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1 - TOXLINE

TI - Arsenic Exposure in Relation to Ischemic Stroke: The Reasons for


Geographic and Racial Differences in Stroke Study.
AU - Tsinovoi CL
AD - From the Departments of Epidemiology and Biostatistics (C.L.T., P.X., K.H.)
and Psychiatry (F.W.U.), Indiana University, Bloomington; Department of
Epidemiology and Biostatistics, Drexel University, Philadelphia, PA (L.A.M.);
University of Missouri Research Reactor Center, University of Missouri, Columbia
(V.M.O.C., J.D.B.); Department of Biostatistics, University of North Carolina at
Chapel Hill (J.C.); Department of Epidemiology, Johns Hopkins University,
Baltimore, MD (E.G.); Department of Medicine, Larner College of Medicine at the
University of Vermont, Burlington (M.C.); and Department of Epidemiology,
University of Alabama at Birmingham (V.J.H.).
AU - Xun P
AD - From the Departments of Epidemiology and Biostatistics (C.L.T., P.X., K.H.)
and Psychiatry (F.W.U.), Indiana University, Bloomington; Department of
Epidemiology and Biostatistics, Drexel University, Philadelphia, PA (L.A.M.);
University of Missouri Research Reactor Center, University of Missouri, Columbia
(V.M.O.C., J.D.B.); Department of Biostatistics, University of North Carolina at
Chapel Hill (J.C.); Department of Epidemiology, Johns Hopkins University,
Baltimore, MD (E.G.); Department of Medicine, Larner College of Medicine at the
University of Vermont, Burlington (M.C.); and Department of Epidemiology,
University of Alabama at Birmingham (V.J.H.).
AU - McClure LA
AD - From the Departments of Epidemiology and Biostatistics (C.L.T., P.X., K.H.)
and Psychiatry (F.W.U.), Indiana University, Bloomington; Department of
Epidemiology and Biostatistics, Drexel University, Philadelphia, PA (L.A.M.);
University of Missouri Research Reactor Center, University of Missouri, Columbia
(V.M.O.C., J.D.B.); Department of Biostatistics, University of North Carolina at
Chapel Hill (J.C.); Department of Epidemiology, Johns Hopkins University,
Baltimore, MD (E.G.); Department of Medicine, Larner College of Medicine at the
University of Vermont, Burlington (M.C.); and Department of Epidemiology,
University of Alabama at Birmingham (V.J.H.).
AU - Carioni VMO
AD - From the Departments of Epidemiology and Biostatistics (C.L.T., P.X., K.H.)
and Psychiatry (F.W.U.), Indiana University, Bloomington; Department of
Epidemiology and Biostatistics, Drexel University, Philadelphia, PA (L.A.M.);
University of Missouri Research Reactor Center, University of Missouri, Columbia
(V.M.O.C., J.D.B.); Department of Biostatistics, University of North Carolina at
Chapel Hill (J.C.); Department of Epidemiology, Johns Hopkins University,
Baltimore, MD (E.G.); Department of Medicine, Larner College of Medicine at the
University of Vermont, Burlington (M.C.); and Department of Epidemiology,
University of Alabama at Birmingham (V.J.H.).
AU - Brockman JD
AD - From the Departments of Epidemiology and Biostatistics (C.L.T., P.X., K.H.)
and Psychiatry (F.W.U.), Indiana University, Bloomington; Department of
Epidemiology and Biostatistics, Drexel University, Philadelphia, PA (L.A.M.);
University of Missouri Research Reactor Center, University of Missouri, Columbia
(V.M.O.C., J.D.B.); Department of Biostatistics, University of North Carolina at
Chapel Hill (J.C.); Department of Epidemiology, Johns Hopkins University,
Baltimore, MD (E.G.); Department of Medicine, Larner College of Medicine at the
University of Vermont, Burlington (M.C.); and Department of Epidemiology,
University of Alabama at Birmingham (V.J.H.).
AU - Cai J
AD - From the Departments of Epidemiology and Biostatistics (C.L.T., P.X., K.H.)
and Psychiatry (F.W.U.), Indiana University, Bloomington; Department of
Epidemiology and Biostatistics, Drexel University, Philadelphia, PA (L.A.M.);
University of Missouri Research Reactor Center, University of Missouri, Columbia
(V.M.O.C., J.D.B.); Department of Biostatistics, University of North Carolina at
Chapel Hill (J.C.); Department of Epidemiology, Johns Hopkins University,
Baltimore, MD (E.G.); Department of Medicine, Larner College of Medicine at the
University of Vermont, Burlington (M.C.); and Department of Epidemiology,
University of Alabama at Birmingham (V.J.H.).
AU - Guallar E
AD - From the Departments of Epidemiology and Biostatistics (C.L.T., P.X., K.H.)
and Psychiatry (F.W.U.), Indiana University, Bloomington; Department of
Epidemiology and Biostatistics, Drexel University, Philadelphia, PA (L.A.M.);
University of Missouri Research Reactor Center, University of Missouri, Columbia
(V.M.O.C., J.D.B.); Department of Biostatistics, University of North Carolina at
Chapel Hill (J.C.); Department of Epidemiology, Johns Hopkins University,
Baltimore, MD (E.G.); Department of Medicine, Larner College of Medicine at the
University of Vermont, Burlington (M.C.); and Department of Epidemiology,
University of Alabama at Birmingham (V.J.H.).
AU - Cushman M
AD - From the Departments of Epidemiology and Biostatistics (C.L.T., P.X., K.H.)
and Psychiatry (F.W.U.), Indiana University, Bloomington; Department of
Epidemiology and Biostatistics, Drexel University, Philadelphia, PA (L.A.M.);
University of Missouri Research Reactor Center, University of Missouri, Columbia
(V.M.O.C., J.D.B.); Department of Biostatistics, University of North Carolina at
Chapel Hill (J.C.); Department of Epidemiology, Johns Hopkins University,
Baltimore, MD (E.G.); Department of Medicine, Larner College of Medicine at the
University of Vermont, Burlington (M.C.); and Department of Epidemiology,
University of Alabama at Birmingham (V.J.H.).
AU - Unverzagt FW
AD - From the Departments of Epidemiology and Biostatistics (C.L.T., P.X., K.H.)
and Psychiatry (F.W.U.), Indiana University, Bloomington; Department of
Epidemiology and Biostatistics, Drexel University, Philadelphia, PA (L.A.M.);
University of Missouri Research Reactor Center, University of Missouri, Columbia
(V.M.O.C., J.D.B.); Department of Biostatistics, University of North Carolina at
Chapel Hill (J.C.); Department of Epidemiology, Johns Hopkins University,
Baltimore, MD (E.G.); Department of Medicine, Larner College of Medicine at the
University of Vermont, Burlington (M.C.); and Department of Epidemiology,
University of Alabama at Birmingham (V.J.H.).
AU - Howard VJ
AD - From the Departments of Epidemiology and Biostatistics (C.L.T., P.X., K.H.)
and Psychiatry (F.W.U.), Indiana University, Bloomington; Department of
Epidemiology and Biostatistics, Drexel University, Philadelphia, PA (L.A.M.);
University of Missouri Research Reactor Center, University of Missouri, Columbia
(V.M.O.C., J.D.B.); Department of Biostatistics, University of North Carolina at
Chapel Hill (J.C.); Department of Epidemiology, Johns Hopkins University,
Baltimore, MD (E.G.); Department of Medicine, Larner College of Medicine at the
University of Vermont, Burlington (M.C.); and Department of Epidemiology,
University of Alabama at Birmingham (V.J.H.).
AU - He K
AD - From the Departments of Epidemiology and Biostatistics (C.L.T., P.X., K.H.)
and Psychiatry (F.W.U.), Indiana University, Bloomington; Department of
Epidemiology and Biostatistics, Drexel University, Philadelphia, PA (L.A.M.);
University of Missouri Research Reactor Center, University of Missouri, Columbia
(V.M.O.C., J.D.B.); Department of Biostatistics, University of North Carolina at
Chapel Hill (J.C.); Department of Epidemiology, Johns Hopkins University,
Baltimore, MD (E.G.); Department of Medicine, Larner College of Medicine at the
University of Vermont, Burlington (M.C.); and Department of Epidemiology,
University of Alabama at Birmingham (V.J.H.). kahe@indiana.edu.
SO - Stroke. 2018, 01; 49(1):19-26. [Stroke]
AB - BACKGROUND AND PURPOSE: The purpose of this case-cohort study was to
examine urinary arsenic levels in relation to incident ischemic stroke in
the United States.
AB - METHODS: We performed a case-cohort study nested within the REGARDS
(REasons for Geographic and Racial Differences in Stroke) cohort. A
subcohort (n=2486) of controls was randomly sampled within region-race-sex
strata while all incident ischemic stroke cases from the full REGARDS
cohort (n=671) were included. Baseline urinary arsenic was measured by
inductively coupled plasma-mass spectrometry. Arsenic species, including
urinary inorganic arsenic and its metabolites monomethylarsonic acid and
dimethylarsinic acid, were measured in a random subset (n=199). Weighted
Cox's proportional hazards models were used to calculate hazard ratios and
95% confidence intervals of ischemic stroke by arsenic and its species.
AB - RESULTS: The average follow-up was 6.7 years. Although incident ischemic
stroke showed no association with total arsenic or total inorganic
arsenic, for each unit higher level of urinary monomethylarsonic acid on a
log-scale, after adjustment for potential confounders, ischemic stroke
risk increased ≈2-fold (hazard ratio=1.98; 95% confidence interval:
1.12-3.50). Effect modification by age, race, sex, or geographic region
was not evident.
AB - CONCLUSIONS: A metabolite of arsenic was positively associated with
incident ischemic stroke in this case-cohort study of the US general
population, a low-to-moderate exposure area. Overall, these findings
suggest a potential role for arsenic methylation in the pathogenesis of
stroke, having important implications for future cerebrovascular research.
KW - *arsenic
KW - *environment exposures
KW - *minerals
KW - *monomethylarsonic acid
KW - *risk
KW - *stroke
KW - *trace elements
RN - J37VJ5709S
RN - N712M78A8G
LA - eng
IS - 1524-4628 (Electronic)
PT - Journal Article
PT - Multicenter Study
PT - Randomized Controlled Trial
PT - Research Support, N.I.H., Extramural
PT - Research Support, U.S. Gov't, Non-P.H.S.
TA - Stroke
YR - 2018
DATE- 20180315
CI - © 2017 American Heart Association, Inc.
CITO- NLM
CS - United States
CSET- IM
FJT - Stroke
EDAT- 20171206
STAT- MEDLINE
CM - Cites: Curr Atheroscler Rep. 2012 Dec;14(6):542-55 (medline /22968315)
CM - Cites: Sci Prog. 1999;82 ( Pt 1):69-88 (medline /10445007)
CM - Cites: Environ Res. 1993 Feb;60(2):161-77 (medline /8472646)
CM - Cites: Toxicol Lett. 2002 Jul 7;133(1):1-16 (medline /12076506)
CM - Cites: Neuroepidemiology. 2005;25(3):135-43 (medline /15990444)
CM - Cites: Biometrics. 1994 Dec;50(4):1064-72 (medline /7786988)
CM - Cites: Am J Epidemiol. 2007 Dec 15;166(12):1381-91 (medline /17875584)
CM - Cites: Ann Intern Med. 2013 Nov 19;159(10):649-59 (medline /24061511)
CM - Cites: Stroke. 2010 Nov;41(11):2499-504 (medline /20947858)
CM - Cites: Talanta. 2017 Apr 1;165:76-83 (medline /28153322)
CM - Cites: Toxicol Appl Pharmacol. 2010 Sep 1;247(2):138-45 (medline
/20600216)
CM - Cites: Environ Health. 2007 Jan 18;6:1 (medline /17233918)
CM - Cites: Am J Epidemiol. 2012 Jun 15;175(12):1252-61 (medline /22534204)
CM - Cites: Int J Environ Res Public Health. 2009 Mar;6(3):1107-23 (medline
/19440436)
CM - Cites: Arch Toxicol. 2000 Aug;74(6):289-99 (medline /11005674)
CM - Cites: J Environ Qual. 2014 Jan;43(1):379-88 (medline /25602572)
CM - Cites: Ann Neurol. 2011 Apr;69(4):619-27 (medline /21416498)
CM - Cites: J Chromatogr Sci. 1999 Sep;37(9):330-44 (medline /10497786)
CM - Cites: Circulation. 2016 Jan 26;133(4):447-54 (medline /26811276)
CM - Cites: Environ Int. 2012 Feb;39(1):150-71 (medline /22208756)
CM - Cites: Am J Kidney Dis. 2008 Aug;52(2):227-34 (medline /18585836)
CM - Cites: Biometrics. 2004 Dec;60(4):1015-24 (medline /15606422)
CM - Cites: Int J Hyg Environ Health. 2015 Aug;218(6):564-74 (medline
/26118750)
CM - Cites: Environ Health. 2007 Feb 02;6:4 (medline /17274811)
CM - Cites: Water Res. 2010 Nov;44(19):5770-6 (medline /20561663)
CM - Cites: Environ Health Perspect. 2013 Jul;121(7):832-8 (medline /23665672)
CM - Cites: Environ Health Perspect. 2003 Aug;111(11):1429-38 (medline
/12928151)
CM - Cites: Stroke. 1995 Jul;26(7):1145-9 (medline /7604404)
CM - Cites: Stroke. 2001 Oct;32(10):2213-20 (medline /11588303)
CM - Cites: Stroke. 1997 Sep;28(9):1717-23 (medline /9303014)
CM - Cites: Environ Health Perspect. 2009 Sep;117(9):1428-33 (medline
/19750109)
CM - Cites: Toxicol Appl Pharmacol. 2004 Aug 1;198(3):327-35 (medline
/15276412)
CM - Cites: Environ Res. 2012 Feb;113:52-7 (medline /22341486)
CM - Cites: Sci Total Environ. 1985 Jun;43(3):255-83 (medline /4012298)
CM - Cites: BMC Public Health. 2014 Feb 18;14:174 (medline /24548416)
CM - Cites: N Engl J Med. 1999 Jan 14;340(2):115-26 (medline /9887164)
CM - Cites: Environ Res. 2010 Jul;110(5):448-54 (medline /19880104)
CM - Cites: Proc Natl Acad Sci U S A. 2011 Dec 20;108(51):20656-60 (medline
/22143778)
CM - Cites: Int J Environ Res Public Health. 2009 Mar;6(3):1010-25 (medline
/19440430)
CM - Cites: BMJ. 2011 May 05;342:d2431 (medline /21546419)
CM - Cites: Environ Res. 2005 Oct;99(2):164-8 (medline /16194666)
CM - Cites: Stroke. 1997 May;28(5):936-40 (medline /9158628)
CM - Cites: Toxicology. 2000 Jul 5;147(3):157-66 (medline /10924798)
CM - Cites: Stroke. 2013 Jul;44(7):1909-14 (medline /23743971)
DOCNO- medline/29212736

2 - TOXLINE
TI - Arsenic Speciation and Accumulation in Selected Organs after Oral
Administration of Rice Extracts in Wistar Rats.
AU - Lewchalermvong K
AD - Center of Excellence on Environmental Health and Toxicology (EHT) , Ministry
of Education , Bangkok 10400 , Thailand.
AU - Rangkadilok N
AD - Center of Excellence on Environmental Health and Toxicology (EHT) , Ministry
of Education , Bangkok 10400 , Thailand.
AU - Nookabkaew S
AD - Center of Excellence on Environmental Health and Toxicology (EHT) , Ministry
of Education , Bangkok 10400 , Thailand.
AU - Suriyo T
AD - Center of Excellence on Environmental Health and Toxicology (EHT) , Ministry
of Education , Bangkok 10400 , Thailand.
AU - Satayavivad J
AD - Center of Excellence on Environmental Health and Toxicology (EHT) , Ministry
of Education , Bangkok 10400 , Thailand.
SO - J Agric Food Chem. 2018, Mar 28; 66(12):3199-3209. [Journal of
agricultural and food chemistry]
AB - Despite its nutritional values, rice also contains arsenic. There has been
increasing concern about health implications associated with exposure to
arsenic through rice consumption. The present study evaluated arsenic
accumulation and its speciation in selected organs of Wistar rats after 28
day repeated oral administrations of polished or unpolished rice and their
control arsenic compounds (sodium arsenite or dimethylarsinic acid; DMA).
Only the treatment of sodium arsenite (2 μg/kg body weight),
significantly increased total arsenic concentrations in blood when
compared to the distilled water control group. In all groups, total
arsenic concentrations were highest in kidney (1.54-1.90 mg/kg) followed
by liver (0.85-1.52 mg/kg), and the predominant arsenic form in these
organs was DMA. However, there was no significant difference in arsenic
accumulation in the measured organs among the control and rice-treated
groups. Therefore, the repeated 28 day administration of
arsenic-contaminated rice did not cause significant arsenic accumulation
in the animal organs.
KW - arsenic accumulation
KW - arsenic speciation
KW - arsenic-contaminated rice
KW - rice extract
RN - N712M78A8G
LA - eng
IS - 1520-5118 (Electronic)
PT - Journal Article
TA - J Agric Food Chem
YR - 2018
DATE- 20180416
CITO- NLM
CS - United States
CSET- IM
FJT - Journal of agricultural and food chemistry
EDAT- 20180319
STAT- MEDLINE
DOCNO- medline/29526085

3 - TOXLINE
TI - Dose and Diet - Sources of Arsenic Intake in Mouse in Utero Exposure
Scenarios.
AU - Murko M
AD - Institute of Chemistry, NAWI Graz, University of Graz , 8010 Graz, Austria.
AU - Elek B
AD - Pharmacokinetics Branch, Integrated Systems Toxicology Division, National
Health and Environmental Effects Laboratory, Office of Research and Development,
United States Environmental Protection Agency , Research Triangle Park, North
Carolina 27709, United States.
AU - Styblo M
AD - Department of Nutrition, Gillings School of Global Public Health, The
University of North Carolina , Chapel Hill, North Carolina 27719, United States.
AU - Thomas DJ
AD - Pharmacokinetics Branch, Integrated Systems Toxicology Division, National
Health and Environmental Effects Laboratory, Office of Research and Development,
United States Environmental Protection Agency , Research Triangle Park, North
Carolina 27709, United States.
AU - Francesconi KA
AD - Institute of Chemistry, NAWI Graz, University of Graz , 8010 Graz, Austria.
SO - Chem Res Toxicol. 2018, Feb 19; 31(2):156-164. [Chemical research in
toxicology]
AB - In humans, early life exposure to inorganic arsenic is associated with
adverse health effects. Inorganic arsenic in utero or in early postnatal
life also produces adverse health effects in offspring of pregnant mice
that consumed drinking water containing low part per billion levels of
inorganic arsenic. Because aggregate exposure of pregnant mice to
inorganic arsenic from both drinking water and food has not been fully
evaluated in experimental studies, quantifying arsenic exposure of the
developing mouse is problematic. Here, we determined levels of total
arsenic and arsenic species in natural ingredient rodent diets that are
composed of many plant and animal-derived foodstuffs and in a purified
ingredient rodent diet that is composed of a more restricted mixture of
foodstuffs. In natural ingredient diets, total arsenic levels ranged from
∼60 to ∼400 parts per billion, and in the purified ingredient
diet, total arsenic level was 13 parts per billion. Inorganic arsenic was
the predominant arsenic species in trifluoroacetic acid extracts of each
diet. Various exposure scenarios were evaluated using information on
inorganic arsenic levels in diet and drinking water and on daily food and
water consumption of pregnant mice. In a scenario in which pregnant mice
consumed drinking water with 10 parts per billion of inorganic arsenic and
a natural ingredient diet containing 89 parts per billion of inorganic
arsenic, drinking water contributed only ∼20% of inorganic arsenic
intake. Quantitation of arsenic species in diets used in studies in which
drinking water is the nominal source of arsenic exposure provides more
accurate dosimetry and improves understanding of dose-response relations.
Use of purified ingredient diets will minimize the discrepancy between the
target dosage level and the actual dosage level attained in utero exposure
studies designed to evaluate effects of low level exposure to inorganic
arsenic.
LA - eng
IS - 1520-5010 (Electronic)
PT - Journal Article
TA - Chem Res Toxicol
YR - 2018
DATE- 20180219
CITO- NLM
CS - United States
FJT - Chemical research in toxicology
EDAT- 20180102
STAT- In-Data-Review
DOCNO- medline/29244955

4 - TOXLINE
TI - Remediation of arsenic in mung bean (Vigna radiata) with growth
enhancement by unique arsenic-resistant bacterium Acinetobacter lwoffii.
AU - Das J
AD - Biosensor Laboratory, Department of Polymer Science and Technology,
University of Calcutta, 92, A.P.C. Road, Kolkata 700009, West Bengal, India.
AU - Sarkar P
AD - Biosensor Laboratory, Department of Polymer Science and Technology,
University of Calcutta, 92, A.P.C. Road, Kolkata 700009, West Bengal, India;
Department of Chemical Engineering, Calcutta Institute of Technology, Banitabla,
Kolkata 711316, West Bengal, India. Electronic address: principalcit@bciedu.org.
SO - Sci Total Environ. 2018, May 15; 624:1106-1118. [The Science of the total
environment]
AB - Arsenic, a carcinogenic and toxic contaminant of soil and water, affects
human health adversely. During last few decades, it has been an important
global environmental issue. Among several arsenic detoxification methods
remediation using arsenic resistant microbes is proved to be
environment-friendly and cost-effective. This study aimed to test the
effects of arsenic utilizing bacterial strain Acinetobacter lwoffii
(RJB-2) on arsenic uptake and growth of mung bean plants (Vigna radiata).
RJB-2 exhibited tolerance up to 125mM of arsenic (V) and 50mM of arsenic
(III). RJB-2 produced plant growth promoting substances e.g. indole acetic
acid (IAA), siderophores, exopolysaccharide (EPS) and phosphate
solubilization in the absence and in presence of arsenic. Pot experiments
were used to scrutinize the role of RJB-2 on arsenic uptake and growth of
mung bean plants grown in soil amended with 22.5mgkg-1 of sodium arsenate
(Na2HAsO4·7H2O). RJB-2 could arrest arsenic uptake in just 7days
and increase plant growth, number of plants per pot, chlorophyll and
carotenoid content of the mung bean plants. RJB-2 formed biofilm and its
root-association helped to abate arsenic uptake in mung bean. Confocal and
light microscopic studies also revealed the abatement of arsenic uptake
and increase in chlorophyll content in mung bean plants in presence of
RJB-2. RJB-2 was also responsible for less production of reactive oxygen
species (ROS) in mung bean plants reducing the oxidative damage caused by
arsenic. The lower percentage of electrolytic leakage (EL) in RJB-2
inoculated mung bean plants proved arsenic abatement. The study also
reported the distribution of arsenic in various parts of mung bean plant.
RJB-2 owing to its intrinsic abilities of plant growth promotion even in
presence of high concentrations of arsenic could inhibit arsenic uptake
completely and therefore it could be used in large-scale cultivation for
phytostabilization of plants.
KW - Acinetobacter lwoffii
KW - Arsenic remediation
KW - Arsenic uptake
KW - Confocal microscopy
KW - Plant growth
KW - Vigna radiata
RN - N712M78A8G
LA - eng
IS - 1879-1026 (Electronic)
PT - Journal Article
TA - Sci Total Environ
YR - 2018
DATE- 20180614
CI - Copyright © 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - The Science of the total environment
EDAT- 20171227
STAT- MEDLINE
DOCNO- medline/29625525

5 - TOXLINE
TI - A novel fungal arsenic methyltransferase, WaarsM reduces grain arsenic
accumulation in transgenic rice (Oryza sativa L.).
AU - Verma S
AD - Genetics and Molecular Biology Division, CSIR-National Botanical Research
Institute, India.
AU - Verma PK
AD - Genetics and Molecular Biology Division, CSIR-National Botanical Research
Institute, India.
AU - Meher AK
AD - Environmental Material Division, CSIR-National Environmental Engineering
Research Institute, India.
AU - Bansiwal AK
AD - Environmental Material Division, CSIR-National Environmental Engineering
Research Institute, India.
AU - Tripathi RD
AD - Plant Ecology and Environmental Science Division, CSIR-National Botanical
Research Institute, India.
AU - Chakrabarty D
AD - Genetics and Molecular Biology Division, CSIR-National Botanical Research
Institute, India. Electronic address: chakrabartyd@nbri.res.in.
SO - J Hazard Mater. 2018, Feb 15; 344(4):626-634. [Journal of hazardous
materials]
AB - Rice (Oryza sativa L.) grown on arsenic-containing soil and water become a
primary dietary source of arsenic and pose a significant health risk. Gene
modification is an important and practical approach to reduce arsenic
accumulation in rice grains. Here, we reported a WaarsM gene of soil
fungus Westerdykella aurantiaca, expressed in rice able to convert toxic
inorganic arsenicals to methylated arsenic species, therefore, reduce
arsenic accumulation in rice grains. In response to arsenic treatment in
hydroponics, WaarsM expressing transgenic lines showed a marked increase
in arsenic resistance and reduces its accumulation compared to NT. Also,
WaarsM expressing transgenic Line 1 evolved ca. 157ng and ca. 43ng
volatile arsenicals (mg-1 fresh weight) after 72h of exposure to 25μM
AsIII and 250μM AsV, respectively. Transgenic Line 1, grown in soil
irrigated with arsenic-containing water accumulates about 50% and 52%
lower arsenic than NT in shoot and root, respectively; while arsenic
concentration in polished seeds and husk of the transgenic line was
reduced by 52% compared to NT. Thus, the present study demonstrates that
the expression of WaarsM in rice induces arsenic methylation and
volatilization, provides a potential strategy to reduce arsenic
accumulation in rice grain.
KW - Arsenic
KW - Arsenic methyltransferase
KW - Rice
KW - Speciation
KW - Volatilization
LA - eng
IS - 1873-3336 (Electronic)
PT - Journal Article
TA - J Hazard Mater
YR - 2018
DATE- 20180103
CI - Copyright © 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Journal of hazardous materials
EDAT- 20171028
STAT- In-Process
DOCNO- medline/29112921

6 - TOXLINE
TI - sEcad and EGF Levels Increased in Urine of Non-ferrous Metal Workers and
Medium of Uroepithelial Cell Line Treated by Arsenic.
AU - Liu J
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
110122, Liaoning Province, People's Republic of China.
AU - Jin P
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
110122, Liaoning Province, People's Republic of China.
AU - Liu S
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
110122, Liaoning Province, People's Republic of China.
AU - Wang F
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
110122, Liaoning Province, People's Republic of China.
AU - Wang X
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
110122, Liaoning Province, People's Republic of China.
AU - Yang L
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
110122, Liaoning Province, People's Republic of China.
AU - Xi S
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
110122, Liaoning Province, People's Republic of China. shxi@cmu.edu.cn.
SO - Biol Trace Elem Res. 2018, May; 183(1):32-39. [Biological trace element
research]
AB - Inorganic arsenic (iAs) is a carcinogen and could increase the risks of
bladder, lung, and skin cancer. Mining and smelting of non-ferrous metals
are common occupational arsenic exposures. In this study, 125 individuals
working in non-ferrous metal smelting plants were separated into two
groups according to urinary total arsenic (TAs) levels: group 1,
TAs < 100 &mu;g/g Cr; group 2,
TAs &ge; 100 &mu;g/g Cr. Demographic characteristics of
participants were obtained by questionnaire interview. Levels of
E-cadherin soluble ectodomain fragment (sEcad) and epidermal growth factor
(EGF) in workers urine were determined by ELISA test. We found that
concentrations of sEcad and EGF present in urine were significantly
elevated in the high urinary arsenic group 2 compared with the low urinary
arsenic group 1. Urinary levels of the shedding of E-cadherin soluble
ectodomain fragment (sEcad) and epidermal growth factor (EGF) were
positively related to the concentrations of iAs in urine after adjusting
for the confounding effects. A positive correlation between sEcad and EGF
concentrations in urine was also observed. In order to verify the effects
of iAs on sEcad and EGF, the human uroepithelial cell line (SV-HUC-1) was
treated with NaAsO2 for 24 h in vitro. sEcad and EGF levels in the
4 &mu;M NaAsO2-treated SV-HUC-1 cell medium significantly increased
compared to the control group. In conclusion, urinary levels of sEcad and
EGF increased in higher urinary arsenic workers of non-ferrous metal
plants and are closely associated with urinary iAs concentration. The
results suggested that sEcad and EGF may potentially be preclinical
prognostic factors of bladder injury and early detection in arsenic
exposure individuals.
KW - Arsenic
KW - EGF
KW - Non-ferrous metals
KW - Uroepithelial cells
KW - sEcad
LA - eng
IS - 1559-0720 (Electronic)
PT - Journal Article
TA - Biol Trace Elem Res
YR - 2018
DATE- 20180406
CITO- NLM
CS - United States
FJT - Biological trace element research
EDAT- 20170817
STAT- In-Process
DOCNO- medline/28819764

7 - TOXLINE
TI - Metabolomic assessment of arsenite toxicity and novel biomarker discovery
in early development of zebrafish embryos.
AU - Wu SY
AD - Department of Radiation Oncology, Wan Fang Hospital, Taipei Medical
University, Taipei, Taiwan; Department of Internal Medicine, School of Medicine,
College of Medicine, Taipei Medical University, Taipei, Taiwan; Graduate Institute
of Biotechnology, Chinese Culture University, YangMingShan, Taipei 11114, Taiwan.
AU - Phan NN
AD - Graduate Institute of Biotechnology, Chinese Culture University,
YangMingShan, Taipei 11114, Taiwan; NTT Institute of Hi-Technology, Nguyen Tat
Thanh University, Ho Chi Minh City, Vietnam.
AU - Ho SH
AD - State Key Lab of Urban Water Resource and Environment, Harbin Institute of
Technology, Harbin, 150090, China.
AU - Lai YH
AD - Department of Chemistry, Chinese Culture University, YangMingShan, Taipei
11114, Taiwan.
AU - Tsai CH
AD - Yu-kang Animal Hospital, Taipei City, Taiwan.
AU - Yang CH
AD - Taiwan Hi-Q Marine Biotech International Ltd, Taiwan.
AU - Yu HG
AD - Graduate Institute of Biotechnology, Chinese Culture University,
YangMingShan, Taipei 11114, Taiwan.
AU - Wang JC
AD - Graduate Institute of Biotechnology, Chinese Culture University,
YangMingShan, Taipei 11114, Taiwan.
AU - Huang PL
AD - Graduate Institute of Biotechnology, Chinese Culture University,
YangMingShan, Taipei 11114, Taiwan.
AU - Lin YC
AD - Graduate Institute of Biotechnology, Chinese Culture University,
YangMingShan, Taipei 11114, Taiwan. Electronic address: LYC10@ulive.pccu.edu.tw.
SO - Toxicol Lett. 2018, Jun 15; 290:116-122. [Toxicology letters]
AB - CONTEXT: Arsenic poisoning commonly occurs through exposure to water
contaminated with arsenic and causes long-term symptoms. Of all the
arsenic derivatives, arsenite is the one of the most toxic compounds.
However, the toxicity of arsenite during developmental stages is still
unclear.
AB - OBJECTIVE: In this study, we performed a metabolomic analysis of arsenite
responses in embryonic zebrafish.
AB - MATERIALS AND METHODS: Embryonic zebrafish were used as an animal model in
this study. They were exposed to sodium arsenite under different
concentrations (0.5, 1.0, 2.0, and 5.0&#8239;mg/L) in 24&#8239;h,
48&#8239;h and 72&#8239;h post fertilization. Changes in morphology were
observed through a light microscope. Changes in metabolomics were
identified using an ultraperformance liquid chromatography quadrupole
time-of-flight system.
AB - RESULTS: The IC50 range was 0.75&#8239;&plusmn;&#8239;0.25&#8239;mg/L.
Compared with the control group, the embryonic lethality rate decreased to
33.3% under 1.0&#8239;mg/L of arsenite treatment, whereas it decreased to
20.0% under 2.0&#8239;mg/L of arsenite treatment. Numerous body axis
curvatures were also observed under treatment with 2.0 and 5.0&#8239;mg/L
of arsenic. Pericardium and yolk sac edema were randomly discovered and
found to worsen over time. Moreover, the 10 metabolites with the highest
variable importance in projection score were identified as potential
biomarkers for arsenic exposure.
AB - CONCLUSION: Arsenic exposure not only leads to a change in the morphology
of embryonic zebrafish but also disturbs the metabolism of zebrafish in
early developmental stages.
KW - Embryonic zebrafish
KW - Metabolomic analysis
KW - Sodium arsenite
RN - 8D239QDW64
RN - N5509X556J
LA - eng
IS - 1879-3169 (Electronic)
PT - Journal Article
TA - Toxicol Lett
YR - 2018
DATE- 20180501
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Toxicology letters
EDAT- 20180315
STAT- MEDLINE
DOCNO- medline/29551592

8 - TOXLINE
TI - Metabolism and disposition of arsenic species from controlled oral dosing
with sodium arsenite in adult female CD-1 mice. I. Pilot study to
determine dosing, analytical measurements, and sampling strategies.
AU - Twaddle NC
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, U.S. Food and Drug Administration, Jefferson, AR 72079, United States.
AU - Vanlandingham M
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, U.S. Food and Drug Administration, Jefferson, AR 72079, United States.
AU - Churchwell MI
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, U.S. Food and Drug Administration, Jefferson, AR 72079, United States.
AU - Doerge DR
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, U.S. Food and Drug Administration, Jefferson, AR 72079, United States.
Electronic address: daniel.doerge@fda.hhs.gov.
SO - Food Chem Toxicol. 2018, Jan; 111:482-493. [Food and chemical toxicology :
an international journal published for the British Industrial Biological
Research Association]
AB - Arsenic (As) is ubiquitous in the earth's crust, with typical dietary
intake in developed countries < 1 &mu;g/kg bw/d, and atypical
groundwater exposures in developing countries approaching
50 &mu;g/kg bw/d. Arsenic exposures are linked with human
diseases and doses of toxicological concern are similar to typical dietary
intake estimates. The methylation of arsenite by
arsenite-3-methyltransferase (As3MT) promotes the clearance of arsenic as
pentavalent species, but also generates reactive trivalent intermediates.
This study measured inorganic arsenic and its metabolites in pentavalent
and trivalent states in blood, tissues, and excreta after oral
administration of arsenite (50-200 &mu;g/kg bw). While liver was a
major site for clearance of arsenite and formation of methylated species,
it also had extensive binding of trivalent intermediates; however, thiol
exchange and oxidation reactions of trivalent arsenic were facile since
dimethylarsinic acid (DMAV) was the predominant species in blood and
urine. Consistent evidence was observed for a non-linear relationship
between doses above 50 &mu;g/kg bw and levels of bound trivalent As
metabolites. The abundance of protein-bound trivalent arsenic within
target tissues should correlate with disruption of critical cellular
processes, which rely on defined interactions of thiol functional groups,
and could provide dose-response relationships from animal models for human
risk assessment.
KW - Arsenic
KW - ICP/MS
KW - Metabolism
KW - Toxicokinetics
RN - 48OVY2OC72
LA - eng
IS - 1873-6351 (Electronic)
PT - Journal Article
TA - Food Chem Toxicol
YR - 2018
DATE- 20180507
CI - Copyright &copy; 2017. Published by Elsevier Ltd.
CITO- NLM
CS - England
CSET- IM
FJT - Food and chemical toxicology : an international journal published for the
British Industrial Biological Research Association
EDAT- 20171205
STAT- MEDLINE
DOCNO- medline/29217265

9 - TOXLINE
TI - Speciation and bioaccessibility of arsenic in traditional Chinese
medicines and assessment of its potential health risk.
AU - Liu L
AD - State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085,
China.
AU - Zhang Y
AD - Wangjing Hospital, China Academy of Chinese Medical Sciences, Beijing 100102,
China.
AU - Yun Z
AD - State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085,
China.
AU - He B
AD - State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085,
China; College of Resources and Environment, University of Chinese Academy of
Sciences, Beijing 100049, China. Electronic address: bhe@rcees.ac.cn.
AU - Zhang Q
AD - State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085,
China; College of Resources and Environment, University of Chinese Academy of
Sciences, Beijing 100049, China.
AU - Hu L
AD - State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085,
China; College of Resources and Environment, University of Chinese Academy of
Sciences, Beijing 100049, China.
AU - Jiang G
AD - State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085,
China; College of Resources and Environment, University of Chinese Academy of
Sciences, Beijing 100049, China.
SO - Sci Total Environ. 2018, Apr 01; 619-620:1088-1097. [The Science of the
total environment]
AB - Arsenic in traditional Chinese medicines (TCMs) has caused public concerns
about its health risk in recent years due to the high toxicity of arsenic
and widespread use of those medicines throughout the world. However, in
previous studies the arsenic toxicity was usually overestimated by
considering the total arsenic concentration only. This work investigated
the total concentration, speciation and bioaccessibility of arsenic in 84
commonly used traditional Chinese patent medicines (CPMs) and Chinese
herbal medicines (CHMs) to evaluate arsenic's potential health risks to
human. Arsenic was found in all the CPMs and 88% of CHMs at concentrations
ranging from 0.033 to 91,000mgkg-1 and 0.012 to 6.6mgkg-1, respectively.
The bioaccessibility of arsenic varied significantly and was in the range
of 0.21%-90% in the CPMs and 15%-96% in the CHMs, with inorganic arsenic
as the predominant species. The average daily intake dose (ADD) and hazard
quotient (HQ) of arsenic in most of medicines were within the safe limits,
while in certain medicines, they exceeded the safe threshold level. These
excesses remind us that the potential health risk by consumption of
several medicines may not be negligible and more control and monitoring of
arsenic in medicines should be carried out.
KW - Arsenic
KW - Bioaccessibility
KW - Simulated gastrointestinal digestion
KW - Speciation
KW - Traditional Chinese medicine
RN - N712M78A8G
LA - eng
IS - 1879-1026 (Electronic)
PT - Journal Article
TA - Sci Total Environ
YR - 2018
DATE- 20180607
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - The Science of the total environment
EDAT- 20171129
STAT- MEDLINE
DOCNO- medline/29734587

10 - TOXLINE
TI - A study of telomere length, arsenic exposure, and arsenic toxicity in a
Bangladeshi cohort.
AU - Zhang C
AD - Department of Public Health Sciences, University of Chicago, Chicago, IL
60615, United States; Department of Epidemiology and Biostatistics, University of
California, San Francisco, San Francisco, CA 94158, United States.
AU - Kibriya MG
AD - Department of Public Health Sciences, University of Chicago, Chicago, IL
60615, United States.
AU - Jasmine F
AD - Department of Public Health Sciences, University of Chicago, Chicago, IL
60615, United States.
AU - Roy S
AD - Department of Public Health Sciences, University of Chicago, Chicago, IL
60615, United States; Centers for Disease Control and Prevention, Atlanta, GA
30329, United States.
AU - Gao J
AD - Department of Public Health Sciences, University of Chicago, Chicago, IL
60615, United States.
AU - Sabarinathan M
AD - Department of Public Health Sciences, University of Chicago, Chicago, IL
60615, United States.
AU - Shinkle J
AD - Department of Public Health Sciences, University of Chicago, Chicago, IL
60615, United States.
AU - Delgado D
AD - Department of Public Health Sciences, University of Chicago, Chicago, IL
60615, United States.
AU - Ahmed A
AD - UChicago Research Bangladesh, Dhaka, Bangladesh.
AU - Islam T
AD - UChicago Research Bangladesh, Dhaka, Bangladesh.
AU - Eunus M
AD - UChicago Research Bangladesh, Dhaka, Bangladesh.
AU - Islam MT
AD - UChicago Research Bangladesh, Dhaka, Bangladesh.
AU - Hasan R
AD - UChicago Research Bangladesh, Dhaka, Bangladesh.
AU - Graziano JH
AD - Department of Environmental Health Sciences, Mailman School of Public Health,
Columbia University, New York, NY 10032, United States.
AU - Ahsan H
AD - Department of Public Health Sciences, University of Chicago, Chicago, IL
60615, United States; Department of Human Genetics, University of Chicago, Chicago,
IL 60615, United States; Comprehensive Cancer Center, University of Chicago,
Chicago, IL 60615, United States; Department of Medicine, University of Chicago,
Chicago, IL 60615, United States.
AU - Pierce BL
AD - Department of Public Health Sciences, University of Chicago, Chicago, IL
60615, United States; Department of Human Genetics, University of Chicago, Chicago,
IL 60615, United States; Comprehensive Cancer Center, University of Chicago,
Chicago, IL 60615, United States. Electronic address: brandonpierce@uchicago.edu.
SO - Environ Res. 2018, Jul; 164:346-355. [Environmental research]
AB - BACKGROUND: Chronic arsenic exposure is associated with increased risk for
arsenical skin lesions, cancer, and other adverse health outcomes. One
potential mechanism of arsenic toxicity is telomere dysfunction. However,
prior epidemiological studies of arsenic exposure, telomere length (TL),
and skin lesion are small and cross-sectional. We investigated the
associations between arsenic exposure and TL and between baseline TL and
incident skin lesion risk among individuals participating in the Health
Effects of Arsenic Longitudinal Study in Bangladesh (2000-2009).
AB - METHODS: Quantitative PCR was used to measure the average TL of peripheral
blood DNA collected at baseline. The association between baseline arsenic
exposure (well water and urine) and TL was estimated in a
randomly-selected subcohort (n&#8239;=&#8239;1469). A nested case-control
study (466 cases and 464 age- and sex-matched controls) was used to
estimate the association between baseline TL and incident skin lesion risk
(diagnosed < &#8239;8 years after baseline).
AB - RESULTS: No association was observed between arsenic exposure (water or
urine) and TL. Among incident skin lesion cases and matched controls, we
observed higher skin lesion risk among individuals with shorter TL (Ptrend
=&#8239;1.5 &times; 10-5) with odds ratios of 2.60, 1.59, and 1.10 for the
first (shortest), second, and third TL quartiles compared to the fourth
(longest).
AB - CONCLUSIONS: Arsenic exposure was not associated with TL among Bangladeshi
adults, suggesting that leukocyte TL may not reflect a primary mode of
action for arsenic's toxicity. However, short TL was associated with
increased skin lesion risk, and may be a biomarker of arsenic
susceptibility modifying arsenic's effect on skin lesion risk.
KW - Arsenic
KW - Bangladesh
KW - Drinking water
KW - Skin lesion
KW - Telomere length
LA - eng
IS - 1096-0953 (Electronic)
PT - Journal Article
TA - Environ Res
YR - 2018
DATE- 20180602
CI - Copyright &copy; 2018. Published by Elsevier Inc.
CITO- NLM
CS - Netherlands
FJT - Environmental research
EDAT- 20180320
STAT- In-Data-Review
DOCNO- medline/29567420

11 - TOXLINE
TI - Effects of Arsenic Compounds on Microminerals Content and Antioxidant
Enzyme Activities in Rat Liver.
AU - Souza ACF
AD - Department of General Biology, Federal University of Vi�osa, Av. P.H. Rolfs,
s/n, Campus Universit�rio, Vi�osa, Minas Gerais, 36570-900, Brazil.
AU - Marchesi SC
AD - Department of General Biology, Federal University of Vi�osa, Av. P.H. Rolfs,
s/n, Campus Universit�rio, Vi�osa, Minas Gerais, 36570-900, Brazil.
AU - de Almeida Lima GD
AD - Department of General Biology, Federal University of Vi�osa, Av. P.H. Rolfs,
s/n, Campus Universit�rio, Vi�osa, Minas Gerais, 36570-900, Brazil.
AU - Machado-Neves M
AD - Department of General Biology, Federal University of Vi�osa, Av. P.H. Rolfs,
s/n, Campus Universit�rio, Vi�osa, Minas Gerais, 36570-900, Brazil.
mariana.mneves@ufv.br.
SO - Biol Trace Elem Res. 2018, Jun; 183(2):305-313. [Biological trace element
research]
AB - Interactions of arsenic with essential trace elements may result in
disturbances on body homeostasis. In the present study, we aimed to
investigate the effects of different arsenic compounds on micromineral
content and antioxidant enzyme activities in rat liver. Male Wistar rats
were randomly divided into five groups and exposed to sodium arsenite and
sodium arsenate at 0.01 and 10 mg/L for 8 weeks in drinking
water. The concentration of arsenic increased in the liver of all
arsenic-exposed animals. The proportion of zinc and copper increased in
animals exposed to 0.01 mg/L sodium arsenite. In addition, these
animals presented a reduction in magnesium and sodium content. Superoxide
dismutase activity decreased mainly in arsenite-exposed animals, whereas
catalase activity decreased in animals exposed to 10 mg/L sodium
arsenate. Further, exposure to sodium arsenate at 10 mg/L altered
copper and magnesium content in the liver, and reduced total protein
levels. Overall, both arsenic compounds altered the liver histology, with
reduction in the proportion of cytoplasm and hepatocyte, and increased the
percentage of sinusoidal capillaries and macrophages. In conclusion, our
findings showed that oral exposure to arsenic compounds disturbs the trace
elements balance in the liver, especially at low concentration, altering
enzymatic and stereological parameters. We concluded that despite the
increase in trace elements content, the antioxidant enzyme activities were
downregulated and did not prevent morphological alterations in the liver
of animals exposed to both arsenic compounds.
KW - Antioxidant defenses
KW - Arsenate
KW - Arsenite
KW - Hepatotoxicity
KW - Mineral microanalysis
LA - eng
IS - 1559-0720 (Electronic)
PT - Journal Article
TA - Biol Trace Elem Res
YR - 2018
DATE- 20180508
CITO- NLM
CS - United States
FJT - Biological trace element research
EDAT- 20170906
STAT- In-Process
DOCNO- medline/28879625

12 - TOXLINE
TI - A unique arsenic speciation profile in Elaphomyces spp. ("deer
truffles")-trimethylarsine oxide and methylarsonous acid as significant
arsenic compounds.
AU - Braeuer S
AD - Institute of Chemistry, Analytical Chemistry for Health and Environment,
University of Graz, Universitaetsplatz 1, 8010, Graz, Austria.
AU - Borovi&#269;ka J
AD - The Czech Academy of Sciences, Institute of Geology, Rozvojov� 269, 16500,
Prague 6, Czech Republic.
AU - Goessler W
AD - Institute of Chemistry, Analytical Chemistry for Health and Environment,
University of Graz, Universitaetsplatz 1, 8010, Graz, Austria. walter.goessler@uni-
graz.at.
SO - Anal Bioanal Chem. 2018, Mar; 410(9):2283-2290. [Analytical and
bioanalytical chemistry]
AB - Arsenic and its species were investigated for the first time in nine
collections of Elaphomyces spp. ("deer truffles") from the Czech Republic
with inductively coupled plasma mass spectrometry (ICPMS) and
high-performance liquid chromatography coupled to ICPMS. The total arsenic
concentrations ranged from 12 to 42 mg kg-1 dry mass in samples of E.
asperulus and from 120 to 660 mg kg-1 dry mass in E. granulatus and
E. muricatus. These concentrations are remarkably high for terrestrial
organisms and demonstrate the arsenic-accumulating ability of these fungi.
The dominating arsenic species in all samples was methylarsonic acid which
accounted for more than 30% of the extractable arsenic. Arsenobetaine,
dimethylarsinic acid, and inorganic arsenic were present as well, but only
at trace concentrations. Surprisingly, we found high amounts of
trimethylarsine oxide in all samples (0.32-28% of the extractable
arsenic). Even more remarkable was that all but two samples contained
significant amounts of the highly toxic trivalent arsenic compound
methylarsonous acid (0.08-0.73% of the extractable arsenic). This is the
first report of the occurrence of trimethylarsine oxide and methylarsonous
acid at significant concentrations in a terrestrial organism. Our findings
point out that there is still a lot to be understood about the
biotransformation pathways of arsenic in the terrestrial environment.
Graphical abstract Trimethylarsine oxide and methylarsonous acid in "deer
truffles".
KW - Arsenic speciation
KW - Deer truffles
KW - Elaphomyces
KW - Fungi
KW - Methylarsonous acid
KW - Trimethylarsine oxide
RN - 4964-14-1
RN - J37VJ5709S
LA - eng
IS - 1618-2650 (Electronic)
PT - Journal Article
TA - Anal Bioanal Chem
YR - 2018
DATE- 20180501
CITO- NLM
CS - Germany
CSET- IM
FJT - Analytical and bioanalytical chemistry
EDAT- 20180212
STAT- MEDLINE
CM - Cites: Chem Res Toxicol. 2014 Apr 21;27(4):457-61 (medline /24517124)
CM - Cites: Sci Total Environ. 2007 May 15;377(2-3):308-18 (medline /17391732)
CM - Cites: Chemosphere. 2008 Apr;71(8):1522-30 (medline /18179812)
CM - Cites: J Sep Sci. 2015 Mar;38(6):943-50 (medline /25594186)
CM - Cites: Toxicol Appl Pharmacol. 2000 Mar 1;163(2):203-7 (medline /10698679)
CM - Cites: Analyst. 2004 May;129(5):373-95 (medline /15116227)
CM - Cites: Arch Toxicol. 2013 Jun;87(6):969-79 (medline /22811022)
CM - Cites: Food Chem. 2018 Mar 1;242:225-231 (medline /29037683)
CM - Cites: Arch Environ Contam Toxicol. 2007 Jan;52(1):38-46 (medline
/17031752)
CM - Cites: Chem Res Toxicol. 2000 Aug;13(8):693-7 (medline /10956055)
CM - Cites: Anal Chem. 2008 Feb 1;80(3):775-82 (medline /18181583)
CM - Cites: Analyst. 2003 Jun;128(6):796-802 (medline /12866906)
CM - Cites: Environ Sci Technol. 2014 Dec 16;48(24):14203-10 (medline
/25417842)
CM - Cites: Anal Methods. 2012;4(2):406-413 (medline /22685491)
CM - Cites: Persoonia. 2017 Jun;38:197-239 (medline /29151633)
CM - Cites: Environ Health Perspect. 2013 Mar;121(3):295-302 (medline
/23458756)
CM - Cites: J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2016
Oct;34(4):217-232 (medline /27635858)
DOCNO- medline/29430602
13 - TOXLINE
TI - Flavonoids inhibit chronically exposed arsenic-induced proliferation and
malignant transformation of HaCaT cells.
AU - Rajput M
AD - Cancer Biology Laboratory, School of Life Sciences, Jawaharlal Nehru
University, New Delhi, India.
AU - Kujur PK
AD - Cancer Biology Laboratory, School of Life Sciences, Jawaharlal Nehru
University, New Delhi, India.
AU - Mishra A
AD - Cancer Biology Laboratory, School of Life Sciences, Jawaharlal Nehru
University, New Delhi, India.
AU - Singh RP
AD - School of Life Sciences, Central University of Gujarat, Gandhinagar, Gujarat,
India.
SO - Photodermatol Photoimmunol Photomed. 2018, Jan; 34(1):91-101.
[Photodermatology, photoimmunology & photomedicine]
AB - BACKGROUND: Apart from exposure to UV-radiation, studies show relationship
between skin cancer and chronic ingestion of arsenic through drinking
water. Chemopreventive strategies could help in reducing the toxic effects
of arsenic and arsenic-induced skin cancer.
AB - METHODS: Cytotoxicity of arsenic on human skin keratinocytes HaCaT cells
was evaluated using MTT and trypan blue assays. Arsenic-induced malignant
transformant HaCaT cells were selected through soft agar colony assay.
Cell cycle progression was analyzed through FACS. The expressions of genes
modulated by arsenic were studied through RT-PCR.
AB - RESULTS: The lower concentrations (0.1-0.5 &mu;mol/L) of arsenic were
non-toxic and transformed HaCaT cells on chronic exposure, and also
enhanced the cell proliferation. Silibinin and fisetin reduced the
arsenic-induced cell proliferation and malignant transformation. A slight
increase in G2-M phase cell population was also observed. The
anti-proliferation effects of flavonoids on HaCaT transformants were
further enhanced when combined with gamma radiation. Chronic and acute
exposure to arsenic modulated the expression of transformation-associated
genes including Bcl-2A1, IGFL-1, Rab31, and TNC in HaCaT cells.
AB - CONCLUSIONS: Chronic exposure to lower arsenic concentrations caused
malignant transformation of skin keratinocytes and that effect was
attenuated by flavonoids silibinin and fisetin. Thus, chemoprevention
could reduce arsenic-caused detrimental effects on skin cells.
KW - arsenic
KW - chemoprevention
KW - phytochemicals
KW - skin cancer
KW - transformation
LA - eng
IS - 1600-0781 (Electronic)
PT - Journal Article
TA - Photodermatol Photoimmunol Photomed
YR - 2018
DATE- 20180109
CI - &copy; 2017 John Wiley &amp; Sons A/S. Published by John Wiley &amp; Sons
Ltd.
CITO- NLM
CS - England
FJT - Photodermatology, photoimmunology &amp; photomedicine
EDAT- 20171128
STAT- In-Process
DOCNO- medline/29049844
14 - TOXLINE
TI - Assessment of arsenic oxidation potential of Microvirga indica S-MI1b sp.
nov. in heavy metal polluted environment.
AU - Tapase SR
AD - Biochemistry Division, Department of Chemistry, Savitribai Phule Pune
University, Pune, 411007, India.
AU - Kodam KM
AD - Biochemistry Division, Department of Chemistry, Savitribai Phule Pune
University, Pune, 411007, India. Electronic address: kodam@chem.unipune.ac.in.
SO - Chemosphere. 2018, Mar; 195:1-10. [Chemosphere]
AB - Arsenic oxidizing &alpha;-proteobacterial strain Microvirga indica S-MI1b
sp. nov. was isolated from metal industry soil and has the ability to
oxidize 15 mM of arsenite [As(III)] completely in 39 h. The
strain S-MI1b resists to different heavy metals and it oxidizes arsenite
in presence of Li, Pb, Hg, Sb(III), Cd, Cr(VI), Ni, and exhibited growth
inhibitory effect in presence of Hg, Cu, and Cd at higher concentration.
The morphology of Microvirga indica S-MI1b changed in presence of heavy
metals however there was no accumulation of As(III) in the cells. The
study showed that Microvirga indica S-MI1b can oxidize arsenite at broad
pH ranges from 4.0 to 9.0 with optimum at pH 7.0. The kinetic studies of
arsenite oxidation by strain S-MI1b signified that it has greater affinity
towards As(III). The arsenite oxidase activity of cells grown in presence
of Li and Cr(VI) supported the cell culture studies. This is first report
on biotransformation of arsenite by Microvirga genus and also arsenite
oxidation in presence of heavy metals.
KW - Arsenic biotransformation
KW - Arsenite oxidase
KW - Heavy metals
KW - Microvirga indica
RN - N5509X556J
RN - N712M78A8G
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180515
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171206
STAT- MEDLINE
DOCNO- medline/29241075

15 - TOXLINE
TI - A new aerobic chemolithoautotrophic arsenic oxidizing microorganism
isolated from a high Andean watershed.
AU - Anguita JM
AD - Centro de Desarrollo Urbano Sustentable (CEDEUS), Santiago, Chile.
AU - Rojas C
AD - Institute of Agricultural Sciences, University of O'Higgins, Rancagua, Chile.
AU - Past�n PA
AD - Centro de Desarrollo Urbano Sustentable (CEDEUS), Santiago, Chile.
AU - Vargas IT
AD - Centro de Desarrollo Urbano Sustentable (CEDEUS), Santiago, Chile.
itvargas@ing.puc.cl.
SO - Biodegradation. 2018, 02; 29(1):59-69. [Biodegradation]
AB - Biological arsenic oxidation has been suggested as a key biogeochemical
process that controls the mobilization and fate of this metalloid in
aqueous environments. To the best of our knowledge, only four aerobic
chemolithoautotrophic arsenite-oxidizing (CAO) bacteria have been shown to
grow via direct arsenic oxidation and to have the essential genes for
chemolithoautotrophic arsenite oxidation. In this study, a new CAO
bacterium was isolated from a high Andean watershed evidencing natural
dissolved arsenic attenuation. The bacterial isolate, designated TS-1, is
closely related to the Ancylobacter genus, in the Alphaproteobacteria
class. Results showed that TS-1 has genes for arsenite oxidation and
carbon fixation. The dependence of bacterial growth from arsenite
oxidation was demonstrated. In addition, a mathematical model was
suggested and the kinetic parameters were obtained by simultaneously
fitting the biomass growth, arsenite depletion curves, and arsenate
production. This research increases the knowledge of chemolithoautotrophic
arsenic oxidizing microorganisms and its potential role as a driver for
natural arsenic attenuation.
KW - *Arsenic
KW - *Biogeochemistry
KW - *Biotransformation
KW - *Chemolithoautotrophic arsenite-oxidizing (CAO) bacteria
RN - N712M78A8G
LA - eng
IS - 1572-9729 (Electronic)
PT - Journal Article
PT - Research Support, Non-U.S. Gov't
TA - Biodegradation
YR - 2018
DATE- 20180430
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Biodegradation
EDAT- 20171116
STAT- MEDLINE
DOCNO- medline/29143902

16 - TOXLINE
TI - Decreasing arsenic accumulation in rice by overexpressing OsNIP1;1 and
OsNIP3;3 through disrupting arsenite radial transport in roots.
AU - Sun SK
AD - State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of
Resources and Environmental Sciences, Nanjing Agricultural University, Nanjing,
210095, China.
AU - Chen Y
AD - Department of Metabolic Biology, John Innes Centre, Norwich Research Park,
Norwich, NR4 7UH, UK.
AU - Che J
AD - Institute of Plant Science and Resources, Okayama University, Chuo 2-20-1,
Kurashiki, 710-0046, Japan.
AU - Konishi N
AD - Institute of Plant Science and Resources, Okayama University, Chuo 2-20-1,
Kurashiki, 710-0046, Japan.
AU - Tang Z
AD - State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of
Resources and Environmental Sciences, Nanjing Agricultural University, Nanjing,
210095, China.
AU - Miller AJ
AD - Department of Metabolic Biology, John Innes Centre, Norwich Research Park,
Norwich, NR4 7UH, UK.
AU - Ma JF
AD - Institute of Plant Science and Resources, Okayama University, Chuo 2-20-1,
Kurashiki, 710-0046, Japan.
AU - Zhao FJ
AD - State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of
Resources and Environmental Sciences, Nanjing Agricultural University, Nanjing,
210095, China.
SO - New Phytol. 2018, May 11. [The New phytologist]
AB - Rice is a major dietary source of the toxic metalloid arsenic. Reducing
arsenic accumulation in rice grain is important for food safety. We
generated transgenic rice overexpressing two aquaporin genes, OsNIP1;1 and
OsNIP3;3, under the control of a maize ubiquitin promoter or the rice
OsLsi1 promoter, and tested the effect on arsenite uptake and
translocation. OsNIP1;1 and OsNIP3;3 were highly permeable to arsenite in
Xenopus oocyte assays. Both transporters were localized at the plasma
membrane. Knockout of either gene had little effect on arsenite uptake or
translocation. Overexpression of OsNIP1;1 or OsNIP3;3 in rice did not
affect arsenite uptake but decreased root-to-shoot translocation of
arsenite and shoot arsenic concentration markedly. The overexpressed
OsNIP1;1 and OsNIP3;3 proteins were localized in all root cells without
polarity. Expression of OsNIP1;1 driven by the OsLsi1 promoter produced
similar effects. When grown in two arsenic-contaminated paddy soils,
overexpressing lines contained significantly lower arsenic concentration
in rice grain than the wild-type without compromising plant growth or the
accumulation of essential nutrients. Overexpression of OsNIP1;1 or
OsNIP3;3 provides a route for arsenite to leak out of the stele, thus
restricting arsenite loading into the xylem. This strategy is effective in
reducing arsenic accumulation in rice grain.
KW - Nodulin 26-like Intrinsic Proteins
KW - arsenic
KW - arsenite
KW - radial transport
KW - rice
KW - root-to-shoot translocation
LA - eng
IS - 1469-8137 (Electronic)
PT - Journal Article
TA - New Phytol
YR - 2018
DATE- 20180511
CI - &copy; 2018 The Authors. New Phytologist &copy; 2018 New Phytologist
Trust.
CITO- NLM
CS - England
FJT - The New phytologist
EDAT- 20180511
STAT- Publisher
DOCNO- medline/29749629

17 - TOXLINE
TI - Arsenic concentrations and speciation in wild birds from an abandoned
realgar mine in China.
AU - Yang F
AD - Institute of Geographic Sciences and Natural Resources Research, Chinese
Academy of Sciences, Beijing, 100101, China; Key Laboratory of Land Surface Pattern
and Simulation, Chinese Academy of Sciences, Beijing, 100101, China; University of
Chinese Academy of Sciences, Beijing, 100049, China.
AU - Xie S
AD - Institute of Geographic Sciences and Natural Resources Research, Chinese
Academy of Sciences, Beijing, 100101, China; Key Laboratory of Land Surface Pattern
and Simulation, Chinese Academy of Sciences, Beijing, 100101, China; University of
Chinese Academy of Sciences, Beijing, 100049, China.
AU - Liu J
AD - Institute of Geographic Sciences and Natural Resources Research, Chinese
Academy of Sciences, Beijing, 100101, China; Key Laboratory of Land Surface Pattern
and Simulation, Chinese Academy of Sciences, Beijing, 100101, China; University of
Chinese Academy of Sciences, Beijing, 100049, China.
AU - Wei C
AD - Institute of Geographic Sciences and Natural Resources Research, Chinese
Academy of Sciences, Beijing, 100101, China; Key Laboratory of Land Surface Pattern
and Simulation, Chinese Academy of Sciences, Beijing, 100101, China. Electronic
address: weicy@igsnrr.ac.cn.
AU - Zhang H
AD - Institute of Geographic Sciences and Natural Resources Research, Chinese
Academy of Sciences, Beijing, 100101, China.
AU - Chen T
AD - University of Chinese Academy of Sciences, Beijing, 100049, China; Beijing
Synchrotron Radiation Facility, Institute of High Energy Physics, Chinese Academy
of Sciences, Beijing, 100049, China.
AU - Zhang J
AD - Beijing Synchrotron Radiation Facility, Institute of High Energy Physics,
Chinese Academy of Sciences, Beijing, 100049, China.
SO - Chemosphere. 2018, Feb; 193:777-784. [Chemosphere]
AB - Birds are at a higher level in the food chain; however, the potential
bioaccumulation and biotransformation of arsenic (As) in birds in As mines
has rarely been studied. In this study, four passerine bird species (tree
sparrow [Passer montanus], light-vented bulbul [Pycnonotus sinensis],
Garrulax canorus [Leucodioptron canorus], and magpie [Pica pica]) were
collected from an abandoned As mine in China. The highest recorded As
concentrations were 4.95 mg/kg and 51.65 mg/kg in muscles and
feathers, respectively. Detection using high-performance liquid
chromatography inductively coupled plasma mass spectrometry (HPLC-ICP-MS)
revealed six As species, including arsenite (As(III)), arsenate (As(V)),
dimethylarsinic acid (DMA), monomethylarsonic acid (MMA), arsenobetaine
(AsB) and arsenocholine (AsC), with the former three species as the
dominant ( > 92%) and the latter three as the minor As species
( < 6.17%). Further analysis of the selected bird samples using the X-ray
absorption near edge structure (XANES) technique revealed the existence of
As(III)-tris-glutathione (As(III)-GSH), which can be regarded as
equivalent to the non-extractable and unidentified As form in the
HPLC-ICP-MS data. Both methods revealed similar patterns of As species in
the birds from the As mine, with muscles containing mainly inorganic As
and DMA and feathers containing mainly inorganic As. The results of this
study contribute to the knowledge regarding As accumulation and speciation
in terrestrial organisms.
KW - Arsenic
KW - Feathers
KW - HPLC-ICP-MS
KW - Muscles
KW - XANES
RN - 39895-81-3
RN - 56320-22-0
RN - AJ2HL7EU8K
RN - J37VJ5709S
RN - N5509X556J
RN - N712M78A8G
RN - N7CIZ75ZPN
RN - UWC1LS4V3I
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180309
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171120
STAT- MEDLINE
DOCNO- medline/29175405

18 - TOXLINE
TI - Phytofiltration of arsenic by aquatic moss (Warnstorfia fluitans).
AU - Sandhi A
AD - Department of Ecology, Environment and Plant Sciences, Stockholm University,
Svante Arrhenius v�g 20A, SE-106 91 Stockholm, Sweden; Land and Water Resources
Engineering Division, Department of Sustainable Development, Environmental Science
and Engineering, KTH Royal Institute of Technology, Teknikringen 76, SE-100 44
Stockholm, Sweden. Electronic address: asandhi@kth.se.
AU - Landberg T
AD - Department of Ecology, Environment and Plant Sciences, Stockholm University,
Svante Arrhenius v�g 20A, SE-106 91 Stockholm, Sweden.
AU - Greger M
AD - Department of Ecology, Environment and Plant Sciences, Stockholm University,
Svante Arrhenius v�g 20A, SE-106 91 Stockholm, Sweden.
SO - Environ Pollut. 2018, Jun; 237:1098-1105. [Environmental pollution
(Barking, Essex : 1987)]
AB - This work investigates whether aquatic moss (Warnstorfia fluitans)
originating from an arsenic (As)-contaminated wetland close to a mine
tailings impoundment may be used for phytofiltration of As. The aim was to
elucidate the capacity of W. fluitans to remove As from arsenite and
arsenate contaminated water, how nutrients affect the As uptake and the
proportion of As adsorption and absorption by the moss plant, which
consists of dead and living parts. Arsenic removal from 0, 1, or 10%
Hoagland nutrient solution containing 0-100 &mu;M arsenate was
followed over 192 h, and the total As in aquatic moss after treatment
was analysed. The uptake and speciation of As in moss cultivated in water
containing 10 &mu;M arsenate or arsenite were examined as As uptake
in living (absorption + adsorption) and dead (adsorption) plant
parts. Results indicated that W. fluitans removed up to 82% of As
from the water within one hour when 1 &mu;M arsenate was added in the
absence of nutrients. The removal time increased with greater nutrient and
As concentrations. Up to 100 &mu;M As had no toxic effect on the
plant biomass. Both arsenite and arsenate were removed from the solution
to similar extents and, independent of the As species added, more arsenate
than arsenite was found in the plant. Of the As taken up, over 90% was
firmly bound to the tissue, a possible mechanism for resisting high As
concentrations. Arsenic was both absorbed and adsorbed by the moss, and
twice as much As was found in living parts as in dead moss tissue. This
study revealed that W. fluitans has potential to serve as a
phytofilter for removing As from As-contaminated water without displaying
any toxic effects of the metalloid.
KW - Absorption
KW - Adsorption
KW - Aquatic moss
KW - Arsenic removal
KW - Arsenic speciation
KW - Arsenic uptake
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180419
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Environmental pollution (Barking, Essex : 1987)
EDAT- 20171120
STAT- In-Process
DOCNO- medline/29157972

19 - TOXLINE
TI - Arsenic hyperaccumulation and speciation in the edible ink stain bolete
(Cyanoboletus pulverulentus).
AU - Braeuer S
AD - University of Graz, Institute of Chemistry, Universit�tsplatz 1, 8010 Graz,
Austria.
AU - Goessler W
AD - University of Graz, Institute of Chemistry, Universit�tsplatz 1, 8010 Graz,
Austria.
AU - Kamen�k J
AD - Nuclear Physics Institute, The Czech Academy of Sciences, Hlavn� 130, 25068
Husinec-&#344;e&#382;, Czech Republic.
AU - Konvalinkov� T
AD - Institute of Microbiology, The Czech Academy of Sciences, V�de&#328;sk� 1083,
14220 Prague 4, Czech Republic.
AU - &#381;igov� A
AD - Institute of Geology, The Czech Academy of Sciences, Rozvojov� 269, 16500
Prague 6, Czech Republic.
AU - Borovi&#269;ka J
AD - Nuclear Physics Institute, The Czech Academy of Sciences, Hlavn� 130, 25068
Husinec-&#344;e&#382;, Czech Republic; Institute of Geology, The Czech Academy of
Sciences, Rozvojov� 269, 16500 Prague 6, Czech Republic. Electronic address:
bore.bor@gmail.com.
SO - Food Chem. 2018, Mar 01; 242:225-231. [Food chemistry]
AB - The edible ink stain bolete (Cyanoboletus pulverulentus) was found to
hyperaccumulate arsenic. We analyzed 39 individual collections determined
as C. pulverulentus, mostly from the Czech Republic. According to our
results, concentrations of arsenic in C. pulverulentus fruit-bodies may
reach 1300mgkg-1 dry weight. In most collections, data for total and
bioavailable arsenic in underlying soils were collected but no significant
correlation between the soil arsenic content and arsenic concentrations in
the associated fruit-bodies was found. Within the fruit-bodies, we found
the majority of arsenic accumulated in the hymenium. Besides occasional
traces of methylarsonic acid (MA), the arsenic speciation in all mushroom
samples consisted solely of dimethylarsinic acid (DMA) and no inorganic
arsenic was detected. Because of the carcinogenic potential of DMA, C.
pulverulentus should not be recommended as an edible mushroom and its
consumption should be restricted.
KW - Dimethylarsinic acid
KW - Edible mushrooms
KW - HPLC-ICPMS
KW - Health risk
KW - Soil
LA - eng
IS - 0308-8146 (Print)
PT - Journal Article
TA - Food Chem
YR - 2018
DATE- 20171017
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Food chemistry
EDAT- 20170908
STAT- In-Process
DOCNO- medline/29037683

20 - TOXLINE
TI - Fertility in male rats: Disentangling adverse effects of arsenic
compounds.
AU - Lima GDA
AD - Department of General Biology, Federal University of Vi�osa (UFV), Vi�osa,
Minas Gerais, 36570-900, Brazil.
AU - Sertorio MN
AD - Department of General Biology, Federal University of Vi�osa (UFV), Vi�osa,
Minas Gerais, 36570-900, Brazil.
AU - Souza ACF
AD - Department of General Biology, Federal University of Vi�osa (UFV), Vi�osa,
Minas Gerais, 36570-900, Brazil.
AU - Menezes TP
AD - Department of General Biology, Federal University of Vi�osa (UFV), Vi�osa,
Minas Gerais, 36570-900, Brazil.
AU - Mouro VGS
AD - Department of General Biology, Federal University of Vi�osa (UFV), Vi�osa,
Minas Gerais, 36570-900, Brazil.
AU - Gon�alves NM
AD - Department of General Biology, Federal University of Vi�osa (UFV), Vi�osa,
Minas Gerais, 36570-900, Brazil.
AU - Oliveira JM
AD - Department of General Biology, Federal University of Vi�osa (UFV), Vi�osa,
Minas Gerais, 36570-900, Brazil.
AU - Henry M
AD - Department of Veterinary Clinic and Surgery, Veterinary School, Federal
University of Minas Gerais (UFMG), Belo Horizonte, Minas Gerais, 31270-901, Brazil.
AU - Machado-Neves M
AD - Department of General Biology, Federal University of Vi�osa (UFV), Vi�osa,
Minas Gerais, 36570-900, Brazil. Electronic address: mariana.mneves@ufv.br.
SO - Reprod Toxicol. 2018, Jun; 78:130-140. [Reproductive toxicology (Elmsford,
N.Y.)]
AB - Arsenic impairs male reproductive functions. However, it is not clear
whether different arsenic compounds similarly affect fertility. In this
study, we compared the impact of sodium arsenite and arsenate on sperm
quality and fertility. After 56&#8239;d exposure, male Wistar rats were
mated and pregnant females were evaluated by fertility indexes. Clearly,
exposure to 10&#8239;mg/L arsenite reduced daily sperm production via H2O2
overproduction and germ cells loss. Animals from this group also showed a
decrease in epididymal sperm counts and percentage of sperm with intact
membranes. Moreover, they presented low fertility potential and high
preimplantation loss. In contrast, 10&#8239;mg/L arsenate caused oxidative
stress in testis, mineral imbalance in epididymis, and sperm membranes
damage, with no effects on fertility. Both arsenic compounds at
0.01&#8239;mg/L altered reproductive parameters. We concluded that
arsenite is more harmful than arsenate to sperm quality and male
fertility, with negative influences in early pregnancy.
KW - Arsenate
KW - Arsenite
KW - Fertility potential
KW - Reproductive toxicity
KW - Sperm viability
KW - Trace elements imbalance
LA - eng
IS - 1873-1708 (Electronic)
PT - Journal Article
TA - Reprod Toxicol
YR - 2018
DATE- 20180601
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - United States
FJT - Reproductive toxicology (Elmsford, N.Y.)
EDAT- 20180424
STAT- In-Data-Review
DOCNO- medline/29702248

21 - TOXLINE
TI - Chronic arsenic intoxication diagnostic score (CAsIDS).
AU - Dani SU
AD - PizolCare Praxis Wartau, Tr�bbach, Switzerland.
AU - Walter GF
AD - International Neuroscience Institute, Hannover, Germany.
SO - J Appl Toxicol. 2018, Jan; 38(1):122-144. [Journal of applied toxicology :
JAT]
AB - Arsenic and its compounds are well-established, potent, environmentally
widespread and persistent toxicants with metabolic, genotoxic, mutagenic,
teratogenic, epigenetic and carcinogenic effects. Arsenic occurs naturally
in the Earth's crust, but anthropogenic arsenic emissions have surmounted
the emissions from important natural sources such as volcanism. Inorganic
arsenicals exhibit acute and chronic toxicities in virtually all cell
types and tissues, and hence arsenic intoxication affects multiple
systems. Whereas acute arsenic intoxication is rare and relatively easy to
diagnose, chronic arsenic intoxication (CAsI) is common but goes often
misdiagnosed. Based on a review of the literature as well as our own
clinical experience, we propose a chronic arsenic intoxication diagnostic
score (CAsIDS). A distinctive feature of CAsIDS is the use of bone arsenic
load as an essential criterion for the individual risk assessment of
chronic arsenic intoxication, combined with a systemic clinical
assessment. We present clinical examples where CAsIDS is applied for the
diagnosis of CAsI, review the main topics of the toxicity of arsenic in
different cell and organ systems and discuss the therapy and prevention of
disease caused or aggravated by chronic arsenic intoxication. CAsIDS can
help physicians establish the diagnosis of CAsI and associated conditions.
KW - CAsIDS
KW - arsenic
KW - bone
KW - chronic
KW - intoxication
KW - risk assessment
LA - eng
IS - 1099-1263 (Electronic)
PT - Journal Article
PT - Review
TA - J Appl Toxicol
YR - 2018
DATE- 20171124
CI - Copyright &copy; 2017 John Wiley &amp; Sons, Ltd.
CITO- NLM
CS - England
FJT - Journal of applied toxicology : JAT
EDAT- 20170831
STAT- In-Process
DOCNO- medline/28857213

22 - TOXLINE
TI - Arsenic exposure, diabetes-related genes and diabetes prevalence in a
general population from Spain.
AU - Grau-Perez M
AD - Area of Cardiometabolic and Renal Risk, Biomedical Research Institute
Hospital Clinic of Valencia (INCLIVA), Valencia, Spain; Department of Statistics
and Operational Research, University of Valencia, Valencia, Spain; Department of
Environmental Health and Engineering, Columbia University Mailman School of Public
Health, New York, NY, USA.
AU - Navas-Acien A
AD - Department of Environmental Health and Engineering, Columbia University
Mailman School of Public Health, New York, NY, USA; Department of Environmental
Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD,
USA.
AU - Galan-Chilet I
AD - Genomic and Genetic Diagnosis Unit, Biomedical Research Institute Hospital
Clinic of Valencia (INCLIVA), Valencia, Spain.
AU - Briongos-Figuero LS
AD - Department of Internal Medicine, University Hospital Rio Hortega, Valladolid,
Spain.
AU - Morchon-Simon D
AD - Department of Internal Medicine, University Hospital Rio Hortega, Valladolid,
Spain.
AU - Bermudez JD
AD - Department of Statistics and Operational Research, University of Valencia,
Valencia, Spain.
AU - Crainiceanu CM
AD - Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health,
Baltimore, MD, USA.
AU - de Marco G
AD - Genomic and Genetic Diagnosis Unit, Biomedical Research Institute Hospital
Clinic of Valencia (INCLIVA), Valencia, Spain.
AU - Rentero-Garrido P
AD - Genomic and Genetic Diagnosis Unit, Biomedical Research Institute Hospital
Clinic of Valencia (INCLIVA), Valencia, Spain.
AU - Garcia-Barrera T
AD - Department of Chemistry, University of Huelva, Huelva, Spain.
AU - Gomez-Ariza JL
AD - Department of Chemistry, University of Huelva, Huelva, Spain.
AU - Casasnovas JA
AD - Unidad de Investigaci�n en Prevenci�n Cardiovascular, Instituto de
Investigaci�n Sanitaria de Arag�n, CIBER Cardiovascular (CIBERCV), Zaragoza, Spain.
AU - Martin-Escudero JC
AD - Department of Internal Medicine, University Hospital Rio Hortega, Valladolid,
Spain.
AU - Redon J
AD - Area of Cardiometabolic and Renal Risk, Biomedical Research Institute
Hospital Clinic of Valencia (INCLIVA), Valencia, Spain; CIBER Physiopathology of
Obesity and Nutrition (CIBEROBN), Institute of Health Carlos III, Minister of
Health, Madrid, Spain; Department of Internal Medicine, Hospital Cl�nico de
Valencia, Valencia, Spain.
AU - Chaves FJ
AD - Genomic and Genetic Diagnosis Unit, Biomedical Research Institute Hospital
Clinic of Valencia (INCLIVA), Valencia, Spain; CIBER of Diabetes and Associated
Metabolic Diseases (CIBERDEM), Barcelona, Spain. Electronic address:
felipe.chaves@uv.es.
AU - Tellez-Plaza M
AD - Area of Cardiometabolic and Renal Risk, Biomedical Research Institute
Hospital Clinic of Valencia (INCLIVA), Valencia, Spain; Department of Environmental
Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD,
USA.
SO - Environ Pollut. 2018, Apr; 235:948-955. [Environmental pollution (Barking,
Essex : 1987)]
AB - Inorganic arsenic exposure may be associated with diabetes, but the
evidence at low-moderate levels is not sufficient. Polymorphisms in
diabetes-related genes have been involved in diabetes risk. We evaluated
the association of inorganic arsenic exposure on diabetes in the Hortega
Study, a representative sample of a general population from Valladolid,
Spain. Total urine arsenic was measured in 1451 adults. Urine arsenic
speciation was available in 295 randomly selected participants. To account
for the confounding introduced by non-toxic seafood arsenicals, we
designed a multiple imputation model to predict the missing arsenobetaine
levels. The prevalence of diabetes was 8.3%. The geometric mean of total
arsenic was 66.0&#8239;&mu;g/g. The adjusted odds ratios (95% confidence
interval) for diabetes comparing the highest with the lowest tertile of
total arsenic were 1.76 (1.01, 3.09) and 2.14 (1.47, 3.11) before and
after arsenobetaine adjustment, respectively. Polymorphisms in several
genes including IL8RA, TXN, NR3C2, COX5A and GCLC showed suggestive
differential associations of urine total arsenic with diabetes. The
findings support the role of arsenic on diabetes and the importance of
controlling for seafood arsenicals in populations with high seafood
intake. Suggestive arsenic-gene interactions require confirmation in
larger studies.
KW - Arsenic
KW - Arsenic species
KW - Diabetes
KW - Gene-environment interaction
KW - Multiple imputation
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180512
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Environmental pollution (Barking, Essex : 1987)
EDAT- 20180221
STAT- In-Process
DOCNO- medline/29751399

23 - TOXLINE
TI - Dilution of rice with other gluten free grains to lower inorganic arsenic
in foods for young children in response to European Union regulations
provides impetus to setting stricter standards.
AU - Carey M
AD - Institute for Global Food Security, Queen's University Belfast, Belfast,
Northern Ireland.
AU - Donaldson E
AD - Institute for Global Food Security, Queen's University Belfast, Belfast,
Northern Ireland.
AU - Signes-Pastor AJ
AD - Department of Epidemiology, Geisel School of Medicine, Dartmouth College,
Lebanon, New Hampshire, United States of America.
AU - Meharg AA
AD - Institute for Global Food Security, Queen's University Belfast, Belfast,
Northern Ireland.
SO - PLoS One. 2018; 13(3):e0194700. [PloS one]
AB - There has been an increasing realisation that young infants are exposed to
elevated concentrations of the carcinogen inorganic arsenic, relative to
adults. This is because many infant food products are rice based, and rice
is ~10-fold elevated in inorganic arsenic compared to most other foods.
The European Commission (EC) has acted on this concern setting stricter
standards for infants, 100 &mu;g of inorganic arsenic per kg of food (100
&mu;g/kg), as compared to adults (200 &mu;g/kg), for rice based foods, a
law that was brought into place in 1st January 2016. Here we investigate
how this law has impacted on inorganic arsenic in baby food products in
the UK market, and compare the findings to previous baby food surveys
taken before and just after the law came into place. We find that for a
wide range of UK infant products that the new regulations are being
adhered to, with all samples surveyed, being under 100 &mu;g/kg inorganic
arsenic. The prevalence of pure rice products had decreased in the UK, and
there appears to be careful sourcing of the rice used in these products to
ensure conformity with regulations. There has been an increased presence
of mixed cereal products, with rice and maize as the main ingredient,
appearing on the UK market, with varying rice contents for infant
porridges, cakes and mueslis, with the latter being a relatively
innovative product for infant foods. There was a highly significant
correlation (P < 0.0001) between rice content and inorganic arsenic
concentration across all infant foods. When UK infant rice cakes,
breakfast cereals and porridges were compare to their general, i.e. not
labelled specifically for being for infant consumption, equivalent it was
found that the adult foods generally exceeded the 100 &mu;g/kg inorganic
arsenic standard for infant foods. Thus, infants should not be given rice
products not specifically labelled as being for them if a lower inorganic
arsenic diet is to be maintained.
LA - eng
IS - 1932-6203 (Electronic)
PT - Journal Article
TA - PLoS One
YR - 2018
DATE- 20180329
CITO- NLM
CS - United States
FJT - PloS one
EDAT- 20180316
STAT- In-Data-Review
CM - Cites: Food Chem Toxicol. 2015 Oct;84:169-80 (medline /26327433)
CM - Cites: Sci Rep. 2017 Oct 30;7(1):14312 (medline /29085002)
CM - Cites: Environ Pollut. 2008 Apr;152(3):746-9 (medline /18339463)
CM - Cites: J Food Sci. 2012 Jan;77(1):T15-9 (medline /22181972)
CM - Cites: Pure Appl Chem. 2012;84(2):215-223 (medline /22701232)
CM -Cites: PLoS One. 2015 Jul 22;10(7):e0131608 (medline /26200355)
CM -Cites: Environ Pollut. 2012 Apr;163:77-83 (medline /22325434)
CM -Cites: Food Chem. 2016 Jan 15;191:128-34 (medline /26258711)
CM -Cites: Environ Sci Technol. 2009 Mar 1;43(5):1612-7 (medline /19350943)
CM -Cites: Food Chem. 2018 Jan 15;239:132-140 (medline /28873550)
CM -Cites: Environ Sci Technol. 2007 Oct 1;41(19):6854-9 (medline /17969706)
CM -Cites: Environ Res. 2016 May;147:537-55 (medline /26891939)
CM -Cites: Environ Sci Technol. 2010 Jun 15;44(12):4395-9 (medline /20465302)
CM -Cites: Annu Rev Nutr. 2009;29:381-99 (medline /19575603)
CM -Cites: PLoS One. 2017 May 4;12 (5):e0176923 (medline /28472079)
CM -Cites: Cortex. 2016 Jan;74:370-82 (medline /25682472)
CM -Cites: Toxicol Appl Pharmacol. 2013 Oct 15;272(2):384-90 (medline
/23859881)
CM - Cites: Mol Plant Pathol. 2004 Nov 1;5(6):515-25 (medline /20565626)
CM - Cites: Food Addit Contam Part B Surveill. 2010;3(4):275-88 (medline
/24779628)
CM - Cites: Food Chem. 2014 May 1;150:199-205 (medline /24360440)
CM - Cites: Environ Health Perspect. 2015 May;123(5):500-6 (medline /25707031)
DOCNO- medline/29547635

24 - TOXLINE
TI - Arsenic Exposure from Drinking Water and Urinary Metabolomics:
Associations and Long-Term Reproducibility in Bangladesh Adults.
AU - Wu F
AD - Department of Environmental Medicine, New York University School of
Medicine , New York, New York, USA.
AU - Chi L
AD - Department of Environmental Sciences and Engineering, University of North
Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
AU - Ru H
AD - Department of Environmental Sciences and Engineering, University of North
Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
AU - Parvez F
AD - Department of Environmental Health Sciences, Mailman School of Public Health,
Columbia University, New York, New York, USA.
AU - Slavkovich V
AD - Department of Environmental Health Sciences, Mailman School of Public Health,
Columbia University, New York, New York, USA.
AU - Eunus M
AD - U-Chicago Research Bangladesh, Ltd., Dhaka, Bangladesh.
AU - Ahmed A
AD - U-Chicago Research Bangladesh, Ltd., Dhaka, Bangladesh.
AU - Islam T
AD - U-Chicago Research Bangladesh, Ltd., Dhaka, Bangladesh.
AU - Rakibuz-Zaman M
AD - U-Chicago Research Bangladesh, Ltd., Dhaka, Bangladesh.
AU - Hasan R
AD - U-Chicago Research Bangladesh, Ltd., Dhaka, Bangladesh.
AU - Sarwar G
AD - U-Chicago Research Bangladesh, Ltd., Dhaka, Bangladesh.
AU - Graziano JH
AD - Department of Environmental Health Sciences, Mailman School of Public Health,
Columbia University, New York, New York, USA.
AU - Ahsan H
AD - Department of Health Studies, Center for Cancer Epidemiology and Prevention,
University of Chicago, Chicago, Illinois, USA.
AU - Lu K
AD - Department of Environmental Sciences and Engineering, University of North
Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
AU - Chen Y
AD - Department of Environmental Medicine, New York University School of
Medicine , New York, New York, USA.
SO - Environ Health Perspect. 2018, Jan 12; 126(1):017005. [Environmental
health perspectives]
AB - BACKGROUND: Chronic exposure to inorganic arsenic from drinking water has
been associated with a host of cancer and noncancer diseases. The
application of metabolomics in epidemiologic studies may allow researchers
to identify biomarkers associated with arsenic exposure and its health
effects.
AB - OBJECTIVE: Our goal was to evaluate the long-term reproducibility of
urinary metabolites and associations between reproducible metabolites and
arsenic exposure.
AB - METHODS: We studied samples and data from 112 nonsmoking participants (58
men and 54 women) who were free of any major chronic diseases and who were
enrolled in the Health Effects of Arsenic Longitudinal Study (HEALS), a
large prospective cohort study in Bangladesh. Using a global gas
chromatography-mass spectrometry platform, we measured metabolites in
their urine samples, which were collected at baseline and again 2 y apart,
and estimated intraclass correlation coefficients (ICCs). Linear
regression was used to assess the association between arsenic exposure at
baseline and metabolite levels in baseline urine samples.
AB - RESULTS: We identified 2,519 molecular features that were present in all
224 urine samples from the 112 participants, of which 301 had an ICC of
&ge;0.60. Of the 301 molecular features, water arsenic was significantly
related to 31 molecular features and urinary arsenic was significantly
related to 74 molecular features after adjusting for multiple comparisons.
Six metabolites with a confirmed identity were identified from the 82
molecular features that were significantly associated with either water
arsenic or urinary arsenic after adjustment for multiple comparisons.
AB - CONCLUSIONS: Our study identified urinary metabolites with long-term
reproducibility that were associated with arsenic exposure. The data
established the feasibility of using metabolomics in future larger
studies. https://doi.org/10.1289/EHP1992.
LA - eng
IS - 1552-9924 (Electronic)
PT - Journal Article
TA - Environ Health Perspect
YR - 2018
DATE- 20180413
CITO- NLM
CS - United States
FJT - Environmental health perspectives
EDAT- 20180112
STAT- In-Data-Review
DOCNO- medline/29329102

25 - TOXLINE
TI - Arsenite increases Cyclin D1 expression through coordinated regulation of
the Ca2+/NFAT2 and NF-&kappa;B pathways via ERK/MAPK in a human
uroepithelial cell line.
AU - Liu J
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
Liaoning Province 110122, P. R. China. shxi@cmu.edu.cn.
AU - Jin P
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
Liaoning Province 110122, P. R. China. shxi@cmu.edu.cn.
AU - Lin X
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
Liaoning Province 110122, P. R. China. shxi@cmu.edu.cn.
AU - Zhou Q
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
Liaoning Province 110122, P. R. China. shxi@cmu.edu.cn.
AU - Wang F
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
Liaoning Province 110122, P. R. China. shxi@cmu.edu.cn.
AU - Liu S
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
Liaoning Province 110122, P. R. China. shxi@cmu.edu.cn.
AU - Xi S
AD - Department of Environmental and Occupational Health, Liaoning Provincial Key
Laboratory of Arsenic Biological Effect and Poisoning, School of Public Health,
China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang,
Liaoning Province 110122, P. R. China. shxi@cmu.edu.cn.
SO - Metallomics. 2018, Mar 01; 10(3):486-495. [Metallomics : integrated
biometal science]
AB - To understand the direct link between Cyclin D1, and nuclear factor of
activated T cells 2 (NFAT2) and nuclear factor (NF)-&kappa;B in
arsenic-treated bladder cells, as well as the association between MAPK and
NFAT signaling, we determined whether or not the Ca2+/NFAT pathway is
activated in an arsenic-treated normal urothelial cell line and determined
the roles of NFAT and NF-&kappa;B signals in the regulation of Cyclin D1
expression. The SV-40 immortalized human uroepithelial cell line,
SV-HUC-1, was treated with NaAsO2 for 24 h (0, 1, 2, 4, 8, and 10 &mu;M)
and 10, 20, 30, and 40 weeks (0 and 0.5 &mu;M). We found that arsenite
increased the intracellular Ca2+ levels and induced NFAT2 nuclear
translocation after treatment for 24 h. The level of NFAT2 mRNA and
expression of total protein and nuclear protein were increased after
long-term treatment with 0.5 &mu;M arsenite for 30 and 40 weeks compared
to the cells treated for 24 h. In addition, NF-&kappa;B p50 and p65
nuclear protein expression increased significantly in cells treated with
2-8 &mu;M arsenite for 24 h, which was consistent with NFAT2 nuclear
expression. Furthermore, an ERK inhibitor (U0126) significantly reduced
the expression of NFAT2 nuclear protein, and an ERK and JNK inhibitor
decreased the levels of p65 and p50 nuclear protein. Cyclin D1 is known as
a proto-oncogene and the level of this protein was increased in SV-HUC-1
cells treated with arsenite for 24 h and long-term. An NFAT inhibitor
(CsA) and NF-&kappa;B inhibitor (PDTC) all markedly reduced Cyclin D1
protein expression. Treatment with U0126 also significantly decreased
Cyclin D1 protein expression while JNK and p38 inhibitors did not
attenuate the arsenite-associated increase in Cyclin D1 protein
expression. The results suggest that regulation of Cyclin D1 protein
expression by arsenite in SV-HUC-1 cells is dependent on ERK/NFAT2 and
ERK/NF-&kappa;B, but is not dependent on JNK or p38.
LA - eng
IS - 1756-591X (Electronic)
PT - Journal Article
TA - Metallomics
YR - 2018
DATE- 20180323
CITO- NLM
CS - England
FJT - Metallomics : integrated biometal science
EDAT- 20180312
STAT- In-Data-Review
DOCNO- medline/29528074

26 - TOXLINE
TI - Characterising microbial reduction of arsenate sorbed to ferrihydrite and
its concurrence with iron reduction.
AU - Huang JH
AD - Environmental Geosciences, University of Basel, CH-4056, Basel, Switzerland.
Electronic address: jen-how.huang@unibas.ch.
SO - Chemosphere. 2018, Mar; 194:49-56. [Chemosphere]
AB - A series of model anoxic incubations were performed to understand the
concurrence between arsenate and ferrihydrite reduction by Shewanella
putrefaciens strain CN-32 at different concentrations of arsenate,
ferrihydrite and lactate, and with given &Delta;Grxn for arsenate and
ferrihydrite reduction in non-growth conditions. The reduction kinetics of
arsenate sorbed to ferrihydrite is predominately controlled by the
availability of dissolved arsenate, which is measured by the integral of
dissolved arsenate concentrations against incubation time and shown to
correlate with the first order rate constants. High lactate concentrations
slightly slowed down the rate of arsenate reduction due to the competition
with arsenate for microbial contact. Under all experimental conditions,
simultaneous arsenate and ferrihydrite reduction occurred following
addition of S. putrefaciens inoculums and suggested no apparent
competition between these two enzymatic reductions. Ferrous ions released
from iron reduction might retard microbial arsenate reduction at high
arsenate and ferrihydrite concentrations due to formation of ferrous
arsenate. At high arsenate to ferrihydrite ratios, reductive dissolution
of ferrihydrite shifted arsenate from sorption to dissolution and hence
accelerated arsenate reduction. The interaction between microbial arsenate
and ferrihydrite reduction did not correlate with &Delta;Grxn, but instead
was governed by other factors such as geochemical and microbial
parameters.
KW - Arsenate reduction
KW - Ferrihydrite
KW - Kinetics
KW - Shewanella
RN - 87PZU03K0K
RN - E1UOL152H7
RN - N7CIZ75ZPN
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180416
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171121
STAT- MEDLINE
DOCNO- medline/29197249

27 - TOXLINE
TI - Metabolism and disposition of arsenic species after repeated oral dosing
with sodium arsenite in drinking water. II. Measurements in pregnant and
fetal CD-1 mice.
AU - Twaddle NC
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, U.S. Food and Drug Administration, Jefferson, AR 72079, United States.
AU - Vanlandingham M
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, U.S. Food and Drug Administration, Jefferson, AR 72079, United States.
AU - Beland FA
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, U.S. Food and Drug Administration, Jefferson, AR 72079, United States.
AU - Doerge DR
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, U.S. Food and Drug Administration, Jefferson, AR 72079, United States.
Electronic address: daniel.doerge@fda.hhs.gov.
SO - Food Chem Toxicol. 2018, May; 115:178-184. [Food and chemical toxicology :
an international journal published for the British Industrial Biological
Research Association]
AB - Arsenic is ubiquitous in the earth's crust, and human diseases are linked
with exposures that are similar to dietary intake estimates. Metabolic
methylation of inorganic arsenic facilitates excretion of pentavalent
metabolites and decreases acute toxicity; however, tissue binding of
trivalent arsenic intermediates is evidence for concomitant metabolic
activation. Pregnant and fetal CD-1 mice comprise a key animal model for
arsenic carcinogenesis since adult-only exposures have minimal effects.
This study evaluated inorganic arsenic and its metabolites in pentavalent
and trivalent states in blood and tissues from maternal and fetal CD-1
mice after repeated administration of arsenite through drinking water.
After 8 days of exposure, DMA species were ubiquitous in dams and fetuses.
Despite the presence of MMAIII in dams, none was observed in any fetal
sample. This difference may be important in assessing fetal susceptibility
to arsenic toxicity because MMA production has been linked with human
disease. Binding of DMAIII in fetal tissues provided evidence for
metabolic activation, although the role for such binding in arsenic
toxicity is unclear. This study provides links between administered dose,
metabolism, and internal exposures from a key animal model of arsenic
toxicity to better understand risks from human exposure to environmental
arsenic.
KW - Arsenic
KW - Carcinogenesis
KW - Fetus
KW - Metabolism
KW - Pregnancy
KW - Toxicokinetics
LA - eng
IS - 1873-6351 (Electronic)
PT - Journal Article
TA - Food Chem Toxicol
YR - 2018
DATE- 20180504
CI - Copyright &copy; 2018. Published by Elsevier Ltd.
CITO- NLM
CS - England
FJT - Food and chemical toxicology : an international journal published for the
British Industrial Biological Research Association
EDAT- 20180310
STAT- In-Process
DOCNO- medline/29530638

28 - TOXLINE
TI - Microbe mediated arsenic release from iron minerals and arsenic
methylation in rhizosphere controls arsenic fate in soil-rice system after
straw incorporation.
AU - Yang YP
AD - State Key Lab of Urban and Regional Ecology, Research Center for Eco-
Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, People's
Republic of China; University of Chinese Academy of Sciences, Beijing 100049,
People's Republic of China.
AU - Zhang HM
AD - Jiaxing Academy of Agricultural Sciences, Xiuzhou District, Jiaxing 314016,
People's Republic of China.
AU - Yuan HY
AD - State Key Lab of Urban and Regional Ecology, Research Center for Eco-
Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, People's
Republic of China; University of Chinese Academy of Sciences, Beijing 100049,
People's Republic of China.
AU - Duan GL
AD - State Key Lab of Urban and Regional Ecology, Research Center for Eco-
Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, People's
Republic of China; University of Chinese Academy of Sciences, Beijing 100049,
People's Republic of China. Electronic address: duangl@rcees.ac.cn.
AU - Jin DC
AD - State Key Lab of Urban and Regional Ecology, Research Center for Eco-
Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, People's
Republic of China.
AU - Zhao FJ
AD - State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of
Resources and Environmental Sciences, Nanjing Agricultural University, Nanjing
210095, People's Republic of China.
AU - Zhu YG
AD - State Key Lab of Urban and Regional Ecology, Research Center for Eco-
Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, People's
Republic of China; University of Chinese Academy of Sciences, Beijing 100049,
People's Republic of China; Key Laboratory of Urban Environment and Health,
Institute of Urban Environment, Chinese Academy of Sciences, Xiamen 361021,
People's Republic of China.
SO - Environ Pollut. 2018, May; 236:598-608. [Environmental pollution (Barking,
Essex : 1987)]
AB - Arsenic (As) contamination is a global problem. Straw incorporation is
widely performed in As contaminated paddy fields. To understand how straw
and straw biochar incorporation affect As transformation and translocation
in the soil-microbe-rice system, a pot experiment was carried out with
different dosages of rice straw and straw biochar application. Results
showed that both straw biochar and straw application significantly
increased As mobility. Straw biochar mobilized As mainly through
increasing soil pH and DOM content. Straw incorporation mainly through
enhancing As release from iron (Fe) minerals and arsenate (As(V))
reduction to arsenite (As(III)). Straw biochar didn't significantly affect
As methylation, while straw incorporation significantly enhanced As
methylation, elevated dimethylarsenate (DMA) concentration in soil
porewater and increased As volatilization. Straw biochar didn't
significantly change total As accumulation in rice grains, but decreased
As(III) accumulation by silicon (Si) inhibition. Straw incorporation
significantly increased DMA, but decreased As(III) concentration in rice
grains. After biochar application, dissolved As was significantly
positively correlated with the abundance of Bacillus, indicating that
Bacillus might be involved in As release, and As(III) concentration in
polished grains was negatively correlated with Si concentration. The
significant positive correlation between dissolved As with Fe and the
abundance of iron-reducing bacteria suggested the coupling of As and Fe
reduction mediated by iron-reducing bacteria. The significant positive
correlation between DMA in rice grains and the abundance of methanogenic
bacteria indicated that methanogenic bacteria could be involved in As
methylation after straw application. The results of this study would
advance the understanding how rice straw incorporation affects As fate in
soil-microbe-rice system, and provide some guidance to straw incorporation
in As contaminated paddy soil. This study also revealed a wealth of
microorganisms in the soil environment that dominate As mobility and
transformation after straw incorporation.
KW - Arsenic methylation
KW - Arsenic mobility
KW - Rice (Oryza sativa L.)
KW - Straw biochar
KW - Straw incorporation
RN - 16291-96-6
RN - AJ2HL7EU8K
RN - E1UOL152H7
RN - N5509X556J
RN - N712M78A8G
RN - N7CIZ75ZPN
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180608
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Environmental pollution (Barking, Essex : 1987)
STAT- MEDLINE
DOCNO- medline/29433100

29 - TOXLINE
TI - Arsenic species in rice and rice-based products consumed by toddlers in
Switzerland.
AU - Guillod-Magnin R
AD - a Division of Risk Assessment , Federal Food Safety and Veterinary Office
(FSVO) , Berne , Switzerland.
AU - Br�schweiler BJ
AD - a Division of Risk Assessment , Federal Food Safety and Veterinary Office
(FSVO) , Berne , Switzerland.
AU - Aubert R
AD - a Division of Risk Assessment , Federal Food Safety and Veterinary Office
(FSVO) , Berne , Switzerland.
AU - Haldimann M
AD - a Division of Risk Assessment , Federal Food Safety and Veterinary Office
(FSVO) , Berne , Switzerland.
SO - Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2018, Feb
27:1-15. [Food additives & contaminants. Part A, Chemistry, analysis,
control, exposure & risk assessment]
AB - Inorganic arsenic (iAs) is a contaminant present in food, especially in
rice and rice-based products. Toxicity of arsenic compounds (As) depends
on species and oxidative state. iAs species, such as arsenite (As(III))
and arsenate (As(V)), are more bioactive and toxic than organic arsenic
species, like methylarsonic acid (MMA(V)) and dimethylarsinic acid
(DMA(V)) or arsenosugars and arsenobetaine. An ion
chromatography-inductively coupled-plasma-mass spectroscopy method was
developed to separate the four following arsenic anions: As(III), As(V),
MMA(V) and DMA(V). Sample preparation was done in mild acidic conditions
to ensure species preservation. The predominant arsenic species found in
rice and rice-based products, except for rice drinks, was As(III), with
60-80% of the total As content, followed by DMA(V) and As(V). MMA(V) was
measured only at low levels ( < 3%). Analyses of rice products
(N = 105) intended for toddlers, including special products
destined for infants and toddlers, such as dry form baby foods
(N = 12) or ready-to-use form (N = 9), were done. It
was found in this study that there is little or no margin of exposure.
Risk assessment, using the occurrence data and indicated intake scenarios
compared to reference BMDLs as established by EFSA, demonstrated toddlers
with a high consumption of rice based cereals and rice drinks are at risk
of high iAs exposure, for which a potential health risk cannot be
excluded.
KW - IC-ICP-MS
KW - arsenic speciation
KW - exposure assessment
KW - rice-based baby foods
KW - risk assessment
LA - eng
IS - 1944-0057 (Electronic)
PT - Journal Article
TA - Food Addit Contam Part A Chem Anal Control Expo Risk Assess
YR - 2018
DATE- 20180227
CITO- NLM
CS - England
FJT - Food additives &amp; contaminants. Part A, Chemistry, analysis, control,
exposure &amp; risk assessment
EDAT- 20180227
STAT- Publisher
DOCNO- medline/29448893

30 - TOXLINE
TI - Purification of arsenic-contaminated water with K-jarosite filters.
AU - Hott RC
AD - Instituto de Ci�ncia, Engenharia e Tecnologia (ICET), Universidade Federal
dos Vales do Jequitinhonha e Mucuri (UFVJM), Te�filo Otoni, Minas Gerais, 39803-
371, Brazil.
AU - Maia LFO
AD - Instituto de Ci�ncia, Engenharia e Tecnologia (ICET), Universidade Federal
dos Vales do Jequitinhonha e Mucuri (UFVJM), Te�filo Otoni, Minas Gerais, 39803-
371, Brazil.
AU - Santos MS
AD - Instituto de Ci�ncia, Engenharia e Tecnologia (ICET), Universidade Federal
dos Vales do Jequitinhonha e Mucuri (UFVJM), Te�filo Otoni, Minas Gerais, 39803-
371, Brazil.
AU - Faria MC
AD - Instituto de Ci�ncia, Engenharia e Tecnologia (ICET), Universidade Federal
dos Vales do Jequitinhonha e Mucuri (UFVJM), Te�filo Otoni, Minas Gerais, 39803-
371, Brazil.
AU - Oliveira LCA
AD - Departamento de Qu�mica, ICEx, Universidade Federal de Minas Gerais, Belo
Horizonte, Minas Gerais, 31270-901, Brazil.
AU - Pereira MC
AD - Instituto de Ci�ncia, Engenharia e Tecnologia (ICET), Universidade Federal
dos Vales do Jequitinhonha e Mucuri (UFVJM), Te�filo Otoni, Minas Gerais, 39803-
371, Brazil.
AU - Bomfeti CA
AD - Instituto de Ci�ncia, Engenharia e Tecnologia (ICET), Universidade Federal
dos Vales do Jequitinhonha e Mucuri (UFVJM), Te�filo Otoni, Minas Gerais, 39803-
371, Brazil.
AU - Rodrigues JL
AD - Instituto de Ci�ncia, Engenharia e Tecnologia (ICET), Universidade Federal
dos Vales do Jequitinhonha e Mucuri (UFVJM), Te�filo Otoni, Minas Gerais, 39803-
371, Brazil. jairo.rodrigues@ufvjm.edu.br.
SO - Environ Sci Pollut Res Int. 2018, May; 25(14):13857-13867. [Environmental
science and pollution research international]
AB - The high toxicity and potential arsenic accumulation in several
environments have encouraged the development of technologies for its
removal from contaminated waters. However, the arsenic released into
aquatic environment comes mainly from extremely acidic mining effluents,
making harder to find stable adsorbents to be used in these conditions. In
this work, K-jarosite particles were synthesized as a stable adsorbent in
acidic medium for eliminating arsenic from contaminated water. The
adsorption capacities of K-jarosite for As3+, As5+, and monomethylarsonic
acid were 9.45, 12.36, and 8.21 mg g-1, respectively. Most
arsenic in water was adsorbed within the first 10 min, suggesting the
fast arsenic adsorption kinetics of K-jarosite particles. Because of that,
a K-jarosite filter was constructed for purifying water at a constant
flow. The K-jarosite filter was highly efficient to treat
arsenic-contaminated water from a Brazilian river, reducing the
concentration of arsenic in water to near zero. These data suggest the
K-jarosite filter can be used as a low-cost technology for purifying
arsenic-contaminated water in acidic medium.
KW - Adsorption
KW - Arsenate
KW - Arsenic
KW - Arsenite
KW - Filter
LA - eng
IS - 1614-7499 (Electronic)
PT - Journal Article
TA - Environ Sci Pollut Res Int
YR - 2018
DATE- 20180525
CITO- NLM
CS - Germany
FJT - Environmental science and pollution research international
EDAT- 20180306
STAT- In-Process
CM - Cites: J Hazard Mater. 2009 Nov 15;171(1-3):965-72 (medline /19628332)
CM - Cites: J Environ Manage. 2017 Jan 15;186(Pt 2):261-267 (medline /27480915)
CM - Cites: J Environ Health Sci Eng. 2014 Mar 06;12(1):58 (medline /24602339)
CM - Cites: J Environ Sci (China). 2016 Nov;49:86-96 (medline /28007183)
CM - Cites: Environ Sci Pollut Res Int. 2014 Mar;21(5):3218-29 (medline
/24203255)
CM - Cites: J Hazard Mater. 2016 Apr 5;306:124-132 (medline /26705889)
CM - Cites: Int J Environ Res Public Health. 2013 Apr 12;10(4):1527-46 (medline
/23583964)
CM - Cites: J Environ Sci (China). 2011;23(9):1544-50 (medline /22432292)
CM - Cites: Environ Sci Pollut Res Int. 2016 Nov;23 (21):21969-21979 (medline
/27539466)
CM - Cites: Environ Toxicol Pharmacol. 2016 Dec;48:214-224 (medline /27829199)
DOCNO- medline/29512010

31 - TOXLINE
TI - The effect of association between inefficient arsenic methylation capacity
and demographic characteristics on the risk of skin lesions.
AU - Rasheed H
AD - water@leeds, School of Geography, University of Leeds, Leeds LS2 s9JT, United
Kingdom. Electronic address: gyhj@leeds.ac.uk.
AU - Kay P
AD - water@leeds, School of Geography, University of Leeds, Leeds LS2 s9JT, United
Kingdom.
AU - Slack R
AD - water@leeds, School of Geography, University of Leeds, Leeds LS2 s9JT, United
Kingdom.
AU - Gong YY
AD - School of Food Science and Nutrition, University of Leeds, Leeds LS2 9JT,
United Kingdom.
SO - Toxicol Appl Pharmacol. 2018, Jan 15; 339:42-51. [Toxicology and applied
pharmacology]
AB - This study was conducted in rural Pakistan to assess the dose-response
relationship between skin lesions and arsenic exposure and their variation
by demographic characteristics. The study included 398 participants (66
participants with skin lesions and 332 without) residing in six previously
unstudied villages exposed to ground water arsenic in the range of < 1
to 3090&mu;gL-1. The skin lesions identification process involved
interview and physical examinations of participants followed by
confirmation by a physician according to UNICEF criteria. Urinary
inorganic arsenic (iAs), total arsenic (tAs), monomethylarsonic acid
(MMA), and dimethylarsinic acid (DMA) were analysed to determine
methylation capacity, methylation efficiency and the dose-response
relationship with skin lesions. Study participants with skin lesions were
found to be exposed to arsenic > 10&mu;gL-1 with a daily arsenic intake
of 3.23&plusmn;3.75mgday-1 from household ground water sources for an
exposure duration of 10-20years. The participants with skin lesions
compared to those without skin lesions showed higher levels of urinary iAs
(133.40&plusmn;242.48 vs. 44.24&plusmn;86.48&mu;gg-1Cr), MMA
(106.38&plusmn;135.04 vs. 35.43&plusmn;39.97&mu;gg-1Cr), MMA%
(15.26&plusmn;6.31 vs.12.11&plusmn;4.68) and lower levels of DMA%
(66.99&plusmn;13.59 vs. 73.39&plusmn;10.44) and secondary methylation
index (SMI) (0.81&plusmn;0.11 vs. 0.86&plusmn;0.07). Study participants
carrying a lower methylation capacity characterized by higher MMA% (OR
5.06, 95% CI: 2.09-12.27), lower DMA% (OR 0.64, 95% CI: 0.33-1.26),
primary methylation index (PMI) (OR 0.56, 95% CI: 0.28-1.12) and SMI (OR
0.43, 95% CI: 0.21-0.88) had a significantly higher risk of skin lesions
compared to their corresponding references after adjusting for occupation
categories. The findings confirmed that inefficient arsenic methylation
capacity was significantly associated with increased skin lesion risks and
the effect might be modified by labour intensive occupations.
KW - Arsenicosis
KW - Hyperpigmentation
KW - Keratosis
KW - Methylation capacity
KW - Monomethylarsonic acid (MMA)
KW - Skin lesions
LA - eng
IS - 1096-0333 (Electronic)
PT - Journal Article
TA - Toxicol Appl Pharmacol
YR - 2018
DATE- 20180108
CI - Crown Copyright &copy; 2017. Published by Elsevier Inc. All rights
reserved.
CITO- NLM
CS - United States
FJT - Toxicology and applied pharmacology
EDAT- 20171129
STAT- In-Data-Review
DOCNO- medline/29197518

32 - TOXLINE
TI - Inorganic arsenic exposure increased expression of Fas and Bax gene in
vivo and vitro.
AU - He Y
AD - School of Public Health, Kunming Medical University, China. Electronic
address: heyuefeng@kmmu.edu.cn.
AU - Zhang R
AD - School of Public Health, Kunming Medical University, China.
AU - Xiaoxiao S
AD - School of Public Health, Kunming Medical University, China.
AU - Li S
AD - School of Public Health, Kunming Medical University, China.
AU - Xinan W
AD - School of Public Health, Kunming Medical University, China.
AU - Huang D
AD - The Second People's Hospital of Yunnan Province, China. Electronic address:
Huangdahai2000@163.com.
SO - Gene. 2018, Jun 01. [Gene]
AB - Accumulating evidences have shown that apoptosis plays an important role
in mediating the therapeutic effects and toxicity of arsenic. Fas and Bax
genes are critical regulatory genes for apoptosis. In this study, we
investigated the association between levels of Fas and Bax expression and
the three arsenic species (inorganic arsenic (iAs), monomethylarsonic acid
(MMA) and dimethylarsinic acid (DMA)) in vivo and vitro. Three arsenic
species in urine were measured and levels of Fas and Bax expression were
examined by the quantitative real-time PCR (qPCR) for all subjects. We
found that Fas and Bax mRNA expression in the exposed group were
significantly higher than that in the control group. The levels of gene
expression were positively correlated with the concentrations of urinary
iAs, MMA and DMA in all subjects. Sodium arsenite induced Fas and Bax mRNA
expression, then MMA and DMA did not induce mRNA expression in MDA-MB-231
and XWLC-05 cells. The findings of the present study indicated that iAs,
MMA, and DMA had different effects on expression of Bax and Fas gene.
KW - Arsenic
KW - Bax
KW - DMA Fas
KW - MMA
LA - eng
IS - 1879-0038 (Electronic)
PT - Journal Article
TA - Gene
YR - 2018
DATE- 20180604
CI - Copyright &copy; 2017. Published by Elsevier B.V.
CITO- NLM
CS - Netherlands
FJT - Gene
EDAT- 20180601
STAT- Publisher
DOCNO- medline/29864498

33 - TOXLINE
TI - A comparison of the determination and speciation of inorganic arsenic
using general HPLC methodology with UV, MS and MS/MS detection.
AU - Gilmartin G
AD - Analytical Development, Discovery &amp; Product Development, Teva Branded
Pharmaceutical Product R&amp;D, West Chester, PA, USA. Electronic address:
Gregory.Gilmartin@tevapharm.com.
AU - Gingrich D
AD - Analytical Development, Discovery &amp; Product Development, Teva Branded
Pharmaceutical Product R&amp;D, West Chester, PA, USA.
SO - J Chromatogr B Analyt Technol Biomed Life Sci. 2018, Apr 15; 1083:20-27.
[Journal of chromatography. B, Analytical technologies in the biomedical
and life sciences]
AB - The determination and speciation of arsenic in natural resources such as
drinking water and agricultural soils has been a growing concern in recent
years due to its many toxicological effects [1-3]. To speciate and
quantitate concentrations of < 1&#8239;ppm of arsenic, typically an ion
chromatograph (IC) interfaced to an inductively coupled plasma mass
spectrometer (ICP-MS) is employed [4-9]. This methodology may be very
robust and sensitive, but it is expensive and not as ubiquitous as high
performance liquid chromatography (HPLC) with ultraviolet (UV) absorbance
detection or electrospray ionization mass spectrometry (ESI-MS). Anion
exchange chromatography is a well-documented means of speciating arsenite
(As(III), As2O3) and arsenate (As(V), AsO4) using UV [10], conductivity
[11], or ESI-MS detection [12,13]. This paper demonstrates the utilization
of common liquid chromatographic instrumentation to speciate and
determines inorganic Arsenic compounds using UV or MS via selected ion
recording (SIR) or multiple reaction monitoring (MRM) detection. This
paper describes the analysis of arsenite and arsenate samples prepared
using both deionized and ground water. The limit of quantitation for the
techniques described in this paper for samples spiked in ground water were
454&#8239;ppb (As(III)) and 562&#8239;ppb (As(V)) for UV detection,
45.4&#8239;ppb (As(III)) and 56.2&#8239;ppb (As(V)) for SIR detection, and
4.54&#8239;ppb (As(III)) and 5.62&#8239;ppb (As(V)) for MRM detection.
KW - Arsenic determination
KW - Arsenic speciation
KW - MS and MS/MS detection
KW - UV detection
RN - N712M78A8G
LA - eng
IS - 1873-376X (Electronic)
PT - Comparative Study
PT - Journal Article
TA - J Chromatogr B Analyt Technol Biomed Life Sci
YR - 2018
DATE- 20180504
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Journal of chromatography. B, Analytical technologies in the biomedical
and life sciences
EDAT- 20180226
STAT- MEDLINE
DOCNO- medline/29518633

34 - TOXLINE
TI - Characterization of arsenite-oxidizing bacteria to decipher their role in
arsenic bioremediation.
AU - Biswas R
AD - a Department of Biotechnology and Medical Engineering , National Institute of
Technology Rourkela , Odisha.
AU - Sarkar A
AD - a Department of Biotechnology and Medical Engineering , National Institute of
Technology Rourkela , Odisha.
SO - Prep Biochem Biotechnol. 2018, Jun 11:1-8. [Preparative biochemistry &
biotechnology]
AB - High arsenic groundwater contamination causes serious health risks in many
developing countries, particularly in India and Bangladesh. The arsenic
fluxes in aquifers are primarily controlled by bacterial populations
through biogeochemical cycle. In this present study, two gram-positive
rod-shaped bacteria were isolated from shallow aquifers of Bhojpur
district in Bihar during the early winter season, able to withstand
arsenite (As3+) concentration upto 70&thinsp;mM and 1000&thinsp;mM of
arsenate (As5+) concentration. They showed high resistance to heavy metals
up to 30&thinsp;mM and utilized some complex sugars along with different
carbon sources. Growth at wide range of temperature, pH and salinity were
observed. Both these isolates showed high efficiency in converting As3+
into less toxic concentrations of As5+ respectively from arsenic enriched
culture media. Along with superior arsenic transformation and arsenic
resistance abilities, the isolates showed a wide variety of metabolic
capacity in terms of utilizing a variety of carbon sources under aerobic
conditions, respectively. This study reports the potential As3+-oxidizing
bacteria that can play an important role in subsurface arsenic
transformation that will aid in designing future bioremediation strategy
for the arsenic affected areas.
KW - Arsenic
KW - bacteria
KW - bioremediation
KW - characterization
KW - groundwater
KW - resistance
LA - eng
IS - 1532-2297 (Electronic)
PT - Journal Article
TA - Prep Biochem Biotechnol
YR - 2018
DATE- 20180611
CITO- NLM
CS - England
FJT - Preparative biochemistry &amp; biotechnology
EDAT- 20180611
STAT- Publisher
DOCNO- medline/29889593

35 - TOXLINE
TI - Arsenite downregulates H3K4 trimethylation and H3K9 dimethylation during
transformation of human bronchial epithelial cells.
AU - Tu W
AD - Department of Occupational and Environmental Health, Key Laboratory of
Environment and Health, Ministry of Education, School of Public Health, Tongji
Medical College, Huazhong University of Science and Technology, Wuhan, Hubei,
430030, People's Republic of China.
AU - Liu Y
AD - Department of Occupational and Environmental Health, Key Laboratory of
Environment and Health, Ministry of Education, School of Public Health, Tongji
Medical College, Huazhong University of Science and Technology, Wuhan, Hubei,
430030, People's Republic of China.
AU - Xie C
AD - Department of Occupational and Environmental Health, Key Laboratory of
Environment and Health, Ministry of Education, School of Public Health, Tongji
Medical College, Huazhong University of Science and Technology, Wuhan, Hubei,
430030, People's Republic of China.
AU - Zhou X
AD - Department of Occupational and Environmental Health, Key Laboratory of
Environment and Health, Ministry of Education, School of Public Health, Tongji
Medical College, Huazhong University of Science and Technology, Wuhan, Hubei,
430030, People's Republic of China.
SO - J Appl Toxicol. 2018, Apr; 38(4):480-488. [Journal of applied toxicology :
JAT]
AB - Arsenic is an established human carcinogen but with weak mutagenic
activity. The mechanisms of arsenic-induced carcinogenesis are not well
understood. In the present study, we investigated the role of histone
methylation in transformation of human bronchial epithelial (BEAS-2B)
cells. After 16 weeks' exposure, cells were transformed by 0.1, 0.5
and 1 &mu;m arsenite. Global trimethylated H3K4 (H3K4me3) was
decreased by 0.1 &mu;m arsenite at 12 weeks, and 0.5 and
1 &mu;m arsenite at 8, 12 and 16 weeks, which could be
attributed to reduced histone methyltransferase activities, increased
histone demethylase (HDM) activities as well as increased protein levels
of H3K4 demethylase KDM5A. Global dimethylated H3K9 (H3K9me2) was also
decreased after exposure to 0.5 &mu;m arsenite for 4, 8, 12 and
16 weeks and 1.0 &mu;m arsenite for 8 and 12 weeks, which
was associated with an increase of HDM activities. Our findings indicated
that arsenite decreased global H3K4me3 and H3K9me2 levels during cell
transformation by modulating the enzymatic activities of histone
methyltransferases and/or HDMs, and by upregulation of KDM5A protein
levels for H3K4me3.
KW - BEAS-2B cells
KW - H3K4 trimethylation
KW - H3K9 dimethylation
KW - arsenite
KW - cell transformation
LA - eng
IS - 1099-1263 (Electronic)
PT - Journal Article
TA - J Appl Toxicol
YR - 2018
DATE- 20180214
CI - Copyright &copy; 2017 John Wiley &amp; Sons, Ltd.
CITO- NLM
CS - England
FJT - Journal of applied toxicology : JAT
EDAT- 20171117
STAT- In-Data-Review
DOCNO- medline/29148585

36 - TOXLINE
TI - Associations between Methylated Metabolites of Arsenic and Selenium in
Urine of Pregnant Bangladeshi Women and Interactions between the Main
Genes Involved.
AU - Skr�der H
AD - Institute of Environmental Medicine, Karolinska Institutet, Stockholm,
Sweden.
AU - Engstr�m K
AD - Division of Occupational and Environmental Medicine, Department of Laboratory
Medicine, Lund University , Lund, Sweden.
AU - Kuehnelt D
AD - Institute of Chemistry, NAWI Graz, University of Graz, Graz, Austria.
AU - Kippler M
AD - Institute of Environmental Medicine, Karolinska Institutet, Stockholm,
Sweden.
AU - Francesconi K
AD - Institute of Chemistry, NAWI Graz, University of Graz, Graz, Austria.
AU - Nermell B
AD - Institute of Environmental Medicine, Karolinska Institutet, Stockholm,
Sweden.
AU - Tofail F
AD - International Centre for Diarrhoeal Disease Research, Bangladesh (icddr,b),
Dhaka, Bangladesh.
AU - Broberg K
AD - Institute of Environmental Medicine, Karolinska Institutet, Stockholm,
Sweden.
AU - Vahter M
AD - Institute of Environmental Medicine, Karolinska Institutet, Stockholm,
Sweden.
SO - Environ Health Perspect. 2018, 02 01; 126(2):027001. [Environmental health
perspectives]
AB - BACKGROUND: It has been proposed that interactions between selenium and
arsenic in the body may affect their kinetics and toxicity. However, it is
unknown how the elements influence each other in humans.
AB - OBJECTIVES: We aimed to investigate potential interactions in the
methylation of selenium and arsenic.
AB - METHODS: Urinary selenium (U-Se) and arsenic (U-As) were measured using
inductively coupled plasma mass spectrometry (ICPMS) in samples collected
from pregnant women (n=226) in rural Bangladesh at gestational weeks (GW)
8, 14, 19, and 30. Urinary concentrations of trimethyl selenonium ion
(TMSe) were measured by HPLC-vapor generation-ICPMS, as were inorganic
arsenic (iAs), methylarsonic acid (MMA), and dimethylarsinic acid (DMA).
Methylation efficiency was assessed based on relative amounts (%) of
arsenic and selenium metabolites in urine. Genotyping for the main
arsenite and selenium methyltransferases, AS3MT and INMT, was performed
using TaqMan probes or Sequenom.
AB - RESULTS: Multivariable-adjusted linear regression analyses indicated that
%TMSe (at GW8) was positively associated with %MMA (&beta;=1.3, 95% CI:
0.56, 2.0) and U-As, and inversely associated with %DMA and U-Se in
producers of TMSe (INMT rs6970396 AG+AA, n=74), who had a wide range of
urinary TMSe (12-42%). Also, %TMSe decreased in parallel to %MMA during
pregnancy, especially in the first trimester (-0.58 %TMSe per gestational
week). We found a gene-gene interaction for %MMA (p-interaction=0.076 for
haplotype 1). In analysis stratified by INMT genotype, the association
between %MMA and both AS3MT haplotypes 1 and 3 was stronger in women with
the INMT GG (TMSe nonproducers, 5th-95th percentile: 0.2-2%TMSe) vs. AG+AA
genotype.
AB - CONCLUSIONS: Our findings for Bangladeshi women suggest a positive
association between urinary %MMA and %TMSe. Genes involved in the
methylation of selenium and arsenic may interact on associations with
urinary %MMA. https://doi.org/10.1289/EHP1912.
LA - eng
IS - 1552-9924 (Electronic)
PT - Journal Article
TA - Environ Health Perspect
YR - 2018
DATE- 20180215
CITO- NLM
CS - United States
FJT - Environmental health perspectives
EDAT- 20180201
STAT- In-Data-Review
DOCNO- medline/29398653

37 - TOXLINE
TI - [Analysis of Arsenic Compounds in Blood and Urine by HPLC-ICP-MS].
AU - Lin L
AD - College of Criminal and Justice, East China University of Political Science
and Law, Shanghai 200042, China.
AU - Zhang SJ
AD - Shanghai Key Laboratory of Forensic Medicine, Shanghai Forensic Service
Platform, Academy of Forensic Science, Shanghai 200063, China.
AU - Xu WC
AD - School of Public Health, Southern Medical University, Guangzhou 510515,
China.
AU - Luo RX
AD - Shanghai Key Laboratory of Forensic Medicine, Shanghai Forensic Service
Platform, Academy of Forensic Science, Shanghai 200063, China.
AU - Ma D
AD - Shanghai Key Laboratory of Forensic Medicine, Shanghai Forensic Service
Platform, Academy of Forensic Science, Shanghai 200063, China.
AU - Shen M
AD - Shanghai Key Laboratory of Forensic Medicine, Shanghai Forensic Service
Platform, Academy of Forensic Science, Shanghai 200063, China.
SO - Fa Yi Xue Za Zhi. 2018, Feb; 34(1):37-43. [Fa yi xue za zhi]
AB - OBJECTIVES: To establish an analysis method for the detection of 6 arsenic
compounds [AsC, AsB, As&#65288;&#8546;&#65289;, DMA, MMA and
As&#65288;V&#65289;] in blood and urine by high-performance liquid
chromatography-inductively coupled plasma-mass spectrometry
&#65288;HPLC-ICP-MS&#65289;, and apply it to real cases.
AB - METHODS: Triton was used to damage cells, and then
EDTA&middot;2Na&middot;2H2O was used to complex arsenic compounds in
cells, and sonication and protein deposition by acetonitrile were
performed for sample pretreatment. With the mobile phase consisted of
ammonium carbonate and ultrapure water, gradient elution was performed for
obtaining the arsenic compounds in samples, which were analysed by ICP-MS
with Hamilton PRP-X100 column.
AB - RESULTS: The limits of detection in blood were 1.66-10 ng/mL, while the
lower limits of quantitation in blood ranged from 5 to 30 ng/mL. The
limits of detection in urine were 0.5-10 ng/mL, while the lower limits of
quantitation in urine were 5-30 ng/mL. The relative standard deviation of
inter-day and intra-day precisions was less than 10%. This method had been
successfully applied to 3 cases.
AB - CONCLUSIONS: This study has established an analysis method for detecting 6
common arsenic compounds in blood and urine, which can be used to detect
the arsenic compounds in the blood and urine from arsenic poisoning cases
as well as the patients under arsenic treatment.
COI - The authors of this article and the planning committee members and staff
have no relevant financial relationships with commercial interests to
disclose.
KW - arsenicals
KW - blood
KW - forensic toxicology
KW - high-performance liquid chromatography-inductively coupled plasma-mass
spectrometry (HPLC-ICP-MS)
KW - urine
LA - chi
IS - 1004-5619 (Print)
PT - Journal Article
TA - Fa Yi Xue Za Zhi
YR - 2018
DATE- 20180604
CI - Copyright&copy; by the Editorial Department of Journal of Forensic
Medicine.
CITO- NLM
CS - China
CSET- IM
FJT - Fa yi xue za zhi
EDAT- 20180225
STAT- MEDLINE
DOCNO- medline/29577703

38 - TOXLINE
TI - Lung, Bladder, and Kidney Cancer Mortality 40&thinsp;Years After Arsenic
Exposure Reduction.
AU - Smith AH
AD - Arsenic Health Effects Research Group, School of Public Health, University of
California, Berkeley, CA.
AU - Marshall G
AD - Departamento de Estad�stica, Facultad de Matem�ticas, Pontificia Universidad
Cat�lica de Chile, Santiago, Chile.
AU - Roh T
AD - Arsenic Health Effects Research Group, School of Public Health, University of
California, Berkeley, CA.
AU - Ferreccio C
AD - Advanced Center for Chronic Diseases, Escuela de Medicina, Pontificia
Universidad Cat�lica de Chile, Santiago, Chile.
AU - Liaw J
AD - Arsenic Health Effects Research Group, School of Public Health, University of
California, Berkeley, CA.
AU - Steinmaus C
AD - Arsenic Health Effects Research Group, School of Public Health, University of
California, Berkeley, CA.
SO - J Natl Cancer Inst. 2018, Mar 01; 110(3):241-249. [Journal of the National
Cancer Institute]
AB - Background: Region II in northern Chile (population 442&thinsp;570)
experienced a sudden major increase in arsenic water concentrations in
1958 in the main city of Antofagasta, followed by a major reduction in
exposure when an arsenic removal plant was installed in 1970. It provides
a unique opportunity to study latency effects of exposure to arsenic, and
this is the first study with mortality data up to 40&thinsp;years after
exposure reduction.
AB - Methods: We previously identified high mortality rates in Region II up to
the year 2000. Here we present rate ratios (RRs) for Region II compared
with all the rest of Chile from 2001 to 2010, and with unexposed Region V
(population 1&thinsp;539&thinsp;852) for all years from 1950 to 2010. All
statistical tests were one-sided.
AB - Results: From 2001 to 2010, comparing Region II with the rest of Chile,
lung and bladder mortality were still greatly elevated
(RR&thinsp;=&thinsp;3.38, 95% confidence interval [CI] = 3.19 to 3.58, P
< .001 for lung cancer in men; RR&thinsp;=&thinsp;2.41, 95%
CI&thinsp;=&thinsp;2.20 to 2.64, P < .001 for lung cancer in women;
RR&thinsp;=&thinsp;4.79, 95% CI&thinsp;=&thinsp;4.20 to 5.46, P < .001
for bladder cancer in men; RR&thinsp;=&thinsp;6.43, 95%
CI&thinsp;=&thinsp;5.49 to 7.54, P < .001 for bladder cancer in women).
Kidney cancer mortality was also elevated (RR&thinsp;=&thinsp;1.75, 95%
CI&thinsp;=&thinsp;1.49 to 2.05, P < .001 for men;
RR&thinsp;=&thinsp;2.09, 95% CI&thinsp;=&thinsp;1.69 to 2.57, P < .001
for women). Earlier short latency acute myocardial infarction mortality
increases had subsided.
AB - Conclusions: Lung, bladder, and kidney cancer mortality due to arsenic
exposure have very long latencies, with increased risks manifesting
40&thinsp;years after exposure reduction. Our findings suggest that
arsenic in drinking water may involve one of the longest cancer latencies
for a human carcinogen.
LA - eng
IS - 1460-2105 (Electronic)
PT - Journal Article
TA - J Natl Cancer Inst
YR - 2018
DATE- 20180319
CITO- NLM
CS - United States
FJT - Journal of the National Cancer Institute
STAT- In-Data-Review
DOCNO- medline/29069505

39 - TOXLINE
TI - Human health risks and socio-economic perspectives of arsenic exposure in
Bangladesh: A scoping review.
AU - Rahman MA
AD - Center for Infrastructure Engineering, Western Sydney University, Australia;
Faculty of Science and Technology, Federation University, Ballarat, Victoria,
Australia. Electronic address: rahmanmazizur@gmail.com.
AU - Rahman A
AD - Water and Environmental Engineering, School of Computing, Engineering and
Mathematics, Western Sydney University, Australia.
AU - Khan MZK
AD - Water and Environmental Engineering, School of Computing, Engineering and
Mathematics, Western Sydney University, Australia.
AU - Renzaho AMN
AD - Humanitarian and Development Research Initiative, School of Social Sciences
and Psychology, Western Sydney University, Australia.
SO - Ecotoxicol Environ Saf. 2018, Apr 15; 150:335-343. [Ecotoxicology and
environmental safety]
AB - Arsenic contamination of drinking water, which can occur naturally or
because of human activities such as mining, is the single most important
public health issue in Bangladesh. Fifty out of the 64 districts in the
country have arsenic concentration of groundwater exceeding 50&micro;gL-1,
the Bangladeshi threshold, affecting 35-77 million people or 21-48% of the
total population. Chronic arsenic exposure through drinking water and
other dietary sources is an important public health issue worldwide
affecting hundreds of millions of people. Consequently, arsenic poisoning
has attracted the attention of researchers and has been profiled
extensively in the literature. Most of the literature has focused on
characterising arsenic poisoning and factors associated with it. However,
studies examining the socio-economic aspects of chronic exposure of
arsenic through either drinking water or foods remain underexplored. The
objectives of this paper are (i) to review arsenic exposure pathways to
humans; (ii) to summarise public health impacts of chronic arsenic
exposure; and (iii) to examine socio-economic implications and
consequences of arsenicosis with a focus on Bangladesh. This scoping
review evaluates the contributions of different exposure pathways by
analysing arsenic concentrations in dietary and non-dietary sources. The
socio-economic consequences of arsenicosis disease in Bangladesh are
discussed in this review by considering food habits, nutritional status,
socio-economic conditions, and socio-cultural behaviours of the people of
the country. The pathways of arsenic exposure in Bangladesh include
drinking water, various plant foods and non-dietary sources such as soil.
Arsenic affected people are often abandoned by the society, lose their
jobs and get divorced and are forced to live a sub-standard life. The
fragile public health system in Bangladesh has been burdened by the
management of thousands of arsenicosis victims in Bangladesh.
KW - Arsenic exposure
KW - Bangladesh
KW - Public health
KW - Socio-cultural
KW - Socio-economic
RN - N712M78A8G
LA - eng
IS - 1090-2414 (Electronic)
PT - Journal Article
PT - Review
TA - Ecotoxicol Environ Saf
YR - 2018
DATE- 20180515
CI - Copyright &copy; 2017 Elsevier Inc. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Ecotoxicology and environmental safety
EDAT- 20180104
STAT- MEDLINE
DOCNO- medline/29304476

40 - TOXLINE
TI - Health Risk Assessment and Urinary Excretion of Children Exposed to
Arsenic through Drinking Water and Soils in Sonora, Mexico.
AU - Garc�a-Rico L
AD - Programa de Doctorado en Ciencias Especialidad en Biotecnolog�a, Instituto
Tecnol�gico de Sonora, 5 de Febrero 818 Sur, 85000, Cd., Obreg�n, Sonora, Mexico.
AU - Meza-Figueroa D
AD - Departamento de Geolog�a, Divisi�n de Ciencias Exactas y Naturales,
Universidad de Sonora, Rosales y Encinas, 83000, Hermosillo, Sonora, Mexico.
AU - Jay Gandolfi A
AD - Department of Pharmacology and Toxicology, University of Arizona, 1723 E.
Mabel Street, Tucson, AZ, 85724, USA.
AU - Del Rivero CI
AD - Programa de Maestr�a, Departamento de Geolog�a, Divisi�n de Ciencias Exactas
y Naturales, Universidad de Sonora, Rosales y Encinas, 83000, Hermosillo, Sonora,
Mexico.
AU - Mart�nez-Cinco MA
AD - Divisi�n de Estudios de Posgrado, Facultad de Ingenier�a Qu�mica, Universidad
Michoacana de San Nicol�s de Hidalgo (UMSNH), Gral. Francisco J. M�gica SN,
Felicitas del R�o, 58040, Morelia, Michoac�n, Mexico.
AU - Meza-Montenegro MM
AD - Departamento de Recursos Naturales, Instituto Tecnol�gico de Sonora, 5 de
Febrero 818 Sur, 85000, Cd. Obreg�n, Sonora, Mexico. mmeza@itson.edu.mx.
SO - Biol Trace Elem Res. 2018, May 02. [Biological trace element research]
AB - Environmental arsenic exposure is associated with increased risk of
non-cancerous chronic diseases and a variety of cancers in humans. The
aims of this study were to carry out for the first time a health risk
assessment for two common arsenic exposure routes (drinking water and soil
ingestion) in children living in the most important agricultural areas in
the Yaqui and Mayo valleys in Sonora, Mexico. Drinking water sampling was
conducted in the wells of 57 towns. A cross-sectional study was done in
306 children from 13 villages in the valleys. First morning void urine
samples were analyzed for inorganic arsenic (InAs) and monomethyl and
dimethyl arsenic (MMA and DMA) by HPLC/ICP-MS. The results showed a wide
range of arsenic levels in drinking water between 2.7 and 98.7 &mu;g
As/L. Arsenic levels in agricultural and backyard soils were in the range
of < &thinsp;10-27 mg As/kg. The hazard index
(HI)&thinsp;=&thinsp;&sum;hazard quotient (HQ) for drinking water,
agricultural soil, and backyard soil showed values > &thinsp;1 in 100%
of the study towns, and the carcinogenic risk (CR) was greater than 1E-04
in 85%. The average of arsenic excreted in urine was 31.7 &mu;g As/L,
and DMA had the highest proportion in urine, with averages of 77.8%,
followed by InAs and MMA with 11.4 and 10.9%, respectively, percentages
similar to those reported in the literature. Additionally, positive
correlations between urinary arsenic levels and HI values were found
(r&thinsp;=&thinsp;0.59, P&thinsp;=&thinsp;0.000). These results indicated
that this population is at high risk of developing chronic diseases
including cancer.
KW - Arsenic
KW - Children
KW - Drinking water
KW - Health risk assessment
KW - Soil
KW - Urinary arsenic
LA - eng
IS - 1559-0720 (Electronic)
PT - Journal Article
TA - Biol Trace Elem Res
YR - 2018
DATE- 20180503
CITO- NLM
CS - United States
FJT - Biological trace element research
EDAT- 20180502
STAT- Publisher
DOCNO- medline/29721859

41 - TOXLINE
TI - Ameliorative effects of selenium on arsenic-induced cytotoxicity in
PC12&#8239;cells via modulating autophagy/apoptosis.
AU - Rahman MM
AD - Graduate School of Environmental Science, Hokkaido University, Japan;
Department of Environmental Sciences, Jahangirnagar University, Bangladesh.
AU - Uson-Lopez RA
AD - Graduate School of Environmental Science, Hokkaido University, Japan.
AU - Sikder MT
AD - Faculty of Health Sciences, Hokkaido University, Japan.
AU - Tan G
AD - Graduate School of Environmental Science, Hokkaido University, Japan.
AU - Hosokawa T
AD - Institute for the Advancement of Higher Education, Hokkaido University,
Japan.
AU - Saito T
AD - Faculty of Health Sciences, Hokkaido University, Japan.
AU - Kurasaki M
AD - Graduate School of Environmental Science, Hokkaido University, Japan; Faculty
of Environmental Earth Science, Hokkaido University, Japan. Electronic address:
kura@ees.hokudai.ac.jp.
SO - Chemosphere. 2018, Apr; 196:453-466. [Chemosphere]
AB - Arsenic is well known toxicant responsible for human diseases including
cancers. On the other hand, selenium is an essential trace element with
significant chemopreventive effects, anticancer potentials and antioxidant
properties. Although previous studies have reported antagonism/synergism
between arsenic and selenium in biological systems, the biomolecular
mechanism/s is still inconclusive. Therefore, to elucidate the molecular
phenomena in cellular level, we hypothesized that co-exposure of selenium
with arsenic may have suppressive effects on arsenic-induced cytotoxicity.
We found that selenium in co-exposure with arsenic increases cell
viability, and suppresses oxidative stress induced by arsenic in
PC12&#8239;cells. Consequently, DNA fragmentation due to arsenic exposure
was also reduced by arsenic and selenium co-exposure. Furthermore, western
blot analyses revealed that simultaneous exposure of both metals
significantly inhibited autophagy which further suppressed apoptosis
through positively regulation of key proteins; p-mTOR, p-Akt, p-Foxo1A,
p62, and expression of ubiquitin, Bax, Bcl2, NF&#1082;B, and caspases 3
and 9, although those are negatively regulated by arsenic. In addition,
reverse transcriptase PCR analysis confirmed the involvement of caspase
cascade in cell death process induced by arsenic and subsequent inhibition
by co-exposure of selenium with arsenic. The cellular accumulation study
of arsenic in presence/absence of selenium via inductively coupled plasma
mass spectrometry confirmed that selenium effectively retarded the uptake
of arsenic in PC12&#8239;cells. Finally, these findings imply that
selenium is capable to modulate arsenic-induced intrinsic apoptosis
pathway via enhancement of mTOR/Akt autophagy signaling pathway through
employing antioxidant potentials and through inhibiting the cellular
accumulation of arsenic in PC12&#8239;cells.
KW - Apoptosis
KW - Autophagy
KW - Cytotoxicity
KW - Glutathione
KW - Malondialdehyde
KW - mTOR/Akt-pathway
RN - EC 2.7.1.1
RN - EC 2.7.1.1
RN - H6241UJ22B
RN - N712M78A8G
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180312
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171228
STAT- MEDLINE
DOCNO- medline/29324385

42 - TOXLINE
TI - Arsenic removal from alkaline leaching solution using Fe (III)
precipitation.
AU - Wang Y
AD - a State Key Laboratory of Multiphase Complex System, Institute of Process
Engineering, Chinese Academy of Sciences , Beijing , People's Republic of China.
AU - Lv C
AD - b School of Chemistry and Chemical Engineering , University of Chinese
Academy of Sciences , Beijing , People's Republic of China.
AU - Xiao L
AD - b School of Chemistry and Chemical Engineering , University of Chinese
Academy of Sciences , Beijing , People's Republic of China.
AU - Fu G
AD - b School of Chemistry and Chemical Engineering , University of Chinese
Academy of Sciences , Beijing , People's Republic of China.
AU - Liu Y
AD - b School of Chemistry and Chemical Engineering , University of Chinese
Academy of Sciences , Beijing , People's Republic of China.
AU - Ye S
AD - a State Key Laboratory of Multiphase Complex System, Institute of Process
Engineering, Chinese Academy of Sciences , Beijing , People's Republic of China.
AU - Chen Y
AD - a State Key Laboratory of Multiphase Complex System, Institute of Process
Engineering, Chinese Academy of Sciences , Beijing , People's Republic of China.
SO - Environ Technol. 2018, Feb 02:1-7. [Environmental technology]
AB - The alkaline leaching solution from arsenic-containing gold concentrate
contains a large amount of arsenate ions, which should be removed because
it is harmful to the production process and to the environment. In this
study, conventional Fe (III) precipitation was used to remove arsenic from
the leaching solution. The precipitation reaction was carried out at the
normal temperature, and the effects of pH value and Fe/As ratio on the
arsenic removal were investigated. The results show that the removal rate
of arsenic is distinctive at different pH values, and the effect is best
within the pH range of 5.25-5.96. The removal rate can be further
increased by increasing the ratio of Fe/As. When the
pH&thinsp;=&thinsp;5.25-5.96 and Fe/As&thinsp; > &thinsp;1.8, the arsenic
in the solution can be reduced to below 5&#8197;mg/L. However, the
crystallinity of ferric arsenate is poor, and the particle size is small,
most of which is about 1&#8197;&mu;m. The leaching toxicity test shows the
leaching toxicity of precipitates gradually decreased by the increase of
Fe/As. The precipitates can be stored safely as the ratio of Fe/As
exceeded 2.5.
KW - Arsenic precipitates
KW - Fe/As ratio
KW - ferric arsenate
KW - leaching toxicity
LA - eng
IS - 0959-3330 (Print)
PT - Journal Article
TA - Environ Technol
YR - 2018
DATE- 20180202
CITO- NLM
CS - England
FJT - Environmental technology
EDAT- 20180202
STAT- Publisher
DOCNO- medline/29345188

43 - TOXLINE
TI - A novel biodegradable arsenic adsorbent by immobilization of iron
oxyhydroxide (FeOOH) on the root powder of long-root Eichhornia crassipes.
AU - Lin S
AD - State Environmental Protection Key Laboratory of Environmental Risk
Assessment and Control on Chemical Process, East China University of Science and
Technology, Shanghai, 200237, China. Electronic address: linsen@ecust.edu.cn.
AU - Yang H
AD - Yunnan Research Institute of Ecological Agriculture, Yunnan, 610203, China.
AU - Na Z
AD - Yunnan Research Institute of Ecological Agriculture, Yunnan, 610203, China.
AU - Lin K
AD - State Environmental Protection Key Laboratory of Environmental Risk
Assessment and Control on Chemical Process, East China University of Science and
Technology, Shanghai, 200237, China. Electronic address: linkuangfei@ecust.edu.cn.
SO - Chemosphere. 2018, Feb; 192:258-266. [Chemosphere]
AB - In this study, FeOOH was immobilized on the biodegradable root powder,
abbreviated as RP, of long-root Eichhornia crassipes, a kind of waste
biomass, to improve the adsorption performances for aqueous arsenic
contaminants. The adsorption kinetics and thermodynamics experiments
showed that the adsorption rates and capacities of the root powder for
arsenate (As(V)) and arsenite (As(III)) were both enhanced markedly after
modification with FeOOH. The adsorption of As(V) and As(III) by the
modified root powder, abbreviated as MRP, could arrive at equilibrium in
50 min and the saturated adsorption capacities reached up to
8.67-9.43 mg/g for As(V) and 5.21-5.65 mg/g for As(V) at
temperature of 10-50 &deg;C, respectively. Besides, the effect of pH
and ionic strength on adsorption was investigated and the results showed
that the optimum pH for the arsenic adsorption using the MRP was 9.0 and
the As(V) adsorption was more sensitive to ionic strength. Furthermore,
the complexation of hydratable hydroxyls on FeOOH with arsenic
contaminants was concluded as the adsorption force according FTIR and XPS
analyses. The MRP used could be regenerated via 0.4 mol/L NaOH
solution and no apparent adsorption capacity losses appeared after 6
cyclic utilizations.
KW - Arsenic adsorption
KW - Complexation
KW - Hydratable hydroxyls
KW - Immobilization
KW - Long-root Eichhornia crassipes
RN - 2UA751211N
RN - N5509X556J
RN - N712M78A8G
RN - N7CIZ75ZPN
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180130
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171030
STAT- MEDLINE
DOCNO- medline/29107877

44 - TOXLINE
TI - In Vitro Model To Assess Arsenic Bioaccessibility and Speciation in Cooked
Shrimp.
AU - Chi H
AD - State Key Laboratory of Urban Environment and Health, Institute of Urban
Environment , Chinese Academy of Sciences , Xiamen , Fujian 361021 , People's
Republic of China.
AU - Zhang Y
AD - State Key Laboratory of Urban Environment and Health, Institute of Urban
Environment , Chinese Academy of Sciences , Xiamen , Fujian 361021 , People's
Republic of China.
AU - Williams PN
AD - Institute for Global Food Security, School of Biological Sciences , Queen's
University Belfast , Belfast BT9 7BL , United Kingdom.
AU - Lin S
AD - State Key Laboratory of Urban Environment and Health, Institute of Urban
Environment , Chinese Academy of Sciences , Xiamen , Fujian 361021 , People's
Republic of China.
AU - Hou Y
AD - Department of Environmental Science and Engineering , Huaqiao University ,
Xiamen , Fujian 361021 , People's Republic of China.
AU - Cai C
AD - State Key Laboratory of Urban Environment and Health, Institute of Urban
Environment , Chinese Academy of Sciences , Xiamen , Fujian 361021 , People's
Republic of China.
SO - J Agric Food Chem. 2018, May 09; 66(18):4710-4715. [Journal of
agricultural and food chemistry]
AB - Shrimp, a popular and readily consumed seafood, contains high
concentrations of arsenic. However, few studies have focused on whether
arsenic in the shrimp could be transformed during the cooking process and
gastrointestinal digestion. In this study, a combined in vitro model
[Unified Bioaccessibility Research Group of Europe (BARGE)
Method-Simulator of Human Intestinal Microbial Ecosystem (UBM-SHIME)] was
used to investigate arsenic bioaccessibility and its speciation in raw and
cooked shrimps. The results showed that the cooking practices had little
effect on the arsenic content and speciation. Bioaccessibility of arsenic
in raw shrimp was at a high level, averaging 76.9 &plusmn; 4.28 and 86.7
&plusmn; 3.74% in gastric and small intestinal phases, respectively.
Arsenic speciation was stable in all of the shrimp digestions, with
nontoxic arsenobetaine (AsB) being the dominated speciation. The cooking
practice significantly increased the bioaccessibility of arsenate ( p <
0.05) in shrimp digests, indicating the increase of the potential health
risks.
KW - arsenic
KW - bioaccessibility
KW - in vitro model
KW - shrimp
KW - speciation
RN - N712M78A8G
LA - eng
IS - 1520-5118 (Electronic)
PT - Journal Article
TA - J Agric Food Chem
YR - 2018
DATE- 20180523
CITO- NLM
CS - United States
CSET- IM
FJT - Journal of agricultural and food chemistry
EDAT- 20180424
STAT- MEDLINE
DOCNO- medline/29633616

45 - TOXLINE
TI - Low-level arsenic causes proteotoxic stress and not oxidative stress.
AU - Dodson M
AD - Department of Pharmacology and Toxicology, College of Pharmacy, University of
Arizona, Tucson, AZ 85721, USA.
AU - de la Vega MR
AD - Department of Pharmacology and Toxicology, College of Pharmacy, University of
Arizona, Tucson, AZ 85721, USA.
AU - Harder B
AD - Department of Pharmacology and Toxicology, College of Pharmacy, University of
Arizona, Tucson, AZ 85721, USA.
AU - Castro-Portuguez R
AD - Department of Pharmacology and Toxicology, College of Pharmacy, University of
Arizona, Tucson, AZ 85721, USA.
AU - Rodrigues SD
AD - Department of Pharmacology and Toxicology, College of Pharmacy, University of
Arizona, Tucson, AZ 85721, USA.
AU - Wong PK
AD - Department of Biomedical Engineering, The Pennsylvania State University,
University Park, PA 16802, USA.
AU - Chapman E
AD - Department of Pharmacology and Toxicology, College of Pharmacy, University of
Arizona, Tucson, AZ 85721, USA.
AU - Zhang DD
AD - Department of Pharmacology and Toxicology, College of Pharmacy, University of
Arizona, Tucson, AZ 85721, USA; Arizona Cancer Center, University of Arizona,
Tucson, AZ 85724, USA. Electronic address: dzhang@pharmacy.arizona.edu.
SO - Toxicol Appl Pharmacol. 2018, Feb 15; 341:106-113. [Toxicology and applied
pharmacology]
AB - Prolonged exposure to arsenic has been shown to increase the risk of
developing a number of diseases, including cancer and type II diabetes.
Arsenic is present throughout the environment in its inorganic forms, and
the level of exposure varies greatly by geographical location. The current
recommended maximum level of arsenic exposure by the EPA is 10&mu;g/L, but
levels > 50-1000&mu;g/L have been detected in some parts of Asia, the
Middle East, and the Southwestern United States. One of the most important
steps in developing treatment options for arsenic-linked pathologies is to
understand the cellular pathways affected by low levels of arsenic. Here,
we show that acute exposure to non-lethal, low-level arsenite, an
environmentally relevant arsenical, inhibits the autophagy pathway.
Furthermore, arsenite-induced autophagy inhibition initiates a transient,
but moderate ER stress response. Significantly, low-level arsenite
exposure does not exhibit an increase in oxidative stress. These findings
indicate that compromised autophagy, and not enhanced oxidative stress
occurs early during arsenite exposure, and that restoring the autophagy
pathway and proper proteostasis could be a viable option for treating
arsenic-linked diseases. As such, our study challenges the existing
paradigm that oxidative stress is the main underlying cause of pathologies
associated with environmental arsenic exposure.
KW - Arsenic
KW - Autophagy inhibitor
KW - ER stress
KW - Oxidative stress
KW - Proteostasis
LA - eng
IS - 1096-0333 (Electronic)
PT - Journal Article
TA - Toxicol Appl Pharmacol
YR - 2018
DATE- 20180503
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - United States
FJT - Toxicology and applied pharmacology
EDAT- 20180203
STAT- In-Data-Review
CM - Cites: Environ Health Perspect. 2016 Jan;124(1):104-11 (medline /26068977)
CM - Cites: Environ Health Perspect. 2000 Jul;108(7):655-61 (medline /10903620)
CM - Cites: Toxicol Sci. 2007 Feb;95(2):321-30 (medline /17093206)
CM - Cites: Toxicol Lett. 2003 Jan 31;137(1-2):15-21 (medline /12505429)
CM - Cites: J Appl Toxicol. 2016 Feb;36(2):179-88 (medline /26510484)
CM - Cites: Water Res. 2014 Jan 1;48:156-69 (medline /24094730)
CM - Cites: Sci Total Environ. 2006 Aug 1;366(2-3):701-21 (medline /16203025)
CM - Cites: Arch Toxicol. 2012 Jun;86(6):923-33 (medline /22622864)
CM - Cites: Toxicol Appl Pharmacol. 2001 Oct 15;176(2):127-44 (medline
/11601889)
CM - Cites: Arch Toxicol. 2000 Aug;74(6):289-99 (medline /11005674)
CM - Cites: Toxicol Appl Pharmacol. 2001 Sep 15;175(3):260-8 (medline
/11559025)
CM - Cites: Mol Cell Biol. 2013 Jun;33(12 ):2436-46 (medline /23589329)
CM - Cites: Environ Health Perspect. 2012 Dec;120(12 ):1658-70 (medline
/22889723)
CM - Cites: Toxicology. 2009 Aug 3;262(2):162-70 (medline /19524636)
CM - Cites: Onco Targets Ther. 2013;6:75-84 (medline /23404534)
CM - Cites: J Exp Clin Cancer Res. 2014 May 16;33:42 (medline /24887205)
CM - Cites: Curr Environ Health Rep. 2015 Mar;2(1):52-68 (medline /26231242)
CM - Cites: Chem Rev. 2013 Oct 9;113(10):7769-92 (medline /23808632)
CM - Cites: Environ Health Perspect. 2008 Feb;116(2):190-5 (medline /18288317)
CM - Cites: Science. 2002 Nov 22;298(5598):1602-6 (medline /12446905)
CM - Cites: Free Radic Biol Med. 2013 Oct;63:207-21 (medline /23702245)
CM - Cites: Environ Toxicol Pharmacol. 2013 Nov;36(3):891-902 (medline
/24004876)
CM - Cites: JAMA. 2008 Aug 20;300(7):814-22 (medline /18714061)
CM - Cites: Curr Pharmacol Rep. 2016 Apr;2(2):57-63 (medline /27134817)
CM - Cites: Cancer Res. 2010 Jun 15;70(12):5127-35 (medline /20516118)
CM - Cites: Free Radic Biol Med. 1999 Dec;27(11-12):1405-12 (medline /10641735)
CM - Cites: Environ Health Perspect. 2000 May;108(5):393-7 (medline /10811564)
CM - Cites: Toxicol Appl Pharmacol. 2004 Aug 1;198(3):243-52 (medline
/15276403)
CM - Cites: J Toxicol. 2011;2011:431287 (medline /22174709)
CM - Cites: Am J Epidemiol. 2014 Dec 1;180(11):1082-7 (medline /25371173)
CM - Cites: Autophagy. 2007 Sep-Oct;3(5):452-60 (medline /17534139)
CM - Cites: Environ Toxicol. 2017 Jan;32(1):197-216 (medline /26677073)
CM - Cites: Environ Int. 2008 Aug;34(6):756-64 (medline /18291528)
CM - Cites: Toxicol Sci. 2015 Aug;146(2):290-300 (medline /25979314)
CM - Cites: Toxicol Sci. 2011 Oct;123(2):305-32 (medline /21750349)
CM - Cites: Environ Health Perspect. 2006 Aug;114(8):1193-8 (medline /16882524)
CM - Cites: Environ Health Perspect. 2013 Feb;121(2):237-43 (medline /23221991)
CM - Cites: J Hazard Mater. 2017 Jan 5;321:432-439 (medline /27669384)
CM - Cites: Cancer Epidemiol Biomarkers Prev. 2013 Apr;22(4):623-30 (medline
/23355602)
CM - Cites: Cancer Res. 2005 Apr 15;65(8):3236-42 (medline /15833855)
CM - Cites: Toxicol Lett. 2014 Jan 3;224(1):130-40 (medline /24157283)
DOCNO- medline/29408041
46 - TOXLINE
TI - Enhanced oxidation of arsenite to arsenate using tunable K+ concentration
in the OMS-2 tunnel.
AU - Hou J
AD - Key Laboratory of Arable Land Conservation (Middle and Lower Reaches of
Yangtse River), Ministry of Agriculture, College of Resources and Environment,
Huazhong Agricultural University, Wuhan, 430070, China; State Key Laboratory of
Silicate Materials for Architectures, Wuhan University of Technology, Wuhan,
430070, China. Electronic address: jthou@mail.hzau.edu.cn.
AU - Sha Z
AD - Key Laboratory of Arable Land Conservation (Middle and Lower Reaches of
Yangtse River), Ministry of Agriculture, College of Resources and Environment,
Huazhong Agricultural University, Wuhan, 430070, China.
AU - Hartley W
AD - Crop and Environment Sciences Department, Harper Adams University, Newport,
Shropshire, TF10 8NB, United Kingdom.
AU - Tan W
AD - Key Laboratory of Arable Land Conservation (Middle and Lower Reaches of
Yangtse River), Ministry of Agriculture, College of Resources and Environment,
Huazhong Agricultural University, Wuhan, 430070, China.
AU - Wang M
AD - Key Laboratory of Arable Land Conservation (Middle and Lower Reaches of
Yangtse River), Ministry of Agriculture, College of Resources and Environment,
Huazhong Agricultural University, Wuhan, 430070, China.
AU - Xiong J
AD - Key Laboratory of Arable Land Conservation (Middle and Lower Reaches of
Yangtse River), Ministry of Agriculture, College of Resources and Environment,
Huazhong Agricultural University, Wuhan, 430070, China.
AU - Li Y
AD - State Key Laboratory of Silicate Materials for Architectures, Wuhan
University of Technology, Wuhan, 430070, China.
AU - Ke Y
AD - School of Materials Science and Engineering, Nanyang Technological
University, 50 Nanyang Avenue, Singapore, 639798, Singapore.
AU - Long Y
AD - School of Materials Science and Engineering, Nanyang Technological
University, 50 Nanyang Avenue, Singapore, 639798, Singapore.
AU - Xue S
AD - Department of Environmental Engineering, School of Metallurgy and
Environment, Central South University, Changsha, 410083, China; Chinese National
Engineering Research Centre for Control and Treatment of Heavy Metal Pollution,
Changsha, 410083, China.
SO - Environ Pollut. 2018, Jul; 238:524-531. [Environmental pollution (Barking,
Essex : 1987)]
AB - Cryptomelane-type octahedral molecular sieve manganese oxide (OMS-2)
possesses high redox potential and has attracted much interest in its
application for oxidation arsenite (As(III)) species of arsenic to
arsenate (As(V)) to decrease arsenic toxicity and promote total arsenic
removal. However, coexisting ions such as As(V) and phosphate are
ubiquitous and readily bond to manganese oxide surface, consequently
passivating surface active sites of manganese oxide and reducing As(III)
oxidation. In this study, we present a novel strategy to significantly
promote As(III) oxidation activity of OMS-2 by tuning K+ concentration in
the tunnel. Batch experimental results reveal that increasing K+
concentration in the tunnel of OMS-2 not only considerably improved
As(III) oxidation kinetics rate from 0.027 to 0.102 min-1, but also
reduced adverse effect of competitive ion on As(III) oxidation. The origin
of K+ concentration effect on As(III) oxidation was investigated through
As(V) and phosphate adsorption kinetics, detection of Mn2+ release in
solution, surface charge characteristics, and density functional theory
(DFT) calculations. Experimental results and theoretical calculations
confirm that by increasing K+ concentration in the OMS-2 tunnel not only
does it improve arsenic adsorption on K+ doped OMS-2, but also accelerates
two electrons transfers from As(III) to each bonded Mn atom on OMS-2
surface, thus considerably improving As(III) oxidation kinetics rate,
which is responsible for counteracting the adverse adsorption effects by
coexisting ions.
KW - Arsenate
KW - Arsenite oxidation
KW - Competitive adsorption
KW - K(+) doping
KW - OMS-2
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180515
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Environmental pollution (Barking, Essex : 1987)
EDAT- 20180330
STAT- In-Process
DOCNO- medline/29605612

47 - TOXLINE
TI - Chronic Arsenic Exposure Increases A&beta;(1-42) Production and Receptor
for Advanced Glycation End Products Expression in Rat Brain.
AU - Ni�o SA
AD - Centro de Biociencias, Universidad Aut�noma de San Luis Potos� , Km. 14.5
carretera San Luis Potos� - Matehuala, Ejido "Palma de la Cruz", CP 78321 Soledad
de Graciano S�nchez, San Luis Potos�, M�xico.
AU - Martel-Gallegos G
AD - Laboratorio Nacional Forense Nuclear, Instituto Nacional de Investigaciones
Nucleares , Carretera M�xico-Toluca s/n, CP 52750 La Marquesa Ocoyoacac, M�xico.
AU - Castro-Zavala A
AD - Laboratorio Nacional Forense Nuclear, Instituto Nacional de Investigaciones
Nucleares , Carretera M�xico-Toluca s/n, CP 52750 La Marquesa Ocoyoacac, M�xico.
AU - Ortega-Berlanga B
AD - Laboratorio Nacional Forense Nuclear, Instituto Nacional de Investigaciones
Nucleares , Carretera M�xico-Toluca s/n, CP 52750 La Marquesa Ocoyoacac, M�xico.
AU - Delgado JM
AD - Laboratorio Nacional Forense Nuclear, Instituto Nacional de Investigaciones
Nucleares , Carretera M�xico-Toluca s/n, CP 52750 La Marquesa Ocoyoacac, M�xico.
AU - Hern�ndez-Mendoza H
AD - Laboratorio Nacional Forense Nuclear, Instituto Nacional de Investigaciones
Nucleares , Carretera M�xico-Toluca s/n, CP 52750 La Marquesa Ocoyoacac, M�xico.
AU - Romero-Guzm�n E
AD - Laboratorio Nacional Forense Nuclear, Instituto Nacional de Investigaciones
Nucleares , Carretera M�xico-Toluca s/n, CP 52750 La Marquesa Ocoyoacac, M�xico.
AU - R�os-Lugo J
AD - Laboratorio Nacional Forense Nuclear, Instituto Nacional de Investigaciones
Nucleares , Carretera M�xico-Toluca s/n, CP 52750 La Marquesa Ocoyoacac, M�xico.
AU - Rosales-Mendoza S
AD - Laboratorio Nacional Forense Nuclear, Instituto Nacional de Investigaciones
Nucleares , Carretera M�xico-Toluca s/n, CP 52750 La Marquesa Ocoyoacac, M�xico.
AU - Jim�nez-Capdeville ME
AD - Laboratorio Nacional Forense Nuclear, Instituto Nacional de Investigaciones
Nucleares , Carretera M�xico-Toluca s/n, CP 52750 La Marquesa Ocoyoacac, M�xico.
AU - Zaraz�a S
AD - Laboratorio Nacional Forense Nuclear, Instituto Nacional de Investigaciones
Nucleares , Carretera M�xico-Toluca s/n, CP 52750 La Marquesa Ocoyoacac, M�xico.
SO - Chem Res Toxicol. 2018, Jan 16; 31(1):13-21. [Chemical research in
toxicology]
AB - Chronic arsenic exposure during development is associated with alterations
of chemical transmission and demyelination, which result in cognitive
deficits and peripheral neuropathies. At the cellular level, arsenic
toxicity involves increased generation of reactive species that induce
severe cellular alterations such as DNA fragmentation, apoptosis, and
lipid peroxidation. It has been proposed that arsenic-associated
neurodegeneration could evolve to Alzheimer disease in later life.1,2 In
this study, the effects of chronic exposure to inorganic arsenic (3 ppm by
drinking water) in Wistar rats on the production and elimination of
Amyloid-&beta; (A&beta;) were evaluated. Male Wistar rats were exposed to
3 ppm of arsenic in drinking water from fetal development until 4 months
of age. After behavioral deficits induced by arsenic exposure through
contextual fear conditioning were verified, the brains were collected for
the determination of total arsenic by inductively coupled plasma-mass
spectrometry, the levels of amyloid precursor protein and receptor for
advanced glycation end products (RAGE) by Western blot analysis as well as
their transcript levels by RT-qPCR, A&beta;(1-42) estimation by ELISA
assay and the enzymatic activity of &beta;-secretase (BACE1). Our results
demonstrate that chronic arsenic exposure induces behavioral deficits
accompanied of higher levels of soluble and membranal RAGE and the
increase of A&beta;(1-42) cleaved. In addition, BACE1 enzymatic activity
was increased, while immunoblot assays showed no differences in the
low-density lipoprotein receptor-related protein 1 (LRP1) receptor among
groups. These results provide evidence of the effects of arsenic exposure
on the production of A&beta;(1-42) and cerebral amyloid clearance through
RAGE in an in vivo model that displays behavioral alterations. This work
supports the hypothesis that early exposure to metals may contribute to
neurodegeneration associated with amyloid accumulation.
LA - eng
IS - 1520-5010 (Electronic)
PT - Journal Article
TA - Chem Res Toxicol
YR - 2018
DATE- 20180116
CITO- NLM
CS - United States
FJT - Chemical research in toxicology
EDAT- 20171204
STAT- In-Data-Review
DOCNO- medline/29155576

48 - TOXLINE
TI - Arsenic uptake by arugula (Eruca vesicaria, L.) cultivars as affected by
phosphate availability.
AU - Tang X
AD - Institute of Hydrobiology, Jinan University, Guangzhou, 510632, China.
AU - Lim MP
AD - Section of Soil and Crop Sciences, School of Integrative Plant Science,
Cornell University, Ithaca, NY, 14850, USA.
AU - McBride MB
AD - Section of Soil and Crop Sciences, School of Integrative Plant Science,
Cornell University, Ithaca, NY, 14850, USA. Electronic address: mbm7@cornell.edu.
SO - Chemosphere. 2018, Mar; 195:559-566. [Chemosphere]
AB - To assess the importance of variation among arugula (Eruca vesicaria
subsp. sativa) cultivars in the ability to accumulate arsenic (As) in
above-ground tissues, uptake of As by 16 cultivars was measured in the
field and in hydroponic culture. In the field trial on soil contaminated
by past pesticide use, As soil-plant uptake coefficients varied by a
factor of 2.7 among different cultivars, approaching a value of one for
the strongest accumulators. Compared to the field assay, hydroponically
grown arugula accumulated much lower concentrations of As when nutrient
solutions contained standard (high) concentrations of phosphate along with
1.0&#8239;mg&#8239;L-1 As in the form of soluble arsenate. However, As
accumulation was much greater in hydroponic culture using low-P nutrient
solutions, an indication that phosphate strongly competed with arsenate
for root uptake. Analysis of arugula roots after exposure to arsenate at
1.0&#8239;mg As L-1 and low phosphate revealed from 24 to 400 times
greater As concentration in roots than tops, with S concentrations
significantly greater in As-exposed than control roots. This indicated
greater sulfate uptake by roots exposed to arsenate, and suggested that
thiol-mediated As immobilization occurred in the roots which strongly
restricted translocation to the tops.
KW - Arsenic bioaccumulation
KW - Arsenic immobilization in roots
KW - Arugula cultivars
KW - Brassicas
KW - Genetic variation
RN - N712M78A8G
RN - N7CIZ75ZPN
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180606
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171227
STAT- MEDLINE
DOCNO- medline/29277036

49 - TOXLINE
TI - Arsenic in agricultural soils across China: Distribution pattern,
accumulation trend, influencing factors, and risk assessment.
AU - Zhou Y
AD - MOE Key Laboratory of Environmental Remediation and Ecosystem Health, College
of Environmental and Resource Sciences, Zhejiang University, Hangzhou 310058,
China.
AU - Niu L
AD - MOE Key Laboratory of Environmental Remediation and Ecosystem Health, College
of Environmental and Resource Sciences, Zhejiang University, Hangzhou 310058,
China.
AU - Liu K
AD - Division of Engineering and Applied Science, California Institute of
Technology, Pasadena, CA 91125, USA. Electronic address: kliu7@caltech.edu.
AU - Yin S
AD - MOE Key Laboratory of Environmental Remediation and Ecosystem Health, College
of Environmental and Resource Sciences, Zhejiang University, Hangzhou 310058,
China.
AU - Liu W
AD - MOE Key Laboratory of Environmental Remediation and Ecosystem Health, College
of Environmental and Resource Sciences, Zhejiang University, Hangzhou 310058,
China. Electronic address: wliu@zju.edu.
SO - Sci Total Environ. 2018, Mar; 616-617:156-163. [The Science of the total
environment]
AB - Arsenic (As) in the environment is of concern due to its strong toxicity
and high risks to the ecosystems and humans. In this study, soil samples
across China collected in 2011 and 2016 were used to determine the
concentrations of arsenic in arable soils. The median concentration of
arsenic in surface soils was 9.7mg/kg. The inventory of arsenic in the
Chinese agricultural surface soils was estimated to be 3.7&times;106tons.
In general, arsenic contamination was found higher in South and Northeast
China than in other regions, with means of 18.7 and 15.8mg/kg,
respectively. Vertically, arsenic concentrations were higher in top layer
(0-15cm) soils (median of 9.8mg/kg) and decreased with soil depth (medians
of 8.9mg/kg at 15-30cm and 8.0mg/kg at 30-45cm). By comparing with
published data, an increasing accumulation trend over the past decades was
found and this enhancement was positively related with the long-term
application of fertilizers in agricultural practice, especially phosphate
fertilizers. Soil pH was found to affect the movement of arsenic in soil,
and high-pH conditions enhanced the pool of arsenic. The ecological risk
assessment revealed that arsenic in Chinese agricultural soil posed a low
risk to the ecosystem. Regarding human health, the mean hazard indices
(HIs) of arsenic were below 1, suggesting an absence of non-carcinogenic
risks. In addition, the cancer risks of arsenic in all soil samples were
within the acceptable range (below 1&times;10-4), indicating low to very
low risks to the exposed population. Findings from this study are valuable
to provide effective management options for risk avoidance and to control
the persistent accumulation of arsenic in the agriculture sector across
the world.
KW - Accumulation trend
KW - Agricultural soil
KW - Arsenic
KW - Distribution pattern
KW - Ecological and human health risk
RN - N712M78A8G
LA - eng
IS - 1879-1026 (Electronic)
PT - Journal Article
TA - Sci Total Environ
YR - 2018
DATE- 20180514
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - The Science of the total environment
EDAT- 20171104
STAT- MEDLINE
DOCNO- medline/29112838

50 - TOXLINE
TI - Effect of the natural arsenic gradient on the diversity and arsenic
resistance of bacterial communities of the sediments of Camarones River
(Atacama Desert, Chile).
AU - Leon CG
AD - Environmental Microbiology Laboratory, Department of Microbiology, Faculty of
Biological Sciences, University of Concepci�n, Concepci�n, Chile.
AU - Moraga R
AD - Microbiology Laboratory, Faculty of Renewable Natural Resources, Arturo Prat
University, Iquique, Chile.
AU - Valenzuela C
AD - Environmental Microbiology Laboratory, Department of Microbiology, Faculty of
Biological Sciences, University of Concepci�n, Concepci�n, Chile.
AU - Gugliandolo C
AD - Department of Chemical, Biological, Pharmaceutical and Environmental
Sciences, University of Messina, Messina, Italy.
AU - Lo Giudice A
AD - Institute for the Coastal Marine Environment, National Research Council
(IAMC-CNR), Messina, Italy.
AU - Papale M
AD - Department of Chemical, Biological, Pharmaceutical and Environmental
Sciences, University of Messina, Messina, Italy.
AU - Vilo C
AD - Environmental Microbiology Laboratory, Department of Microbiology, Faculty of
Biological Sciences, University of Concepci�n, Concepci�n, Chile.
AU - Dong Q
AD - Center for Biomedical Informatics, Department of Public Health Sciences,
Loyola University Chicago, Maywood, Illinois, United States of America.
AU - Smith CT
AD - Environmental Microbiology Laboratory, Department of Microbiology, Faculty of
Biological Sciences, University of Concepci�n, Concepci�n, Chile.
AU - Rossello-Mora R
AD - Marine Microbiology Group, Institut Mediterrani d'Estudis Avancats (CSIC-
UIB), Esporles, Spain.
AU - Ya�ez J
AD - Department of Analytical and Inorganic Chemistry, Faculty of Chemical
Sciences, University of Concepcion, Concepcion, Chile.
AU - Campos VL
AD - Environmental Microbiology Laboratory, Department of Microbiology, Faculty of
Biological Sciences, University of Concepci�n, Concepci�n, Chile.
SO - PLoS One. 2018; 13(5):e0195080. [PloS one]
AB - Arsenic (As), a highly toxic metalloid, naturally present in Camarones
River (Atacama Desert, Chile) is a great health concern for the local
population and authorities. In this study, the taxonomic and functional
characterization of bacterial communities associated to metal-rich
sediments from three sites of the river (sites M1, M2 and M3), showing
different arsenic concentrations, were evaluated using a combination of
approaches. Diversity of bacterial communities was evaluated by Illumina
sequencing. Strains resistant to arsenic concentrations varying from 0.5
to 100 mM arsenite or arsenate were isolated and the presence of genes
coding for enzymes involved in arsenic oxidation (aio) or reduction (arsC)
investigated. Bacterial communities showed a moderate diversity which
increased as arsenic concentrations decreased along the river. Sequences
of the dominant taxonomic groups (abundances &ge;1%) present in all three
sites were affiliated to Proteobacteria (range 40.3-47.2%), Firmicutes
(8.4-24.8%), Acidobacteria (10.4-17.1%), Actinobacteria (5.4-8.1%),
Chloroflexi (3.9-7.5%), Planctomycetes (1.2-5.3%), Gemmatimonadetes
(1.2-1.5%), and Nitrospirae (1.1-1.2%). Bacterial communities from sites
M2 and M3 showed no significant differences in diversity between each
other (p = 0.9753) but they were significantly more diverse than M1
(p < 0.001 and p < 0.001, respectively). Sequences affiliated with
Proteobacteria, Firmicutes, Acidobacteria, Chloroflexi and Actinobacteria
at M1 accounted for more than 89% of the total classified bacterial
sequences present but these phyla were present in lesser proportions in M2
and M3 sites. Strains isolated from the sediment of sample M1, having the
greatest arsenic concentration (498 mg kg-1), showed the largest
percentages of arsenic oxidation and reduction. Genes aio were more
frequently detected in isolates from M1 (54%), whereas arsC genes were
present in almost all isolates from all three sediments, suggesting that
bacterial communities play an important role in the arsenic biogeochemical
cycle and detoxification of arsenical compounds. Overall, results provide
further knowledge on the microbial diversity of arsenic contaminated
fresh-water sediments.
LA - eng
IS - 1932-6203 (Electronic)
PT - Journal Article
TA - PLoS One
YR - 2018
DATE- 20180513
CITO- NLM
CS - United States
FJT - PloS one
EDAT- 20180501
STAT- In-Data-Review
CM - Cites: J Environ Monit. 2005 Dec;7(12):1335-41 (medline /16307093)
CM - Cites: PLoS One. 2014 Apr 22;9(4):e95655 (medline /24755825)
CM - Cites: Biochimie. 2009 Oct;91(10):1229-37 (medline /19567262)
CM - Cites: J Environ Sci Health A Tox Hazard Subst Environ Eng. 2015;50(1):1-8
(medline /25438126)
CM - Cites: Annu Rev Microbiol. 2006;60:107-30 (medline /16704340)
CM - Cites: Extremophiles. 2009 May;13(3):557-65 (medline /19363644)
CM - Cites: J Biol Chem. 1992 Nov 25;267(33):23674-82 (medline /1331097)
CM - Cites: Bull Environ Contam Toxicol. 2009 Nov;83(5):657-61 (medline
/19779656)
CM - Cites: Environ Sci Technol. 2001 Sep 15;35(18):3676-82 (medline /11783644)
CM - Cites: Int J Syst Evol Microbiol. 2006 Aug;56(Pt 8):1765-9 (medline
/16902005)
CM - Cites: Arch Biochem Biophys. 1991 Feb 1;284(2):381-5 (medline /1703401)
CM - Cites: Biochim Biophys Acta. 2004 Jun 7;1656(2-3):148-55 (medline
/15178476)
CM - Cites: J Hazard Mater. 2000 Aug 28;76(1):125-38 (medline /10863019)
CM - Cites: PLoS One. 2014 Oct 09;9(10):e108185 (medline /25299175)
CM - Cites: Biosci Biotechnol Biochem. 2014;78(11):1963-70 (medline /25051896)
CM - Cites: Environ Microbiol. 2007 Apr;9(4):934-43 (medline /17359265)
CM - Cites: J Bacteriol. 2010 Jul;192(14):3755-62 (medline /20453090)
CM - Cites: Arch Environ Contam Toxicol. 2011 Aug;61(2):185-92 (medline
/20859623)
CM - Cites: Reprod Toxicol. 1995 Mar-Apr;9(2):105-13 (medline /7795320)
CM - Cites: Bioinformatics. 2011 Aug 15;27(16):2194-200 (medline /21700674)
CM - Cites: Front Microbiol. 2015 May 06;6:360 (medline /25999920)
CM - Cites: J Bacteriol. 2006 Feb;188(3):1081-8 (medline /16428412)
CM - Cites: Appl Environ Microbiol. 2008 Jul;74(14):4567-73 (medline /18502920)
CM - Cites: PLoS One. 2012;7(6):e40059 (medline /22768219)
CM - Cites: Biodegradation. 2012 Nov;23(6):803-12 (medline /22760225)
CM - Cites: Environ Microbiol. 2015 Jun;17(6):1991-2005 (medline /25244307)
CM - Cites: Nucleic Acids Res. 2013 Jan;41(Database issue):D590-6 (medline
/23193283)
CM - Cites: J Bacteriol. 2012 Jan;194(2):207-8 (medline /22056935)
CM - Cites: Rev Med Chil. 2010 Apr;138(4):461-9 (medline /20668794)
CM - Cites: FEMS Microbiol Rev. 1999 Oct;23(5):615-27 (medline /10525169)
CM - Cites: J Bacteriol. 2003 Jan;185(1):135-41 (medline /12486049)
CM - Cites: Environ Toxicol Chem. 2001 Nov;20(11):2639-43 (medline /11699792)
CM - Cites: Environ Sci Technol. 2004 Jan 1;38(1):104-11 (medline /14740724)
CM - Cites: PLoS One. 2015 Mar 05;10(3):e0119465 (medline /25742617)
CM -Cites: Chemosphere. 2007 Jan;66(4):775-82 (medline /16949129)
CM -Cites: PLoS One. 2017 May 5;12 (5):e0176696 (medline /28475654)
CM -Cites: J Appl Microbiol. 2002;93(4):656-67 (medline /12234349)
CM -Cites: Chemosphere. 2009 Sep;77(2):169-74 (medline /19716583)
CM -Cites: J Basic Microbiol. 2009 Sep;49 Suppl 1:S93-7 (medline /19718679)
CM -Cites: J Biosci Bioeng. 2014 Jul;118(1):1-9 (medline /24507904)
CM -Cites: World J Microbiol Biotechnol. 2012 Apr;28(4):1511-21 (medline
/22805933)
CM - Cites: J Bacteriol. 2012 Aug;194(16):4473-4 (medline /22843599)
CM - Cites: Environ Sci Technol. 2010 Jan 1;44(1):15-23 (medline /20000681)
CM - Cites: PLoS One. 2013 Aug 30;8(8):e72535 (medline /24023621)
CM - Cites: BMC Microbiol. 2009 Jan 08;9:4 (medline /19128515)
CM - Cites: Trends Microbiol. 2005 Feb;13(2):45-9 (medline /15680760)
CM - Cites: Biometals. 2009 Feb;22(1):117-30 (medline /19130261)
CM - Cites: Environ Sci Technol. 2001 Oct 1;35(19):3857-62 (medline /11642444)
CM - Cites: Appl Environ Microbiol. 2010 Jul;76(13):4566-70 (medline /20453153)
CM - Cites: Appl Environ Microbiol. 2002 Jan;68(1):280-8 (medline /11772637)
CM - Cites: Bull Environ Contam Toxicol. 2009 May;82(5):593-6 (medline
/19190837)
CM - Cites: Sci Rep. 2017 Feb 06;7:42037 (medline /28165031)
CM - Cites: Curr Microbiol. 2012 Aug;65(2):212-8 (medline /22638843)
CM - Cites: Res Microbiol. 2007 Mar;158(2):128-37 (medline /17258434)
CM - Cites: J Hazard Mater. 2006 Dec 1;138(3):459-70 (medline /17049728)
CM - Cites: Front Microbiol. 2016 Dec 06;7:1917 (medline /27999565)
DOCNO- medline/29715297

51 - TOXLINE
TI - Sensitive arsenic speciation by capillary electrophoresis using UV
absorbance detection with on-line sample preconcentration techniques.
AU - Lee HG
AD - Department of Chemistry, Seoul National University, Seoul 08826, Republic of
Korea.
AU - Kwon JY
AD - Department of Chemistry, Seoul National University, Seoul 08826, Republic of
Korea.
AU - Chung DS
AD - Department of Chemistry, Seoul National University, Seoul 08826, Republic of
Korea. Electronic address: dschung@snu.ac.kr.
SO - Talanta. 2018, May 01; 181:366-372. [Talanta]
AB - The World Health Organization (WHO) guideline states that the total
arsenic concentration in drinking water must not exceed 10 ppb. However,
arsenic toxicity varies significantly, with inorganic arsenic species
being more toxic than organic species. Arsenic speciation is therefore
important for evaluating the health risks from arsenic-contaminated
drinking water. Capillary electrophoresis provides the necessary high
performance separation to determine arsenic species in water, but its
sensitivity with absorbance detection is far below than needed. Using a
coated capillary, several on-line sample preconcentration techniques such
as large volume sample stacking with an electroosmotic flow pump, field
amplified sample injection (FASI), transient isotachophoresis (tITP),
electrokinetic supercharging (EKS) combining FASI and tITP, and counter
flow (CF)-EKS, were therefore investigated. With CF-EKS using phosphate
and N-cyclohexyl-2-aminoethanesulfonate as leading and terminating
electrolytes, respectively, standard samples of arsenite, arsenate,
monomethylarsonic acid, and dimethylarsinic acid were preconcentrated from
6,300- to 45,000-fold. The limits of detection obtained with UV absorbance
detection were 0.08-0.3 ppb As. For a spring water sample spiked with the
four arsenic species, LODs of 2-9 ppb As were obtained, which are lower
than the WHO guideline of 10 ppb total As.
KW - Arsenic speciation
KW - Capillary electrophoresis
KW - Counter flow electrokinetic supercharging
KW - Isotachophoresis
KW - Sample stacking technique
LA - eng
IS - 1873-3573 (Electronic)
PT - Journal Article
TA - Talanta
YR - 2018
DATE- 20180328
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Talanta
EDAT- 20180203
STAT- PubMed-not-MEDLINE
DOCNO- medline/29426526

52 - TOXLINE
TI - Maternal arsenic exposure and birth outcomes: A birth cohort study in
Wuhan, China.
AU - Liu H
AD - Key Laboratory of Environment and Health (HUST), Ministry of Education &amp;
Ministry of Environmental Protection, State Key Laboratory of Environmental Health,
School of Public Health, Tongji Medical College, Huazhong University of Science and
Technology, Wuhan, Hubei, China.
AU - Lu S
AD - Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical
College, Huazhong University of Science and Technology, Wuhan, China.
AU - Zhang B
AD - Wuhan Medical and Health Center for Women and Children, Wuhan, Hubei, China.
AU - Xia W
AD - Key Laboratory of Environment and Health (HUST), Ministry of Education &amp;
Ministry of Environmental Protection, State Key Laboratory of Environmental Health,
School of Public Health, Tongji Medical College, Huazhong University of Science and
Technology, Wuhan, Hubei, China.
AU - Liu W
AD - Key Laboratory of Environment and Health (HUST), Ministry of Education &amp;
Ministry of Environmental Protection, State Key Laboratory of Environmental Health,
School of Public Health, Tongji Medical College, Huazhong University of Science and
Technology, Wuhan, Hubei, China.
AU - Peng Y
AD - Key Laboratory of Environment and Health (HUST), Ministry of Education &amp;
Ministry of Environmental Protection, State Key Laboratory of Environmental Health,
School of Public Health, Tongji Medical College, Huazhong University of Science and
Technology, Wuhan, Hubei, China.
AU - Zhang H
AD - Wuhan Polytechnic University, Wuhan, Hubei, China.
AU - Wu K
AD - Department of Chemistry, Huazhong University of Science and Technology,
Wuhan, China.
AU - Xu S
AD - Key Laboratory of Environment and Health (HUST), Ministry of Education &amp;
Ministry of Environmental Protection, State Key Laboratory of Environmental Health,
School of Public Health, Tongji Medical College, Huazhong University of Science and
Technology, Wuhan, Hubei, China.
AU - Li Y
AD - Key Laboratory of Environment and Health (HUST), Ministry of Education &amp;
Ministry of Environmental Protection, State Key Laboratory of Environmental Health,
School of Public Health, Tongji Medical College, Huazhong University of Science and
Technology, Wuhan, Hubei, China. Electronic address: liyuanyuan@hust.edu.cn.
SO - Environ Pollut. 2018, May; 236:817-823. [Environmental pollution (Barking,
Essex : 1987)]
AB - Maternal arsenic exposure leads to adverse birth outcomes, but the
critical window of this susceptibility keeps unclear. To determine whether
the associations between maternal arsenic exposure and birth outcomes were
trimester-specific, we conducted a birth cohort study of 1390 women from
2014 to 2016 in Wuhan, China. We examined associations between total
urinary arsenic concentrations in three trimesters and birth weight, birth
length and the risk of small for gestational age (SGA), and the
differences of these associations across trimesters using generalized
estimating equations. Maternal urinary arsenic concentrations varied
across trimesters and were weakly correlated. Arsenic concentrations in
the 3rd trimester, but not in the 1st and 2nd trimesters, were associated
with birth outcomes. For each doubling of arsenic levels in the 3rd
trimester, birth weight was decreased 24.27&#8239;g (95% confidence
interval (CI): -46.99, -1.55), birth length was decreased
0.13&#8239;cm (95% CI: -0.22, -0.04), and the risk for SGA birth
was increased 25% (95% CI: 1.03, 1.49). Further, stratified analyses
indicated that these associations were only observed in female infants.
Our findings indicate maternal arsenic levels in the 3rd trimester seemed
to have significant impacts on birth outcomes, and also emphasize the
public health interventions relevance to arsenic exposure in late
pregnancy.
KW - Cohort
KW - Critical window
KW - Low-level arsenic
KW - Sex specific
KW - Urine
RN - N712M78A8G
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180615
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Environmental pollution (Barking, Essex : 1987)
STAT- MEDLINE
DOCNO- medline/29462776

53 - TOXLINE
TI - Embryonic-only arsenic exposure alters skeletal muscle satellite cell
function in killifish (Fundulus heteroclitus).
AU - Szymkowicz DB
AD - Environmental Toxicology Graduate Program, Clemson University, Clemson, SC,
United States.
AU - Schwendinger KL
AD - Department of Biological Sciences, Clemson University, Clemson, SC, United
States.
AU - Tatnall CM
AD - Department of Biological Sciences, Clemson University, Clemson, SC, United
States.
AU - Swetenburg JR
AD - Department of Biological Sciences, Clemson University, Clemson, SC, United
States.
AU - Bain LJ
AD - Environmental Toxicology Graduate Program, Clemson University, Clemson, SC,
United States; Department of Biological Sciences, Clemson University, Clemson, SC,
United States. Electronic address: lbain@clemson.edu.
SO - Aquat Toxicol. 2018, May; 198:276-286. [Aquatic toxicology (Amsterdam,
Netherlands)]
AB - Arsenic is a contaminant found worldwide in drinking water and food.
Epidemiological studies have correlated arsenic exposure with reduced
weight gain and improper muscular development, while in vitro studies show
that arsenic exposure impairs myogenic differentiation. The purpose of
this study was to use Fundulus heteroclitus or killifish as a model
organism to determine if embryonic-only arsenic exposure permanently
reduces the number or function of muscle satellite cells. Killifish
embryos were exposed to 0, 50, 200, or 800&#8239;ppb arsenite (AsIII)
until hatching, and then juvenile fish were raised in clean water. At 28,
40, and 52 weeks after hatching, skeletal muscle injuries were induced by
injecting cardiotoxin into the trunk of the fish just posterior to the
dorsal fin. Muscle sections were collected at 0, 3 and 10&#8239;days
post-injury. Collagen levels were used to assess muscle tissue damage and
recovery, while levels of proliferating cell nuclear antigen (PCNA) and
myogenin were quantified to compare proliferating cells and newly formed
myoblasts. At 28 weeks of age, baseline collagen levels were 105% and 112%
greater in 200 and 800&#8239;ppb groups, respectively, and at 52 weeks of
age, were 58% higher than controls in the 200&#8239;ppb fish. After
cardiotoxin injury, collagen levels tend to increase to a greater extent
and take longer to resolve in the arsenic exposed fish. The number of
baseline PCNA(+) cells were 48-216% greater in 800&#8239;ppb exposed fish
compared to controls, depending on the week examined. However, following
cardiotoxin injury, PCNA is reduced at 28 weeks in 200 and 800&#8239;ppb
fish at day 3 during the recovery period. By 52 weeks, there are
significant reductions in PCNA in all exposure groups at day 3 of the
recovery period. Based on these results, embryonic arsenic exposure
increases baseline collagen levels and PCNA(+) cells in skeletal muscle.
However, when these fish are challenged with a muscle injury, the
proliferation and differentiation of satellite cells into myogenic
precursors is impaired and instead, the fish appear to be favoring a
fibrotic resolution to the injury.
KW - Arsenic
KW - Collagen
KW - Embryo
KW - Fish
KW - Myogenin
KW - Satellite cell
RN - 9007-34-5
RN - N5509X556J
RN - N712M78A8G
LA - eng
IS - 1879-1514 (Electronic)
PT - Journal Article
TA - Aquat Toxicol
YR - 2018
DATE- 20180604
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Aquatic toxicology (Amsterdam, Netherlands)
EDAT- 20180319
STAT- MEDLINE
CM - Cites: PLoS One. 2012;7(5):e38249 (medline /22693606)
CM - Cites: Toxicol Sci. 2012 Sep;129(1):146-56 (medline /22641621)
CM - Cites: Nat Commun. 2013;4:1964 (medline /23743995)
CM - Cites: Toxicol Lett. 2002 Jul 7;133(1):1-16 (medline /12076506)
CM - Cites: Aquat Toxicol. 2017 May;186:1-10 (medline /28237603)
CM - Cites: Environ Int. 2009 May;35(4):743-59 (medline /19232730)
CM - Cites: J Prev Med Public Health. 2014 Sep;47(5):245-52 (medline /25284195)
CM - Cites: Cold Spring Harb Perspect Biol. 2012 Feb 01;4(2):null (medline
/22300977)
CM - Cites: Am J Epidemiol. 2009 Feb 1;169(3):304-12 (medline /19037006)
CM - Cites: Postgrad Med J. 2003 Jul;79(933):391-6 (medline /12897217)
CM - Cites: PLoS One. 2015 Sep 11;10(9):e0137907 (medline /26359868)
CM - Cites: Trends Cell Biol. 2016 Jun;26(6):434-444 (medline /26948993)
CM - Cites: Ecotoxicol Environ Saf. 2015 Feb;112:247-70 (medline /25463877)
CM - Cites: J Cell Sci. 2014 Nov 1;127(Pt 21):4543-8 (medline /25300792)
CM - Cites: Am J Physiol Regul Integr Comp Physiol. 2010 May;298(5):R1173-87
(medline /20219869)
CM - Cites: Proc Natl Acad Sci U S A. 2015 Sep 22;112(38):E5246-52 (medline
/26372956)
CM - Cites: Talanta. 2002 Aug 16;58(1):201-35 (medline /18968746)
CM - Cites: Gen Comp Endocrinol. 2013 Oct 1;192:136-48 (medline /23791761)
CM - Cites: Aquat Toxicol. 2014 Jan;146:196-204 (medline /24316437)
CM - Cites: Compr Physiol. 2015 Jul 1;5(3):1027-59 (medline /26140708)
CM - Cites: J Exp Biol. 2006 Jun;209(Pt 12):2249-64 (medline /16731802)
CM - Cites: Epidemiology. 2016 Mar;27(2):173-81 (medline /26583609)
CM - Cites: Ann Anat. 2015 Nov;202:18-27 (medline /26340019)
CM - Cites: Int J Biochem Cell Biol. 2004 Jun;36(6):1031-7 (medline /15094118)
CM - Cites: J Expo Sci Environ Epidemiol. 2015 Nov-Dec;25(6):599-603 (medline
/25805251)
CM - Cites: Environ Health Perspect. 2010 Jul;118(7):949-56 (medline /20299303)
CM - Cites: J Environ Sci Health A Tox Hazard Subst Environ Eng.
2006;41(10):2399-428 (medline /17018421)
CM - Cites: Free Radic Biol Med. 2014 Sep;74:64-73 (medline /24960579)
CM - Cites: J Exp Biol. 2011 May 15;214(Pt 10):1617-28 (medline /21525308)
CM - Cites: Chemosphere. 2003 Sep;52(9):1353-9 (medline /12867164)
CM - Cites: J Cell Sci. 2015 Oct 1;128(19):3525-31 (medline /26377767)
CM - Cites: Toxicol Sci. 2012 Feb;125(2):522-31 (medline /22058191)
CM - Cites: Environ Res. 2017 Aug;157:52-59 (medline /28521257)
CM - Cites: Stem Cells. 2016 Mar;34(3):732-42 (medline /26537186)
CM - Cites: PLoS One. 2016 Jan 25;11(1):e0147198 (medline /26807982)
CM - Cites: Environ Health Perspect. 2016 Aug;124(8):1308-15 (medline
/26859631)
CM - Cites: Toxicon. 2003 Dec 15;42(8):933-45 (medline /15019492)
CM - Cites: Adv Drug Deliv Rev. 2017 Nov 1;121:43-56 (medline /28736303)
DOCNO- medline/29574248

54 - TOXLINE
TI - Arsenic-containing hydrocarbons disrupt a model in vitro
blood-cerebrospinal fluid barrier.
AU - M�ller SM
AD - Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-
Allee 114-116, 14558 Nuthetal, Germany; Heinrich-Stockmeyer Foundation,
Parkstra&szlig;e 44-46, 49214 Bad Rothenfelde, Germany.
AU - Ebert F
AD - Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-
Allee 114-116, 14558 Nuthetal, Germany.
AU - Bornhorst J
AD - Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-
Allee 114-116, 14558 Nuthetal, Germany.
AU - Galla HJ
AD - Institute of Biochemistry, University of M�nster, Wilhelm-Klemm-Str. 2, 48149
M�nster, Germany.
AU - Francesconi KA
AD - Institute of Chemistry, NAWI Graz, University of Graz, Universit�tsplatz 1,
8010 Graz, Austria.
AU - Schwerdtle T
AD - Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-
Allee 114-116, 14558 Nuthetal, Germany. Electronic address: tanja.schwerdtle@uni-
potsdam.de.
SO - J Trace Elem Med Biol. 2018, Sep; 49:171-177. [Journal of trace elements
in medicine and biology : organ of the Society for Minerals and Trace
Elements (GMS)]
AB - Lipid-soluble arsenicals, so-called arsenolipids, have gained a lot of
attention in the last few years because of their presence in many seafoods
and reports showing substantial cytotoxicity emanating from
arsenic-containing hydrocarbons (AsHCs), a prominent subgroup of the
arsenolipids. More recent in vivo and in vitro studies indicate that some
arsenolipids might have adverse effects on brain health. In the present
study, we focused on the effects of selected arsenolipids and three
representative metabolites on the blood-cerebrospinal fluid barrier
(B-CSF-B), a brain-regulating interface. For this purpose, we incubated an
in vitro model of the B-CSF-B composed of porcine choroid plexus
epithelial cells (PCPECs) with three AsHCs, two arsenic-containing fatty
acids (AsFAs) and three representative arsenolipid metabolites
(dimethylarsinic acid, thio/oxo-dimethylpropanoic acid) to examine their
cytotoxic potential and impact on barrier integrity. The toxic arsenic
species arsenite was also tested in this way and served as a reference
substance. While AsFAs and the metabolites showed no cytotoxic effects in
the conducted assays, AsHCs showed a strong cytotoxicity, being up to
1.5-fold more cytotoxic than arsenite. Analysis of the in vitro B-CSF-B
integrity showed a concentration-dependent disruption of the barrier
within 72&#8239;h. The correlation with the decreased plasma membrane
surface area (measured as capacitance) indicates cytotoxic effects. These
findings suggest exposure to elevated levels of certain arsenolipids may
have detrimental consequences for the central nervous system.
KW - Arsenic-containing fatty acids
KW - Arsenic-containing hydrocarbons
KW - Arsenolipids
KW - Blood-cerebrospinal fluid barrier
KW - Blood-liquor barrier
LA - eng
IS - 1878-3252 (Electronic)
PT - Journal Article
TA - J Trace Elem Med Biol
YR - 2018
DATE- 20180613
CI - Copyright &copy; 2018 Elsevier GmbH. All rights reserved.
CITO- NLM
CS - Germany
FJT - Journal of trace elements in medicine and biology : organ of the Society
for Minerals and Trace Elements (GMS)
EDAT- 20180206
STAT- In-Process
DOCNO- medline/29449109

55 - TOXLINE
TI - Species-specific bioaccumulation and correlated health risk of arsenic
compounds in freshwater fish from a typical mine-impacted river.
AU - Jia Y
AD - College of Chemistry and Chemical Engineering, Central South University,
Changsha 410083, China.
AU - Wang L
AD - College of Chemistry and Chemical Engineering, Central South University,
Changsha 410083, China; Hunan Provincial Key Laboratory of Efficient and Clean
Utilization of Manganese Resources, Central South University, Changsha 410083,
China. Electronic address: linwang@csu.edu.cn.
AU - Li S
AD - College of Chemistry and Chemical Engineering, Central South University,
Changsha 410083, China.
AU - Cao J
AD - College of Chemistry and Chemical Engineering, Central South University,
Changsha 410083, China.
AU - Yang Z
AD - College of Chemistry and Chemical Engineering, Central South University,
Changsha 410083, China; Hunan Provincial Key Laboratory of Efficient and Clean
Utilization of Manganese Resources, Central South University, Changsha 410083,
China; Center for Environment and Water Resources, Central South University,
Changsha 410083, China. Electronic address: zgyang@csu.edu.cn.
SO - Sci Total Environ. 2018, Jun 01; 625:600-607. [The Science of the total
environment]
AB - Arsenic (As) speciation and bioaccumulation in fish muscle tissues have
been intensively investigated in marine ecosystem. However, little is
known about these in freshwater fish. In this study, freshwater fish
including 120 specimens and 8 species were collected from the Xiang River,
a typical mine-impacted river in China. Six As species including arsenite
(AsIII), arsenate (AsV), monomethylarsonic acid (MMA), dimethylarsinic
acid (DMA), arsenocholine (AsC) and arsenobetaine (AsB) were
simultaneously separated and determined using HPLC-ICP-MS. The mean
(&plusmn;SD) concentration of total As (tAs) in the dried fish muscle was
0.748&plusmn;0.651mg&middot;kg-1. AsB was found as the predominant As
species in most of the studied fish samples, in accordance with the
reports in marine fish. However, the diversity of inorganic/organic As
proportion observed in the studied freshwater fish species was larger than
that in marine fish species due to greater spatial variability of As
contamination, mobilization and origination in the studied catchments. The
percentage of AsB (AsB%) in fish muscle was irrelevant to tAs
concentration, while the percentage of iAs (iAs%) decreased with tAs
concentration in a hyperbolic pattern. This can be attributed to
restricted assimilation and accumulation of toxic iAs with increasing tAs
concentration in fish. Chronic non-carcinogenic and carcinogenic health
risks were evaluated through Monte-Carlo simulation. The result indicated
that consuming freshwater fish in the Xiang River could cause considerable
carcinogenic risk to local inhabitants.
KW - Arsenic
KW - Arsenobetaine
KW - Fish
KW - Inorganic arsenic
LA - eng
IS - 1879-1026 (Electronic)
PT - Journal Article
TA - Sci Total Environ
YR - 2018
DATE- 20180227
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - The Science of the total environment
EDAT- 20171230
STAT- In-Process
DOCNO- medline/29294442

56 - TOXLINE
TI - Prenatal arsenic exposure, child marriage, and pregnancy weight gain:
Associations with preterm birth in Bangladesh.
AU - Rahman ML
AD - Harvard T.H. Chan School of Public Health, Department of Environmental
Health, Boston, MA, USA.
AU - Kile ML
AD - Oregon State University, College of Public Health and Human Sciences,
Corvallis, OR, USA.
AU - Rodrigues EG
AD - Harvard T.H. Chan School of Public Health, Department of Environmental
Health, Boston, MA, USA.
AU - Valeri L
AD - McLean Hospital, Belmont, Massachusetts, USA and Harvard Medical School,
Boston, MA, USA.
AU - Raj A
AD - Center on Gender Equity and Health, Department of Medicine, University of
California, San Diego, CA, USA.
AU - Mazumdar M
AD - Harvard T.H. Chan School of Public Health, Department of Environmental
Health, Boston, MA, USA.
AU - Mostofa G
AD - Dhaka Community Hospital Trust, Dhaka, Bangladesh.
AU - Quamruzzaman Q
AD - Dhaka Community Hospital Trust, Dhaka, Bangladesh.
AU - Rahman M
AD - Dhaka Community Hospital Trust, Dhaka, Bangladesh.
AU - Hauser R
AD - Harvard T.H. Chan School of Public Health, Department of Environmental
Health, Boston, MA, USA; Harvard T.H. Chan School of Public Health, Department of
Epidemiology, Boston, MA, USA.
AU - Baccarelli A
AD - Columbia University, Mailman School of Public Health, Department of
Environmental Health, New York, NY, USA.
AU - Liang L
AD - Harvard T.H. Chan School of Public Health, Department of Biostatistics,
Boston, MA, USA.
AU - Christiani DC
AD - Harvard T.H. Chan School of Public Health, Department of Environmental
Health, Boston, MA, USA; Harvard T.H. Chan School of Public Health, Department of
Epidemiology, Boston, MA, USA. Electronic address: dchris@hsph.harvard.edu.
SO - Environ Int. 2018, Mar; 112:23-32. [Environment international]
AB - BACKGROUND: Preterm birth is a disease of multifactorial etiologies that
has environmental, social, and maternal health components. Individual
studies have shown that exposure to arsenic contaminated drinking water,
child marriage, and low maternal weight gain during pregnancy contribute
to preterm birth. These factors are highly prevalent and often co-exist in
Bangladesh, a country in South Asia with one of the world's highest
prevalences of preterm birth.
AB - OBJECTIVE: To evaluate the individual and interactive effects of prenatal
arsenic exposure, child marriage, and pregnancy weight gain on preterm
birth in a prospective birth cohort in Bangladesh.
AB - METHODS: During 2008-2011, we recruited 1613 pregnant women aged
&ge;18years at &le;16weeks of gestation and followed them until 1-month
post-partum. We measured total arsenic in drinking water (n=1184) and in
maternal toenails (n=1115) collected at enrollment and &le;1-month
post-partum, respectively using inductively coupled plasma mass
spectrometry. Child marriage ( < 18years old) was defined using
self-report, and 2nd and 3rd trimester pregnancy weight gain was
calculated using monthly records. Gestational age was determined at
enrollment by ultrasound.
AB - RESULTS: In multivariate adjusted Poisson regression models, the risk
ratios (RR) for preterm birth were 1.12 (95% CI: 1.07-1.18) for a unit
change in natural log water arsenic exposure, 2.28 (95% CI: 1.76-2.95) for
child marriage, and 0.64 (95% CI: 0.42-0.97) for a pound per week increase
in maternal weight during the 2nd and 3rd trimesters. In stratified
analysis by child marriage, pregnancy weight gain was inversely associated
with preterm birth among women with a history of child marriage (RR=0.58;
95% CI: 0.37-0.92), but not among women with no history of child marriage
(RR=86; 95% CI: 0.37-2.01). Mediation analysis revealed that both arsenic
exposure and child marriage had small but significant associations with
preterm birth via lowering pregnancy weight gain. Similar associations
were observed when arsenic exposure was assessed using maternal toenail
arsenic concentrations.
AB - CONCLUSIONS: Reducing arsenic exposure and ending child marriage could
reduce the risk of preterm birth in Bangladesh. Furthermore, enhancing
nutritional support to ensure adequate weight gain during pregnancy may
provide additional benefits especially for women with a history of child
marriage.
LA - eng
IS - 1873-6750 (Electronic)
PT - Journal Article
TA - Environ Int
YR - 2018
DATE- 20180413
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Environment international
EDAT- 20171212
STAT- In-Data-Review
DOCNO- medline/29245039

57 - TOXLINE
TI - Statistical optimization of arsenic biosorption by microbial enzyme via
Ca-alginate beads.
AU - Banerjee S
AD - a Department of Polymer Science and technology , Biosensor Laboratory,
University of Calcutta , Kolkata , West Bengal , India.
AU - Banerjee A
AD - a Department of Polymer Science and technology , Biosensor Laboratory,
University of Calcutta , Kolkata , West Bengal , India.
AU - Sarkar P
AD - a Department of Polymer Science and technology , Biosensor Laboratory,
University of Calcutta , Kolkata , West Bengal , India.
SO - J Environ Sci Health A Tox Hazard Subst Environ Eng. 2018, Apr 16;
53(5):436-442. [Journal of environmental science and health. Part A,
Toxic/hazardous substances & environmental engineering]
AB - Bioremediation of arsenic using green technology via microbial enzymes has
attracted scientists due to its simplicity and cost effectiveness.
Statistical optimization of arsenate bioremediation was conducted by the
enzyme arsenate reductase extracted from arsenic tolerant bacterium
Pseudomonas alcaligenes. Response surface methodology based on Box-Behnken
design matrix was performed to determine the optimal operational
conditions of a multivariable system and their interactive effects on the
bioremediation process. The highest biosorptive activity of
96.2 &micro;g gm-1 of beads was achieved under optimized conditions
(pH = 7.0; As (V) concentration = 1000 ppb; time = 2 h). SEM
analysis showed the morphological changes on the surface of enzyme
immobilized gluteraldehyde crosslinked Ca-alginate beads. The immobilized
enzyme retained its activity for 8 cycles. ANOVA with a high correlation
coefficient (R2 > 0.99) and lower "Prob > F"value ( < 0.0001)
corroborated the second-order polynomial model for the biosorption
process. This study on the adsorptive removal of As (V) by enzyme-loaded
biosorbent revealed a possible way of its application in large scale
treatment of As (V)-contaminated water bodies.
KW - Arsenate
KW - arsenate reductase
KW - biosorption
KW - box–behnken design
KW - response surface methodology
KW - statistical optimization
RN - 8A5D83Q4RW
RN - 8C3Z4148WZ
RN - N712M78A8G
RN - N7CIZ75ZPN
RN - SY7Q814VUP
LA - eng
IS - 1532-4117 (Electronic)
PT - Journal Article
TA - J Environ Sci Health A Tox Hazard Subst Environ Eng
YR - 2018
DATE- 20180525
CITO- NLM
CS - England
CSET- IM
FJT - Journal of environmental science and health. Part A, Toxic/hazardous
substances &amp; environmental engineering
EDAT- 20171226
STAT- MEDLINE
DOCNO- medline/29278978

58 - TOXLINE
TI - Taxonomically-linked growth phenotypes during arsenic stress among arsenic
resistant bacteria isolated from soils overlying the Centralia coal seam
fire.
AU - Dunivin TK
AD - Environmental and Integrative Toxicological Sciences Doctoral Program,
Michigan State University, East Lansing, Michigan, United States of America.
AU - Miller J
AD - Lyman Briggs College, Michigan State University, East Lansing, Michigan,
United States of America.
AU - Shade A
AD - Program in Ecology, Evolutionary Biology and Behavior, Michigan State
University, East Lansing, Michigan, United States of America.
SO - PLoS One. 2018; 13(1):e0191893. [PloS one]
AB - Arsenic (As), a toxic element, has impacted life since early Earth. Thus,
microorganisms have evolved many As resistance and tolerance mechanisms to
improve their survival outcomes given As exposure. We isolated As
resistant bacteria from Centralia, PA, the site of an underground coal
seam fire that has been burning since 1962. From a 57.4&deg;C soil
collected from a vent above the fire, we isolated 25 unique aerobic As
resistant bacterial strains spanning seven genera. We examined their
diversity, resistance gene content, transformation abilities, inhibitory
concentrations, and growth phenotypes. Although As concentrations were low
at the time of soil collection (2.58 ppm), isolates had high minimum
inhibitory concentrations (MICs) of arsenate and arsenite ( > 300 mM and
20 mM respectively), and most isolates were capable of arsenate reduction.
We screened isolates (PCR and sequencing) using 12 published primer sets
for six As resistance genes (AsRGs). Genes encoding arsenate reductase
(arsC) and arsenite efflux pumps (arsB, ACR3(2)) were present, and
phylogenetic incongruence between 16S rRNA genes and AsRGs provided
evidence for horizontal gene transfer. A detailed investigation of
differences in isolate growth phenotypes across As concentrations (lag
time to exponential growth, maximum growth rate, and maximum OD590) showed
a relationship with taxonomy, providing information that could help to
predict an isolate's performance given As exposure in situ. Our results
suggest that microbiological management and remediation of environmental
As could be informed by taxonomically-linked As tolerance, potential for
resistance gene transferability, and the rare biosphere.
RN - N712M78A8G
LA - eng
IS - 1932-6203 (Electronic)
PT - Journal Article
PT - Research Support, Non-U.S. Gov't
TA - PLoS One
YR - 2018
DATE- 20180312
CITO- NLM
CS - United States
CSET- IM
FJT - PloS one
EDAT- 20180125
STAT- MEDLINE
CM - Cites: FEMS Microbiol Lett. 2004 Aug 15;237(2):249-53 (medline /15321669)
CM - Cites: Appl Microbiol Biotechnol. 2013 Jan;97(1):51-62 (medline /23138712)
CM - Cites: Environ Geochem Health. 2010 Apr;32(2):95-105 (medline /19548094)
CM - Cites: Appl Environ Microbiol. 2010 Apr;76(8):2445-50 (medline /20173072)
CM - Cites: Ecotoxicology. 2013 Mar;22(2):363-76 (medline /23238642)
CM - Cites: Can J Microbiol. 1978 Dec;24(12):1468-74 (medline /747810)
CM - Cites: Nat Rev Microbiol. 2016 Apr;14 (5):320-30 (medline /27080241)
CM - Cites: Annu Rev Microbiol. 2017 Sep 8;71:711-730 (medline /28731846)
CM - Cites: Appl Environ Microbiol. 2011 Jul;77(13):4685-92 (medline /21571879)
CM - Cites: BMC Genomics. 2008 Mar 24;9:136 (medline /18366724)
CM - Cites: BMC Evol Biol. 2003 Jul 23;3:18 (medline /12877744)
CM - Cites: Curr Microbiol. 2004 May;48(5):341-7 (medline /15060729)
CM - Cites: Naturwissenschaften. 2003 Sep;90(9):395-401 (medline /14504781)
CM - Cites: J Microbiol Methods. 2004 Sep;58(3):335-49 (medline /15279938)
CM - Cites: Chemosphere. 2011 Sep;85(1):129-34 (medline /21724233)
CM - Cites: Appl Environ Microbiol. 2008 Jul;74(14):4567-73 (medline /18502920)
CM - Cites: Appl Microbiol Biotechnol. 2008 Aug;80(1):155-65 (medline
/18560832)
CM - Cites: Environ Pollut. 2008 Dec;156(3):1069-74 (medline /18550235)
CM - Cites: Front Microbiol. 2016 May 02;7:636 (medline /27199962)
CM - Cites: Environ Sci Technol. 2004 Jan 1;38(1):104-11 (medline /14740724)
CM - Cites: Appl Environ Microbiol. 2007 Aug;73(16):5261-7 (medline /17586664)
CM - Cites: Can J Microbiol. 2010 Mar;56(3):236-46 (medline /20453910)
CM - Cites: Syst Appl Microbiol. 2010 Apr;33(3):154-64 (medline /20303688)
CM - Cites: Mol Biol Evol. 2016 Jul;33(7):1870-4 (medline /27004904)
CM - Cites: Nucleic Acids Res. 2014 Jan;42(Database issue):D633-42 (medline
/24288368)
CM -Cites: FEMS Microbiol Ecol. 2009 Apr;68(1):108-17 (medline /19291024)
CM -Cites: J Microbiol Methods. 2003 Dec;55(3):541-55 (medline /14607398)
CM -Cites: Environ Microbiol. 2012 Sep;14(9):2247-52 (medline /22788977)
CM -Cites: Nat Methods. 2012 Jun 28;9(7):676-82 (medline /22743772)
CM -Cites: J Bacteriol. 2005 Jul;187(14):4853-64 (medline /15995200)
CM -Cites: FEMS Microbiol Rev. 2016 Mar;40(2):299-322 (medline /26790947)
CM -Cites: Int J Syst Evol Microbiol. 2012 Mar;62(Pt 3):716-21 (medline
/22140171)
CM - Cites: BMC Microbiol. 2009 Jan 08;9:4 (medline /19128515)
CM - Cites: Folia Microbiol (Praha). 2011 Jan;56(1):29-35 (medline /21394480)
CM - Cites: J Biol Methods. 2014;1(2):null (medline /25606571)
CM - Cites: J Antibiot (Tokyo). 2010 Aug;63(8):468-76 (medline /20648021)
CM - Cites: Sci Total Environ. 2016 Aug 15;562:588-595 (medline /27110973)
CM - Cites: J Hazard Mater. 2014 May 15;272:112-20 (medline /24685527)
CM - Cites: Appl Environ Microbiol. 2016 Nov 21;82(24):7019-7029 (medline
/27663031)
CM - Cites: ISME J. 2017 Jun;11(6):1447-1459 (medline /28282042)
CM - Cites: Syst Appl Microbiol. 2005 Oct;28(8):727-34 (medline /16261862)
CM - Cites: Appl Environ Microbiol. 2006 May;72(5):3738-42 (medline /16672525)
CM - Cites: J Appl Microbiol. 2007 Dec;103(6):2299-308 (medline /18045414)
CM - Cites: Nat Rev Microbiol. 2005 May;3(5):439-46 (medline /15864265)
CM - Cites: J Environ Sci Health A Tox Hazard Subst Environ Eng.
2011;46(14):1736-47 (medline /22175878)
CM - Cites: Environ Sci Technol. 2013 Apr 2;47(7):3141-8 (medline /23469919)
CM - Cites: Genome Res. 1999 Sep;9(9):868-77 (medline /10508846)
CM - Cites: FEMS Microbiol Rev. 2002 Aug;26(3):311-25 (medline /12165430)
CM - Cites: Res Microbiol. 2007 Mar;158(2):128-37 (medline /17258434)
CM - Cites: Int J Syst Evol Microbiol. 2004 Jul;54(Pt 4):1369-75 (medline
/15280316)
CM - Cites: Extremophiles. 2013 May;17(3):421-31 (medline /23525943)
DOCNO- medline/29370270

59 - TOXLINE
TI - &alpha;-Lipoic acid inhibits testicular and epididymal oxidative damage
and improves fertility efficacy in arsenic-intoxicated rats.
AU - Prathima P
AD - Department of Biotechnology, Vikrama Simhapuri University, Nellore, AP
524003, India.
AU - Pavani R
AD - Department of Biotechnology, Vikrama Simhapuri University, Nellore, AP
524003, India.
AU - Sukeerthi S
AD - Department of Biotechnology, Vikrama Simhapuri University, Nellore, AP
524003, India.
AU - Sainath SB
AD - Department of Biotechnology, Vikrama Simhapuri University, Nellore, AP
524003, India.
SO - J Biochem Mol Toxicol. 2018, Feb. [Journal of biochemical and molecular
toxicology]
AB - The present study evaluates the protective effect of &alpha;-lipoic acid
(LA) against arsenic-induced testicular and epididymal oxidative damage in
rats. Arsenic caused significant reduction in the reproductive organ
weights, serum testosterone levels, testicular daily sperm count,
epididymal sperm count, sperm motility, sperm viability, and sperm
membrane integrity. Significant reduction in the activity levels of
superoxide dismutase, catalase, and glutathione levels with a concomitant
increase in the lipid peroxidation and protein carbonyl content in the
testis and the cauda epididymis of arsenic-exposed rats. Arsenic
intoxication also enhanced the testicular caspase-3 mRNA levels,
disorganization of testicular and cauda epididymal architecture as well as
increased arsenic content in the testis and the cauda epididymis of rats.
Arsenic exposure also deteriorated fertility ability in male rats over
controls. Conversely, &alpha;-LA negated the testicular and cauda
epididymal oxidative stress and restored the male reproductive health in
arsenic-exposed rats.
KW - arsenic
KW - lipoic acid
KW - rats
KW - spermatogenesis
KW - testicular steroidogenesis
RN - 3XMK78S47O
RN - 48OVY2OC72
RN - 73Y7P0K73Y
RN - EC 1.-
RN - GAN16C9B8O
LA - eng
IS - 1099-0461 (Electronic)
PT - Journal Article
TA - J Biochem Mol Toxicol
YR - 2018
DATE- 20180618
CI - &copy; 2017 Wiley Periodicals, Inc.
CITO- NLM
CS - United States
CSET- IM
FJT - Journal of biochemical and molecular toxicology
EDAT- 20171207
STAT- MEDLINE
DOCNO- medline/29214690

60 - TOXLINE
TI - Lithium Treatment Aggregates the Adverse Effects on Erythrocytes Subjected
to Arsenic Exposure.
AU - Bhardwaj P
AD - Department of Biophysics, Panjab University Chandigarh, Chandigarh, 160014,
India.
AU - Jain K
AD - Centre of Nuclear Medicine, Panjab University Chandigarh, Chandigarh, India.
AU - Dhawan DK
AD - Department of Biophysics, Panjab University Chandigarh, Chandigarh, 160014,
India. dhawan@pu.ac.in.
SO - Biol Trace Elem Res. 2018, Jul; 184(1):206-213. [Biological trace element
research]
AB - The present study was designed to investigate the effects of lithium
treatment on red blood cells which were given arsenic exposure. Long-term
lithium therapy is being extensively used for the treatment of bipolar
disorders. Arsenic is a group I carcinogen and a major toxic pollutant in
drinking water that affects millions of people worldwide. Male SD rats
were segregated into four groups, viz. normal control, lithium treated,
arsenic treated, and lithium + arsenic treated. Lithium was supplemented
as lithium carbonate at a dose level of 1.1 g/kg diet for a period of
8 weeks. Arsenic was given in the form of sodium arsenite at a dose
level of 100 ppm in drinking water, ad libitum, for the same period.
Lysates of red blood cells were used to investigate the effects of lithium
and arsenic treatments on anti-oxidant enzymes, reduced glutathione (GSH),
and lipid peroxidation (LPO) levels. Various hematological parameters,
activities of Na+ K+ ATPase and delta-aminolevulinic acid dehydratase
(&delta;-ALAD) were also assessed. A significant reduction was observed in
the activities of antioxidant enzymes, GSH levels, total erythrocyte
counts, Na+ K+ ATPase, and ALAD enzyme activities in lysates of red blood
cells when exposed either to lithium or arsenic. In addition, a
significant increase in the levels of malondialdehyde (MDA), lymphocytes,
neutrophils, and total leukocytes was also observed following lithium as
well as arsenic treatments. However, when arsenic-treated rats were
subjected to lithium treatment, a pronounced alteration was noticed in all
the above parameters. Therefore, we conclude that lithium supplementation
to the arsenic-treated rats enhances the adverse effects on red blood
cells and therefore use of lithium may not be medicated to patients who
are vulnerable to arsenic exposure through drinking water. It can also be
inferred that adverse effects of lithium therapy may get aggravated in
patients thriving in the arsenic-contaminated area.
KW - Arsenic
KW - Lithium therapy
KW - Oxidative stress
KW - Red blood cell lysates
LA - eng
IS - 1559-0720 (Electronic)
PT - Journal Article
TA - Biol Trace Elem Res
YR - 2018
DATE- 20180608
CITO- NLM
CS - United States
FJT - Biological trace element research
EDAT- 20171007
STAT- In-Process
DOCNO- medline/28988373

61 - TOXLINE
TI - Chronic exposure to arsenic and high fat diet additively induced
cardiotoxicity in male mice.
AU - Ahangarpour A
AD - Health Research Institute, Diabetes Research Center, Department of
Physiology, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, I.R. Iran.
AU - Zeidooni L
AD - Department of Toxicology and Student Research Committee, School of Pharmacy,
Ahvaz Jundishapur University of Medical Sciences, Ahvaz, I.R. Iran.
AU - Samimi A
AD - Department of Toxicology and Student Research Committee, School of Pharmacy,
Ahvaz Jundishapur University of Medical Sciences, Ahvaz, I.R. Iran.
AU - Alboghobeish S
AD - Department of Pharmacology and Student Research Committee, School of
Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, I.R. Iran.
AU - Khorsandi LS
AD - Cell and Molecular Research Center, Faculty of Medicine, Ahvaz Jundishapur
University of Medical Sciences, Ahvaz, I.R. Iran.
AU - Moradi M
AD - Health Research Institute, Diabetes Research Center, Department of
Physiology, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, I.R. Iran.
SO - Res Pharm Sci. 2018, Feb; 13(1):47-56. [Research in pharmaceutical
sciences]
AB - Diet is one of the important risk factors that could potentially affect
arsenic-induced cardiotoxicity. The present study was undertaken to
investigate the effect of high fat diet on arsenic-induced cardiotoxicity
in mice. Mice were divided into six different groups (n = 12), two control
groups received either low fat diet (LFD) or high fat diet (HFD) along
with deionized drinking water and four test groups given LFD + 25 ppm
arsenic, LFD + 50 ppm arsenic, HFD + 25 ppm arsenic, and HFD + 50 ppm
arsenic in drinking water for 5 months. The body weight, heart weight to
body weight ratio, cardiac biochemical markers, lipid profile, and
histological examination of heart were evaluated. The results demonstrated
that arsenic exposure led to a significant decrease in heart glutathione
level, catalase enzyme activity, and a significant increase in reactive
oxygen species (ROS), malondialdehyde levels, and biochemical enzymes. The
administration of HFD resulted in above-mentioned changes as well as an
alteration in lipid profile; however, arsenic exposure alone or along with
HFD caused a reduction in lipid profile factors, except HDL level. Our
results revealed that HFD increased arsenic-induced heart injury in the
mice. This effect may be because of reduction in antioxidant activities
and/or increase in oxidative stress and ROS in mice heart tissues. These
findings could be important for clinical intervention to protect against
or prevent arsenic-induced cardiotoxicity in humans.
KW - Arsenic
KW - Cardiotoxicity
KW - Chronic exposure
KW - Heart
KW - High fat diet
LA - eng
IS - 1735-5362 (Print)
PT - Journal Article
TA - Res Pharm Sci
YR - 2018
DATE- 20180204
CITO- NLM
CS - Iran
FJT - Research in pharmaceutical sciences
STAT- PubMed-not-MEDLINE
CM - Cites: Food Chem Toxicol. 2006 Sep;44(9):1579-84 (medline /16774805)
CM - Cites: Sci Rep. 2014 Nov 04;4:6894 (medline /25367288)
CM - Cites: Diabetol Metab Syndr. 2011 Dec 23;3(1):37 (medline /22196253)
CM - Cites: Toxicol Appl Pharmacol. 2007 Aug 1;222(3):315-26 (medline
/17433393)
CM - Cites: Arch Toxicol. 2008 Mar;82(3):137-49 (medline /18197399)
CM - Cites: Toxicol Sci. 2009 Feb;107(2):312-23 (medline /19015167)
CM - Cites: Ecotoxicol Environ Saf. 2011 May;74(4):607-14 (medline /20719385)
CM - Cites: Toxicol Lett. 2003 Jan 31;137(1-2):15-21 (medline /12505429)
CM - Cites: Food Chem Toxicol. 2014 Apr;66:262-77 (medline /24508525)
CM - Cites: Exp Biol Med (Maywood). 2008 Mar;233(3):377-84 (medline /18296743)
CM - Cites: Diabetol Metab Syndr. 2011 Aug 03;3(1):17 (medline /21812977)
CM - Cites: Hypertension. 1999 Jan;33(1):74-8 (medline /9931084)
CM - Cites: J Neurochem. 2005 Jun;93(6):1561-7 (medline /15935072)
CM - Cites: Chem Rev. 2011 Oct 12;111(10):5944-72 (medline /21861450)
CM - Cites: Med Clin North Am. 2011 Sep;95(5):919-37 (medline /21855700)
CM - Cites: Biol Trace Elem Res. 1995 Nov;50(2):119-24 (medline /8605079)
CM - Cites: Gastroenterol Hepatol Bed Bench. 2017 Winter;10 (1):44-53 (medline
/28331564)
CM - Cites: Mutagenesis. 1994 May;9(3):253-7 (medline /7934966)
CM - Cites: PLoS One. 2012;7(6):e38713 (medline /22719926)
CM - Cites: J Invest Dermatol. 1999 Nov;113(5):760-5 (medline /10571731)
CM - Cites: Curr Vasc Pharmacol. 2006 Jul;4(3):215-27 (medline /16842139)
CM - Cites: J Cell Physiol. 1998 Nov;177(2):324-33 (medline /9766529)
CM - Cites: Toxicol Appl Pharmacol. 2009 Sep 15;239(3):320-4 (medline
/19573547)
CM - Cites: Biochim Biophys Acta. 1998 Apr 29;1397(2):223-30 (medline /9565690)
CM - Cites: Basic Clin Pharmacol Toxicol. 2006 Jan;98(1):38-43 (medline
/16433889)
CM -Cites: Indian J Med Res. 2008 Oct;128(4):501-23 (medline /19106443)
CM -Cites: Int J Epidemiol. 2001 Oct;30(5):983-8 (medline /11689508)
CM -Cites: J Proteome Res. 2014 Feb 7;13(2):547-554 (medline /24328084)
CM -Cites: Hypertension. 1995 Jan;25(1):53-60 (medline /7843753)
CM -Cites: Pathophysiology. 2008 Oct;15(3):147-56 (medline /18434106)
CM -Cites: J Radiat Res. 2008 Nov;49(6):579-86 (medline /18827438)
CM -Cites: Toxicol Appl Pharmacol. 2005 Aug 7;206(2):169-75 (medline
/15967205)
CM - Cites: Neurotoxicology. 2003 Aug;24(4-5):747-53 (medline /12900089)
CM - Cites: Life Sci. 2005 Sep 16;77(18):2324-37 (medline /15964026)
CM - Cites: Cardiovasc Toxicol. 2002;2(1):63-73 (medline /12189281)
CM - Cites: Cardiovasc Toxicol. 2014 Mar;14 (1):83-97 (medline /24062023)
CM - Cites: Proc Natl Acad Sci U S A. 1984 Jul;81(14):4343-7 (medline /6589599)
CM - Cites: Environ Health Perspect. 2011 Aug;119(8):1104-9 (medline /21592922)
DOCNO- medline/29387111

62 - TOXLINE
TI - Role of miR-31 and SATB2 in arsenic-induced malignant BEAS-2B cell
transformation.
AU - Chen QY
AD - Department of Environmental Medicine, New York University School of Medicine,
New York, New York.
AU - Li J
AD - Hubei Province Key Laboratory of Occupational Hazard Identification and
Control, Medical college, Wuhan University of Science and Technology, Wuhan, China.
AU - Sun H
AD - Department of Environmental Medicine, New York University School of Medicine,
New York, New York.
AU - Wu F
AD - Department of Environmental Medicine, New York University School of Medicine,
New York, New York.
AU - Zhu Y
AD - Department of Environmental Medicine, New York University School of Medicine,
New York, New York.
AU - Kluz T
AD - Department of Environmental Medicine, New York University School of Medicine,
New York, New York.
AU - Jordan A
AD - Department of Environmental Medicine, New York University School of Medicine,
New York, New York.
AU - DesMarais T
AD - Department of Environmental Medicine, New York University School of Medicine,
New York, New York.
AU - Zhang X
AD - Department of Environmental Medicine, New York University School of Medicine,
New York, New York.
AU - Murphy A
AD - Department of Environmental Medicine, New York University School of Medicine,
New York, New York.
AU - Costa M
AD - Department of Environmental Medicine, New York University School of Medicine,
New York, New York.
SO - Mol Carcinog. 2018, Mar 30. [Molecular carcinogenesis]
AB - Arsenic is a naturally occurring and highly potent metalloid known to
elicit serious public health concerns. Today, approximately 200 million
people around the globe are exposed to arsenic-contaminated drinking water
at levels greater than the World Health Organization's recommended limit
of 10 parts per billion. As a class I human carcinogen, arsenic exposure
is known to elicit various cancers, including lung, skin, liver, and
kidney. Current evidence suggests that arsenic is capable of inducing both
genotoxic and cytotoxic injury, as well as activating epigenetic pathways
to induce carcinogenesis. Our study identifies a novel pathway that is
implicated in arsenic-induced carcinogenesis. Arsenic down-regulated
miRNA-31 and the release of this inhibition caused overexpression of
special AT-rich sequence-binding protein 2 (SATB2). Arsenic is known to
disrupt miRNA expression, and here we report for the first time that
arsenic is capable of inhibiting miR-31 expression. As a direct downstream
target of miR-31, SATB2 is a prominent transcription factor, and nuclear
matrix binding protein implicated in many types of human diseases
including lung cancer. Results from this study show that arsenic induces
the overexpressing SATB2 by inhibiting miR-31 expression, which blocks the
translation of SATB2 mRNA, since levels of SATB2 mRNA remain the same but
protein levels decrease. Overexpression of SATB2 induces malignant
transformation of human bronchial epithelial (BEAS-2B) cells indicating
the importance of the expression of miR-31 in preventing carcinogenesis by
suppressing SATB2 protein levels.
KW - carcinogenesis
KW - human bronchial epithelial cells
KW - metals
KW - non-coding RNAs
LA - eng
IS - 1098-2744 (Electronic)
PT - Journal Article
TA - Mol Carcinog
YR - 2018
DATE- 20180417
CI - &copy; 2018 Wiley Periodicals, Inc.
CITO- NLM
CS - United States
FJT - Molecular carcinogenesis
EDAT- 20180330
STAT- Publisher
DOCNO- medline/29603397

63 - TOXLINE
TI - Serum folate and cobalamin levels and urinary dimethylarsinic acid in US
children and adults.
AU - Zhu J
AD - Department of Mathematics and Computer Science, Fort Valley State University,
Fort Valley, GA, 31030, USA.
AU - Gao Y
AD - Center for Endemic Disease Control, Chinese Center for Disease Control and
Prevention, Harbin Medical University, Harbin, 150081, China.
AU - Sun D
AD - Center for Endemic Disease Control, Chinese Center for Disease Control and
Prevention, Harbin Medical University, Harbin, 150081, China.
AU - Wei Y
AD - Department of Community Medicine, Mercer University School of Medicine, 1550
College St, Macon, GA, 31207, USA. wei_yd@mercer.edu.
SO - Environ Sci Pollut Res Int. 2018, Apr 12. [Environmental science and
pollution research international]
AB - Nutritional status could affect arsenic metabolism and toxicity in the
general population chronically exposed to low levels of inorganic arsenic.
In this study, we examined the association of serum folate and cobalamin
with urinary concentrations of dimethylarsinic acid (DMA), the most
abundant metabolite of inorganic arsenic measured in urine, in children
and adults who participated in the 2003-2006 US National Health and
Nutrition Examination Surveys. A total of 1161 children (aged
6-19 years) and 1938 adults (aged 20-85 years) were analyzed for
the association using multivariate general linear models, adjusting for
potential confounders. We observed a positive association between serum
levels of folate and cobalamin and creatinine-corrected urinary
concentrations of DMA in both children and adults. Furthermore, serum
levels of folate and cobalamin were inversely associated with homocysteine
(Hcy). These results suggest that dietary intake of folate and cobalamin
may exhibit protective functions against arsenic toxicity by increasing
arsenic metabolism to the less toxic metabolite DMA and decreasing serum
levels of Hcy.
KW - Arsenic metabolism
KW - Cobalamin
KW - Folate
KW - Homocysteine
KW - Urinary dimethylarsinic acid
LA - eng
IS - 1614-7499 (Electronic)
PT - Journal Article
TA - Environ Sci Pollut Res Int
YR - 2018
DATE- 20180413
CITO- NLM
CS - Germany
FJT - Environmental science and pollution research international
EDAT- 20180412
STAT- Publisher
DOCNO- medline/29651724

64 - TOXLINE
TI - Realistic risk assessment of arsenic in rice.
AU - Althobiti RA
AD - Queen's University, Department of Chemistry, 90 Bader Lane, Kingston, ON K7L
3N6, Canada.
AU - Sadiq NW
AD - Queen's University, Department of Chemistry, 90 Bader Lane, Kingston, ON K7L
3N6, Canada.
AU - Beauchemin D
AD - Queen's University, Department of Chemistry, 90 Bader Lane, Kingston, ON K7L
3N6, Canada. Electronic address: diane.beauchemin@chem.queensu.ca.
SO - Food Chem. 2018, Aug 15; 257:230-236. [Food chemistry]
AB - Over 3 billion people share a diet consisting mainly of rice, which may
contain significant amounts of arsenic. Because the toxicity of arsenic is
dependent on its chemical form and that it may be in a form that is not
bio-accessible (i.e. dissolved in the gastrointestinal tract) and can thus
not become bio-available (i.e. end up in the blood stream, where it may
exert its toxic effect), the bio-accessibility of arsenic was determined
in thirteen different types of rice. The effects of washing and cooking
were also studied. The total concentration of arsenic ranged from 93 to
989&#8239;&micro;g&#8239;kg-1 and its bio-accessibility ranged from 16 to
93%. Cooking only changed arsenic speciation in a few cases. However,
simply washing rice with arsenic-free water before cooking removed 3-43%
of the arsenic, resulting in all the rice tested except the most
contaminated one being safe to consume by adults.
KW - Arsenic
KW - Bio-accessibility
KW - Inductively coupled plasma mass spectrometry
KW - Rice
KW - Speciation analysis
LA - eng
IS - 0308-8146 (Print)
PT - Journal Article
TA - Food Chem
YR - 2018
DATE- 20180406
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Food chemistry
EDAT- 20180307
STAT- In-Process
DOCNO- medline/29622204

65 - TOXLINE
TI - Role of microRNAs in senescence and its contribution to peripheral
neuropathy in the arsenic exposed population of West Bengal, India.
AU - Chatterjee D
AD - Molecular Genetics Division, CSIR-Indian Institute of Chemical Biology,
Kolkata 700032, India.
AU - Bandyopadhyay A
AD - Health Point Multispeciality Hospital, Kolkata 700025, India; Ramakrishna
Sarada Mission Matri Bhavan, Kolkata 700 026, India.
AU - Sarma N
AD - Dr. B.C. Roy Post Graduate Institute of Paediatric Science, Kolkata 700054,
India.
AU - Basu S
AD - Department of General Medicine, Sri Aurobindo Seva Kendra, Kolkata 700068,
India.
AU - Roychowdhury T
AD - School of Environmental Studies, Jadavpur University, Kolkata 700032, India.
AU - Roy SS
AD - Cell Biology &amp; Physiology Division, CSIR-Indian Institute of Chemical
Biology, Kolkata 700032, India.
AU - Giri AK
AD - Molecular Genetics Division, CSIR-Indian Institute of Chemical Biology,
Kolkata 700032, India. Electronic address: akgiri15@yahoo.com.
SO - Environ Pollut. 2018, Feb; 233:596-603. [Environmental pollution (Barking,
Essex : 1987)]
AB - Arsenic induced senescence (AIS) has been identified in the population of
West Bengal, India very recently. Also there is a high incidence of
arsenic induced peripheral neuropathy (PN) throughout India. However, the
epigenetic regulation of AIS and its contribution in arsenic induced PN
remains unexplored. We recruited seventy two arsenic exposed and forty
unexposed individuals from West Bengal to evaluate the role of senescence
associated miRNAs (SA-miRs) in AIS and their involvement if any, in PN.
The downstream molecules of the miRNA associated with the disease outcome,
was also checked by immuoblotting. In vitro studies were conducted
with HEK 293 cells and sodium arsenite exposure. Our results show
that all the SA-miRs were upregulated in comparison to unexposed controls.
miR-29a was the most significantly altered, highest expression being in
the arsenic exposed group with PN, suggesting its association with the
occurrence of PN. We looked for the expression of peripheral myelin
protein 22 (PMP22), a specific target of miR-29a associated with
myelination and found that both in vitro and in vivo results
showed over-expression of the protein. Since this was quite contrary to
miRNA regulation, we checked for intermediate players &beta;-catenin and
GSK-3&beta; upon arsenic exposure which affects PMP22 expression. We found
that &beta;-catenin was upregulated in vitro and was also highest in
the arsenic exposed group with PN while GSK-3&beta; followed the reverse
pattern. Our findings suggest that arsenic exposure alters the expression
of SA-miRs and the mir-29a/beta catenin/PMP22 axis might be responsible
for arsenic induced PN.
KW - Arsenic
KW - Health effects
KW - Neuropathy
KW - Senescence
KW - miRNA
RN - EC 2.7.11.26
RN - N712M78A8G
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180406
CI - Copyright &copy; 2017. Published by Elsevier Ltd.
CITO- NLM
CS - England
CSET- IM
FJT - Environmental pollution (Barking, Essex : 1987)
EDAT- 20171105
STAT- MEDLINE
DOCNO- medline/29107899

66 - TOXLINE
TI - Antioxidant enzymes responses in shoots of arsenic hyperaccumulator,
Isatis cappadocica Desv., under interaction of arsenate and phosphate.
AU - Souri Z
AD - a Department of Biology, Laboratory of Plant Physiology, Faculty of Science ,
Razi University , Kermanshah , Iran.
AU - Karimi N
AD - a Department of Biology, Laboratory of Plant Physiology, Faculty of Science ,
Razi University , Kermanshah , Iran.
AU - de Oliveira LM
AD - b Soil and Water Science Department , University of Florida , Gainesville ,
FL , USA.
SO - Environ Technol. 2018, May; 39(10):1316-1327. [Environmental technology]
AB - The present study investigated the effects of arsenate and phosphate
interaction on growth, lipid peroxidation, arsenic (As) accumulation,
phosphorus (P) accumulation, and the activities of some antioxidant
enzymes in Isatis cappadocica. Plants were exposed to (50-1200 &mu;mol
L-1) arsenate and (5-1600 &mu;mol L-1) phosphate for 28 days in a
hydroponic system. At a phosphate concentration of 1600&ensp;&micro;M,
biomass production and chlorophyll content increased, demonstrating
clearly that phosphate was able to provide protection against As toxicity.
In case of joint application of 1600 &micro;M phosphate with arsenate, the
As accumulation and then lipid peroxidation were decreased when compared
to samples treated with arsenate and 5 &micro;M phosphate. The activities
of superoxide dismutase (SOD), ascorbate peroxidase (APX), catalase (CAT)
and glutathione reductase (GR) increased with increasing arsenate supply
levels. Addition of P decreased activities of SOD, APX and CAT, while high
phosphate treatments had a positive effect on GR activity, which may be
due to regulation of glutathione biosynthesis within the plants. In
conclusion, high arsenate treatment (800-1200 &micro;M) could cause an
increasing oxidative stress, which can be scavenged by the antioxidant
enzyme. Furthermore, P may affect As-induced oxidative stress through
nutrient condition and As accumulation.
KW - Isatis cappadocica
KW - antioxidant enzymes
KW - arsenic
KW - phosphorus
KW - plant tolerance
LA - eng
IS - 0959-3330 (Print)
PT - Journal Article
TA - Environ Technol
YR - 2018
DATE- 20180322
CITO- NLM
CS - England
FJT - Environmental technology
EDAT- 20170527
STAT- In-Process
DOCNO- medline/28488470

67 - TOXLINE
TI - Environmental arsenic exposure: From genetic susceptibility to
pathogenesis.
AU - Minatel BC
AD - Department of Integrative Oncology, British Columbia Cancer Research Centre,
Vancouver, British Columbia, Canada.
AU - Sage AP
AD - Department of Integrative Oncology, British Columbia Cancer Research Centre,
Vancouver, British Columbia, Canada.
AU - Anderson C
AD - Department of Integrative Oncology, British Columbia Cancer Research Centre,
Vancouver, British Columbia, Canada.
AU - Hubaux R
AD - Department of Integrative Oncology, British Columbia Cancer Research Centre,
Vancouver, British Columbia, Canada.
AU - Marshall EA
AD - Department of Integrative Oncology, British Columbia Cancer Research Centre,
Vancouver, British Columbia, Canada.
AU - Lam WL
AD - Department of Integrative Oncology, British Columbia Cancer Research Centre,
Vancouver, British Columbia, Canada.
AU - Martinez VD
AD - Department of Integrative Oncology, British Columbia Cancer Research Centre,
Vancouver, British Columbia, Canada. Electronic address: vmartinez@bccrc.ca.
SO - Environ Int. 2018, Mar; 112:183-197. [Environment international]
AB - More than 200 million people in 70 countries are exposed to arsenic
through drinking water. Chronic exposure to this metalloid has been
associated with the onset of many diseases, including cancer.
Epidemiological evidence supports its carcinogenic potential, however,
detailed molecular mechanisms remain to be elucidated. Despite the global
magnitude of this problem, not all individuals face the same risk.
Susceptibility to the toxic effects of arsenic is influenced by
alterations in genes involved in arsenic metabolism, as well as biological
factors, such as age, gender and nutrition. Moreover, chronic arsenic
exposure results in several genotoxic and epigenetic alterations tightly
associated with the arsenic biotransformation process, resulting in an
increased cancer risk. In this review, we: 1) review the roles of
inter-individual DNA-level variations influencing the susceptibility to
arsenic-induced carcinogenesis; 2) discuss the contribution of arsenic
biotransformation to cancer initiation; 3) provide insights into emerging
research areas and the challenges in the field; and 4) compile a resource
of publicly available arsenic-related DNA-level variations, transcriptome
and methylation data. Understanding the molecular mechanisms of arsenic
exposure and its subsequent health effects will support efforts to reduce
the worldwide health burden and encourage the development of strategies
for managing arsenic-related diseases in the era of personalized medicine.
KW - Arsenic
KW - Cancer
KW - Drinking water
KW - Environmental carcinogens
KW - Epigenetics
KW - Genetic susceptibility
LA - eng
IS - 1873-6750 (Electronic)
PT - Journal Article
PT - Review
TA - Environ Int
YR - 2018
DATE- 20180413
CI - Copyright &copy; 2017 The Authors. Published by Elsevier Ltd.. All rights
reserved.
CITO- NLM
CS - Netherlands
FJT - Environment international
EDAT- 20171222
STAT- In-Data-Review
DOCNO- medline/29275244

68 - TOXLINE
TI - A new family of periplasmic-binding proteins that sense arsenic oxyanions.
AU - Badilla C
AD - Institute of Structural &amp; Molecular Biology, Division of Biosciences,
University College London, London, WC1E 6BT, UK.
AU - Osborne TH
AD - Institute of Structural &amp; Molecular Biology, Division of Biosciences,
University College London, London, WC1E 6BT, UK.
AU - Cole A
AD - Institute of Structural &amp; Molecular Biology, Department of Biological
Sciences, Birkbeck College, University of London, WC1E 7HX, London, UK.
AU - Watson C
AD - Institute of Structural &amp; Molecular Biology, Division of Biosciences,
University College London, London, WC1E 6BT, UK.
AU - Djordjevic S
AD - Institute of Structural &amp; Molecular Biology, Division of Biosciences,
University College London, London, WC1E 6BT, UK. s.djordjevic@ucl.ac.uk.
AU - Santini JM
AD - Institute of Structural &amp; Molecular Biology, Division of Biosciences,
University College London, London, WC1E 6BT, UK. j.santini@ucl.ac.uk.
SO - Sci Rep. 2018, Apr 19; 8(1):6282. [Scientific reports]
AB - Arsenic contamination of drinking water affects more than 140 million
people worldwide. While toxic to humans, inorganic forms of arsenic
(arsenite and arsenate), can be used as energy sources for microbial
respiration. AioX and its orthologues (ArxX and ArrX) represent the first
members of a new sub-family of periplasmic-binding proteins that serve as
the first component of a signal transduction system, that's role is to
positively regulate expression of arsenic metabolism enzymes. As
determined by X-ray crystallography for AioX, arsenite binding only
requires subtle conformational changes in protein structure, providing
insights into protein-ligand interactions. The binding pocket of all
orthologues is conserved but this alone is not sufficient for oxyanion
selectivity, with proteins selectively binding either arsenite or
arsenate. Phylogenetic evidence, clearly demonstrates that the regulatory
proteins evolved together early in prokaryotic evolution and had a
separate origin from the metabolic enzymes whose expression they regulate.
LA - eng
IS - 2045-2322 (Electronic)
PT - Journal Article
TA - Sci Rep
YR - 2018
DATE- 20180501
CITO- NLM
CS - England
FJT - Scientific reports
EDAT- 20180419
STAT- In-Data-Review
CM - Cites: Biochemistry. 2005 Nov 15;44(45):14835-44 (medline /16274231)
CM - Cites: BMC Evol Biol. 2015 Jun 12;15:110 (medline /26067063)
CM - Cites: J Biol Chem. 1992 Nov 25;267(33):23674-82 (medline /1331097)
CM - Cites: J Appl Crystallogr. 2007 Aug 1;40(Pt 4):658-674 (medline /19461840)
CM - Cites: J Mol Biol. 1993 Jan 5;229(1):105-24 (medline /7678431)
CM - Cites: J Mol Biol. 1997 Jun 27;269(5):719-31 (medline /9223636)
CM - Cites: Environ Sci Technol. 2017 Nov 21;51(22):13353-13362 (medline
/29064247)
CM - Cites: Protein Sci. 1995 Nov;4(11):2411-23 (medline /8563639)
CM - Cites: J Bacteriol. 2010 Jul;192(14):3755-62 (medline /20453090)
CM - Cites: Environ Microbiol. 2012 Jul;14(7):1624-34 (medline /22176720)
CM - Cites: BMC Evol Biol. 2008 Jul 16;8:206 (medline /18631373)
CM - Cites: Mol Biol Evol. 2003 May;20(5):686-93 (medline /12679550)
CM - Cites: Mol Biol Evol. 2013 Dec;30(12):2725-9 (medline /24132122)
CM - Cites: Environ Microbiol. 2012 Jul;14(7):1635-45 (medline /22404962)
CM - Cites: J Bacteriol. 2006 Feb;188(3):1081-8 (medline /16428412)
CM - Cites: Microbiologyopen. 2017 Dec 17;:null (medline /29250936)
CM - Cites: FEBS Lett. 2002 Apr 24;517(1-3):185-9 (medline /12062434)
CM - Cites: FEMS Microbiol Lett. 2017 Aug 15;364(15):null (medline /28859313)
CM - Cites: Cell. 2006 Sep 22;126(6):1095-108 (medline /16990134)
CM - Cites: Biochemistry. 1967 Jul;6(7):1948-54 (medline /6049437)
CM - Cites: J Bacteriol. 1987 May;169(5):2096-102 (medline /2883171)
CM - Cites: Acta Crystallogr D Biol Crystallogr. 2011 Apr;67(Pt 4):235-42
(medline /21460441)
CM - Cites: J Bacteriol. 2004 Mar;186(6):1614-9 (medline /14996791)
CM - Cites: Nucleic Acids Res. 2004 Mar 19;32(5):1792-7 (medline /15034147)
CM - Cites: Environ Microbiol Rep. 2012 Dec;4(6):571-86 (medline /23760928)
CM - Cites: Structure. 2001 Feb 7;9(2):125-32 (medline /11250197)
CM - Cites: BMC Microbiol. 2010 Feb 18;10:53 (medline /20167112)
CM - Cites: J Bacteriol. 2008 Jan;190(1):135-42 (medline /17951391)
CM - Cites: FEMS Microbiol Lett. 2003 Sep 12;226(1):107-12 (medline /13129615)
CM - Cites: J Mol Biol. 1999 Feb 12;286(1):279-90 (medline /9931266)
CM - Cites: Genome Biol Evol. 2013;5(5):934-53 (medline /23589360)
CM - Cites: J Mol Biol. 1990 Oct 5;215(3):403-10 (medline /2231712)
CM - Cites: Genome Biol Evol. 2012;4(3):307-15 (medline /22333491)
CM - Cites: Eur J Biochem. 1998 Aug 1;255(3):647-53 (medline /9738904)
CM - Cites: Appl Environ Microbiol. 2000 Jan;66(1):92-7 (medline /10618208)
CM - Cites: PLoS One. 2013 Aug 30;8(8):e72535 (medline /24023621)
CM - Cites: FEBS Lett. 2016 Dec;590(23 ):4393-4401 (medline /27714801)
CM - Cites: Metallomics. 2013 Apr;5(4):318-24 (medline /23150098)
CM - Cites: Acta Crystallogr D Biol Crystallogr. 2011 Apr;67(Pt 4):355-67
(medline /21460454)
CM - Cites: Appl Environ Microbiol. 2002 Oct;68(10):4795-802 (medline
/12324322)
CM -Cites: FEMS Microbiol Ecol. 2016 Dec;92 (12 ): (medline /27612494)
CM -Cites: J Mol Biol. 2011 Dec 2;414(3):356-69 (medline /22019591)
CM -Cites: J Bacteriol. 1996 Feb;178(4):1219-23 (medline /8576063)
CM -Cites: Acta Crystallogr D Biol Crystallogr. 2004 Dec;60(Pt 12 Pt
1):2126-32 (medline /15572765)
CM - Cites: FEMS Microbiol Lett. 2010 Dec;313(1):20-8 (medline /21039781)
CM - Cites: J Biol Chem. 2006 Dec 15;281(50):38189-99 (medline /17040909)
CM - Cites: Nature. 2002 Jan 31;415(6871):545-9 (medline /11823863)
CM - Cites: Biochim Biophys Acta. 2007 Feb;1767(2):189-96 (medline /17306216)
DOCNO- medline/29674678

69 - TOXLINE
TI - MicroRNA-191, regulated by HIF-2&alpha;, is involved in EMT and
acquisition of a stem cell-like phenotype in arsenite-transformed human
liver epithelial cells.
AU - Chen C
AD - Institute of Toxicology, School of Public Health, Nanjing Medical University,
Nanjing 211166, Jiangsu, People's Republic of China; The Key Laboratory of Modern
Toxicology, Ministry of Education, School of Public Health, Nanjing Medical
University, Nanjing 211166, Jiangsu, People's Republic of China.
AU - Yang Q
AD - Institute of Toxicology, School of Public Health, Nanjing Medical University,
Nanjing 211166, Jiangsu, People's Republic of China; The Key Laboratory of Modern
Toxicology, Ministry of Education, School of Public Health, Nanjing Medical
University, Nanjing 211166, Jiangsu, People's Republic of China.
AU - Wang D
AD - The Key Laboratory of Environmental Pollution Monitoring and Disease Control,
Ministry of Education, School of Public Health, Guizhou Medical University, Guiyang
550025, Guizhou, People's Republic of China.
AU - Luo F
AD - Institute of Toxicology, School of Public Health, Nanjing Medical University,
Nanjing 211166, Jiangsu, People's Republic of China; The Key Laboratory of Modern
Toxicology, Ministry of Education, School of Public Health, Nanjing Medical
University, Nanjing 211166, Jiangsu, People's Republic of China.
AU - Liu X
AD - Institute of Toxicology, School of Public Health, Nanjing Medical University,
Nanjing 211166, Jiangsu, People's Republic of China; The Key Laboratory of Modern
Toxicology, Ministry of Education, School of Public Health, Nanjing Medical
University, Nanjing 211166, Jiangsu, People's Republic of China.
AU - Xue J
AD - Institute of Toxicology, School of Public Health, Nanjing Medical University,
Nanjing 211166, Jiangsu, People's Republic of China; The Key Laboratory of Modern
Toxicology, Ministry of Education, School of Public Health, Nanjing Medical
University, Nanjing 211166, Jiangsu, People's Republic of China.
AU - Yang P
AD - The School of Public Health, Institute for Chemical Carcinogenesis, Guangzhou
Medical University, Guangzhou 510182, Guangdong, People's Republic of China.
AU - Xu H
AD - Institute of Toxicology, School of Public Health, Nanjing Medical University,
Nanjing 211166, Jiangsu, People's Republic of China; The Key Laboratory of Modern
Toxicology, Ministry of Education, School of Public Health, Nanjing Medical
University, Nanjing 211166, Jiangsu, People's Republic of China.
AU - Lu J
AD - The School of Public Health, Institute for Chemical Carcinogenesis, Guangzhou
Medical University, Guangzhou 510182, Guangdong, People's Republic of China.
AU - Zhang A
AD - The Key Laboratory of Environmental Pollution Monitoring and Disease Control,
Ministry of Education, School of Public Health, Guizhou Medical University, Guiyang
550025, Guizhou, People's Republic of China. Electronic address:
aihuagzykd@163.com.
AU - Liu Q
AD - Institute of Toxicology, School of Public Health, Nanjing Medical University,
Nanjing 211166, Jiangsu, People's Republic of China; The Key Laboratory of Modern
Toxicology, Ministry of Education, School of Public Health, Nanjing Medical
University, Nanjing 211166, Jiangsu, People's Republic of China. Electronic
address: qzliu@njmu.edu.cn.
SO - Toxicol In Vitro. 2018, Apr; 48:128-136. [Toxicology in vitro : an
international journal published in association with BIBRA]
AB - Inorganic arsenic is widely distributed in the environment, and
epidemiologic data show a strong association between arsenic exposure and
risk of liver cancer. An understanding of the mechanisms underlying
development of liver cancer and metastasis would be useful in reducing the
incidence and mortality of liver cancer. MicroRNAs (miRs) act as
regulators in liver cancer. Here, we show that acute or chronic exposure
of human liver epithelial L-02 cells to arsenite increased expression of
miR-191. There were decreased levels of BASP-1 and E-cadherin and
increased levels of WT-1 and N-cadherin, indicating that arsenite induced
epithelial-mesenchymal transition (EMT). Moreover, arsenite increased
EpCAM and CD90 mRNA levels, showing the acquisition of stem cell-like
properties by these cells. Suppression of miR-191 resulted in repression
of EMT and reduced expression of stem-cell markers. Further, a miR-191
inhibitor blocked spheroid formation and production of side population
cells. Luciferase reporter assays indicated that miR-191 was a target of
HIF-2&alpha;, and inhibition of miR-191 decreased the neoplastic and
metastatic properties of arsenite-transformed L-02 cells. Thus, in
arsenite-transformed liver epithelial cells, transcriptional activation of
the miR-191 promoter by HIF-2&alpha; is involved in EMT and in the
acquisition of a stem cell-like phenotype.
KW - Arsenic poisoning
KW - Cancer stem cells (CSCs)
KW - Epithelial-mesenchymal transition (EMT)
KW - Experimental carcinogenesis
KW - miR-191
LA - eng
IS - 1879-3177 (Electronic)
PT - Journal Article
TA - Toxicol In Vitro
YR - 2018
DATE- 20180305
CI - Copyright &copy; 2017. Published by Elsevier Ltd.
CITO- NLM
CS - England
FJT - Toxicology in vitro : an international journal published in association
with BIBRA
EDAT- 20171224
STAT- In-Process
DOCNO- medline/29277653

70 - TOXLINE
TI - High catalytic oxidation of As(III) by molecular oxygen over Fe-loaded
silicon carbide with MW activation.
AU - Pan H
AD - School of Environmental Science and Engineering, Huazhong University of
Science and Technology, 1037 Luoyu Road, Wuhan, 430074, PR China.
AU - Hou H
AD - School of Environmental Science and Engineering, Huazhong University of
Science and Technology, 1037 Luoyu Road, Wuhan, 430074, PR China.
AU - Shi Y
AD - School of Environmental Science and Engineering, Huazhong University of
Science and Technology, 1037 Luoyu Road, Wuhan, 430074, PR China.
AU - Li H
AD - School of Environmental Science and Engineering, Huazhong University of
Science and Technology, 1037 Luoyu Road, Wuhan, 430074, PR China.
AU - Chen J
AD - School of Environmental Science and Engineering, Huazhong University of
Science and Technology, 1037 Luoyu Road, Wuhan, 430074, PR China. Electronic
address: chenjing@mail.hust.edu.cn.
AU - Wang L
AD - School of Environmental Science and Engineering, Huazhong University of
Science and Technology, 1037 Luoyu Road, Wuhan, 430074, PR China. Electronic
address: wanglinling@mail.hust.edu.cn.
AU - Crittenden JC
AD - Brook Byers Institute for Sustainable Systems, School of Civil and
Environmental Engineering, Georgia Institute of Technology, Atlanta, GA 30332, USA.
SO - Chemosphere. 2018, May; 198:537-545. [Chemosphere]
AB - The catalytic oxidation of arsenite (As(III)) to arsenate (As(V)) and the
removal of arsenic (As) in an iron loaded silicon carbide (Fe/SiC) system
under microwave (MW) irradiation were studied. Fe/SiC was synthesized by
electro-deposition and its capability of activating molecular oxygen was
also characterized. Highly efficient As(III) removal in a wide pH range of
2.5-9.5 was achieved, involving oxidation by reactive oxidation species
(OH and O2-) induced by MW irradiation and adsorption by the generated Fe
(hrdro)oxide precipitates. Significant enhancement of As(III) oxidation
was achieved at acidic pH, where sequential fresh Fe(0) exposure with MW
irradiation could improve the Fenton-like reactions and oxidation
efficiency for As(III). As(III) removal was accelerated via adsorption at
alkaline conditions, where the adsorbed Fe(II) on Fe/SiC showed
significant catalytic activity for molecular oxygen and high pH further
favored the formation of (hydro)oxides and the As sequestration by
adsorption. Fe/SiC showed superior performance for the treatment of As in
water with MW irradiation.
KW - Arsenite
KW - Fe arsenic complex
KW - Fe/SiC
KW - MW irradiation
KW - Molecular oxygen activation
RN - E1UOL152H7
RN - N5509X556J
RN - N712M78A8G
RN - N7CIZ75ZPN
RN - S88TT14065
RN - WXQ6E537EW
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180612
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20180208
STAT- MEDLINE
DOCNO- medline/29428768
71 - TOXLINE
TI - Combinatorial drug delivery strategy employing nano-curcumin and
nano-MiADMSA for the treatment of arsenic intoxication in mouse.
AU - Kushwaha P
AD - Division of Regulatory Toxicology, Defence Research and Development
Establishment, Jhansi Road, Gwalior 474002, M.P., India.
AU - Yadav A
AD - Division of Regulatory Toxicology, Defence Research and Development
Establishment, Jhansi Road, Gwalior 474002, M.P., India.
AU - Samim M
AD - Jamia Hamdard, New Delhi, India.
AU - Flora SJS
AD - National Institute of Pharmaceutical Education and Research, Raebareli
209010, U.P., India. Electronic address: sjsflora@hotmail.com.
SO - Chem Biol Interact. 2018, Apr 25; 286:78-87. [Chemico-biological
interactions]
AB - Chelation therapy is the mainstream treatment for heavy metal poisoning.
Apart from this, therapy using antioxidant/herbal extracts are the other
strategies now commonly being tried for the treatment. We have previously
reported individual beneficial efficacy of nanoparticle mediated
administration of an antioxidant like 'curcumin' and an arsenic chelator
'monoisoamyl 2,3-dimercaptosuccinic acid (MiADMSA)' for the treatment of
arsenic toxicity compared to bulk drugs. The present paper investigates
our hypothesis that a combination drug delivery therapy employing two
nanosystems, a chelator and a strong antioxidant, may produce more
pronounced therapeutic effects compared to individual effects in the
treatment of arsenic toxicity. An in-vivo study was conducted wherein
arsenic as sodium arsenite (100&#8239;ppm) was administered in drinking
water for 5 months to Swiss albino mice. This was followed by a treatment
protocol comprising of curcumin encapsulated chitosan nanoparticles
(nano-curcumin, 15&#8239;mg/kg, orally for 1 month) either alone or in
combination with MiADMSA encapsulated polymeric nanoparticles
(nano-MiADMSA, 50&#8239;mg/kg for last 5 days) to evaluate the therapeutic
potential of the combination treatment. Our results demonstrated that
co-treatment with nano-curcumin and nano-MiADMSA provided beneficial
effects in a synergistic way on the adverse changes in oxidative stress
parameters and metal status induced by arsenic.
KW - Arsenic
KW - Curcumin
KW - DMSA monoester
KW - Metal toxicity
KW - Nanoencapsulation
KW - Nanotherapy
KW - Oxidative stress
RN - 88847-89-6
RN - DX1U2629QE
RN - G9481N71RO
RN - GAN16C9B8O
RN - IT942ZTH98
RN - N712M78A8G
LA - eng
IS - 1872-7786 (Electronic)
PT - Journal Article
TA - Chem Biol Interact
YR - 2018
DATE- 20180418
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Ireland
CSET- IM
FJT - Chemico-biological interactions
EDAT- 20180313
STAT- MEDLINE
DOCNO- medline/29548727

72 - TOXLINE
TI - Possible bioremediation of arsenic toxicity by isolating indigenous
bacteria from the middle Gangetic plain of Bihar, India.
AU - Satyapal GK
AD - Centre for Biological Sciences (Biotechnology), Central University of South
Bihar, Patna, Bihar, India.
AU - Mishra SK
AD - Centre for Biological Sciences (Biotechnology), Central University of South
Bihar, Patna, Bihar, India.
AU - Srivastava A
AD - Centre for Biological Sciences (Life Science), Central University of South
Bihar, Patna, Bihar, India.
AU - Ranjan RK
AD - Centre for Environmental Sciences, Central University of South Bihar, Patna,
Bihar, India.
AU - Prakash K
AD - Centre for Biological Sciences (Biotechnology), Central University of South
Bihar, Patna, Bihar, India.
AU - Haque R
AD - Centre for Biological Sciences (Biotechnology), Central University of South
Bihar, Patna, Bihar, India.
AU - Kumar N
AD - Centre for Biological Sciences (Biotechnology), Central University of South
Bihar, Patna, Bihar, India.
SO - Biotechnol Rep (Amst). 2018, Mar; 17:117-125. [Biotechnology reports
(Amsterdam, Netherlands)]
AB - In middle Gangetic plain, high arsenic concentration is present in water,
which causes a significant health risk. Total 48 morphologically distinct
arsenite resistant bacteria were isolated from middle Gangetic plain. The
minimum inhibitory concentration (MIC) values of arsenite varied widely in
the range 1-15&#8239;mM of the isolates. On the basis of their MIC, two
isolates, AK1 (KY569423) and AK9 (KY569424) were selected. The analysis of
the 16S rRNA gene sequence of selected isolates revealed that they are
belong to the genus Pseudomonas. The AgNO3 test based microplate method
revealed that isolates, AK1 and AK9, have potential in transformation of
arsenic species. Further, the presence of aoxR, aoxB and aoxC genes in the
both isolated strain AK1 and AK9 was confirmed, which play an important
role in arsenic bioremediation by arsenite oxidation. Isolated strains
also showed heavy metal resistance against Cr(IV), Ni(II), Co(II), Pb(II),
Cu(II), Hg(II), Ag(I) and Cd(II).
KW - Arsenic
KW - Bacteria
KW - Bioremediation
KW - Middle Gangetic plain
KW - Oxidation
LA - eng
IS - 2215-017X (Print)
PT - Journal Article
TA - Biotechnol Rep (Amst)
YR - 2018
DATE- 20180318
CITO- NLM
CS - Netherlands
FJT - Biotechnology reports (Amsterdam, Netherlands)
EDAT- 20180208
STAT- PubMed-not-MEDLINE
CM - Cites: FEMS Microbiol Lett. 2004 Aug 15;237(2):249-53 (medline /15321669)
CM - Cites: Environ Geochem Health. 2010 Apr;32(2):95-105 (medline /19548094)
CM - Cites: Appl Microbiol Biotechnol. 2013 May;97(9):3827-41 (medline
/23546422)
CM - Cites: FEBS Lett. 2002 Oct 2;529(1):86-92 (medline /12354618)
CM - Cites: Appl Environ Microbiol. 2005 Feb;71(2):599-608 (medline /15691908)
CM - Cites: J Biotechnol. 2010 Oct 1;150(1):101-7 (medline /20638426)
CM - Cites: J Environ Sci Health A Tox Hazard Subst Environ Eng.
2014;49(12):1349-60 (medline /25072766)
CM - Cites: Environ Health Perspect. 2003 Jul;111(9):1194-201 (medline
/12842773)
CM - Cites: J Contam Hydrol. 2011 Apr 1;123(1-2):20-9 (medline /21216490)
CM - Cites: Int Microbiol. 2006 Sep;9(3):207-15 (medline /17061211)
CM - Cites: J Environ Sci Health A Tox Hazard Subst Environ Eng.
2011;46(14):1736-47 (medline /22175878)
DOCNO- medline/29541605

73 - TOXLINE
TI - Arsenic exposure to breast-fed infants: contaminated breastfeeding in the
first month of birth.
AU - Salmani MH
AD - Department of Environmental Health Engineering, School of Public Health,
Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
AU - Rezaie Z
AD - Research Center for Food Hygiene and Safety, School of Public Health, Shahid
Sadoughi University of Medical Sciences, Yazd, Iran. rezaeizeynab91@gmail.com.
AU - Mozaffari-Khosravi H
AD - Department of Nutrition, School of Public Health, Shahid Sadoughi University
of Medical Sciences, Yazd, Iran.
AU - Ehrampoush MH
AD - Environmental Science and Research Center,School of Public Health, Shahid
Sadoughi University of Medical Sciences, Yazd, Iran.
SO - Environ Sci Pollut Res Int. 2018, Mar; 25(7):6680-6684. [Environmental
science and pollution research international]
AB - Humans are exposed to heavy metals through ingestion, inhalation, and
dermal absorption. Exposure to these chemicals may be possible during
lactation. Although breastfeeding has import benefits of physical growth
and development of breastfed infants, it may be a source of exposure to
toxicants. The present study was conducted to determine infant exposure to
the arsenic via breastfeeding. The milk samples were collected from the
150 volunteering mothers three times during the first month of lactation
after delivery. The average arsenic concentration in breast milk samples
was measured by atomic absorption spectrometer (AAS). The demographic
parameters of lactating mothers were collected by a questionnaire and were
analyzed using SPSS 18 software. Arsenic was not detectable in 71 of 150
samples (47.3%). The highest arsenic concentration was 3.73 &mu;g/L,
and overall mean of arsenic concentration was
0.87&thinsp;&plusmn;&thinsp;0.66 &mu;g/L. The daily infant intake of
arsenic ranged in the 0.01-0.17 &mu;g/kg of body weight, which is
below the limit of daily permissible intake for adults. Our results showed
the need to strengthen national food safety programs and to further
promote avoidance of unhealthy foods consuming during pregnancy. Most of
the study samples had detectable levels of arsenic indicate that there was
maternal exposure prior to pregnancy, nevertheless, it is recommended that
the toxic metal levels should be regularly monitored in biological
environments.
KW - Arsenic
KW - Breastfeeding
KW - Infant exposure
KW - Lactation
LA - eng
IS - 1614-7499 (Electronic)
PT - Journal Article
TA - Environ Sci Pollut Res Int
YR - 2018
DATE- 20180305
CITO- NLM
CS - Germany
FJT - Environmental science and pollution research international
EDAT- 20171219
STAT- In-Process
CM - Cites: J Prev Med Public Health. 2014 Sep;47(5):245-52 (medline /25284195)
CM - Cites: Biol Trace Elem Res. 2012 Oct;149(1):117-22 (medline /22528772)
CM - Cites: Environ Health Perspect. 2008 Jul;116(7):963-9 (medline /18629322)
CM - Cites: Trends Plant Sci. 2004 Sep;9(9):415-7 (medline /15337490)
CM - Cites: Environ Int. 2009 Apr;35(3):473-5 (medline /18775567)
CM - Cites: J Hazard Mater. 2007 Apr 2;142(1-2):1-53 (medline /17324507)
CM - Cites: Int J Hyg Environ Health. 2002 Jul;205(5):405-9 (medline /12173541)
CM - Cites: Matern Child Health J. 2010 Jan;14(1):141-5 (medline /19093194)
CM - Cites: Food Chem Toxicol. 1999 Aug;37(8):839-46 (medline /10506007)
CM - Cites: BMC Med. 2004 Jul 01;2:26 (medline /15230974)
CM - Cites: Environ Health Perspect. 2015 May;123(5):500-6 (medline /25707031)
DOCNO- medline/29260474

74 - TOXLINE
TI - Detection of arsenic-binding siderophores in arsenic-tolerating
Actinobacteria by a modified CAS assay.
AU - Retamal-Morales G
AD - Universidad de Santiago de Chile, Laboratorio de Microbiolog�a B�sica y
Aplicada, Facultad de Qu�mica y Biolog�a, Santiago, Chile; TU Bergakademie
Freiberg, Interdisciplinary Ecological Center, 09599 Freiberg, Germany. Electronic
address: gerardo.retamal@usach.cl.
AU - Mehnert M
AD - TU Bergakademie Freiberg, Interdisciplinary Ecological Center, 09599
Freiberg, Germany.
AU - Schwabe R
AD - TU Bergakademie Freiberg, Interdisciplinary Ecological Center, 09599
Freiberg, Germany.
AU - Tischler D
AD - TU Bergakademie Freiberg, Interdisciplinary Ecological Center, 09599
Freiberg, Germany. Electronic address: dirk.tischler@ioez.tu-freiberg.de.
AU - Zapata C
AD - Universidad de Santiago de Chile, Laboratorio de Microbiolog�a B�sica y
Aplicada, Facultad de Qu�mica y Biolog�a, Santiago, Chile.
AU - Ch�vez R
AD - Universidad de Santiago de Chile, Laboratorio de Microbiolog�a B�sica y
Aplicada, Facultad de Qu�mica y Biolog�a, Santiago, Chile.
AU - Schl�mann M
AD - TU Bergakademie Freiberg, Interdisciplinary Ecological Center, 09599
Freiberg, Germany. Electronic address: michael.schloemann@ioez.tu-freiberg.de.
AU - Levic�n G
AD - Universidad de Santiago de Chile, Laboratorio de Microbiolog�a B�sica y
Aplicada, Facultad de Qu�mica y Biolog�a, Santiago, Chile. Electronic address:
gloria.levican@usach.cl.
SO - Ecotoxicol Environ Saf. 2018, Aug 15; 157:176-181. [Ecotoxicology and
environmental safety]
AB - The metalloid arsenic is highly toxic to all forms of life, and in many
countries decontamination of water and soil is still required. Some
bacteria have mechanisms to detoxify arsenic and can live in its presence.
Actinobacteria are well known for their ability to produce a myriad of
biologically-active compounds. In the present study, we isolated
arsenic-tolerant Actinobacteria from contaminated water in Saxony,
Germany, and determined their ability to produce siderophores able to bind
arsenic. The binding capacity of different siderophore-like compounds was
determined by a modified chrome azurol S (As-mCAS) assay with As(III) at
high pH and using CAS decolorization as a readout. Arsenic-tolerant
isolates from three actinobacterial genera were identified by 16&#8239;S
rRNA gene sequence analysis: Rhodococcus, Arthrobacter and Kocuria. The
isolated Actinobacteria showed a high As(III)-binding activity by
siderophore-like compounds, resulting in 82-100% CAS decolorization, as
compared to the results with EDTA. The interaction between As(III) and
siderophore-like compounds was also detected at neutral pH. In summary,
our results suggest that the isolated arsenic-tolerant Actinobacteria
produce siderophores that bind arsenic, and open new perspectives on
potential candidates for decontaminating environments with arsenic and for
other biotechnological applications.
KW - Actinobacteria
KW - Arsenic
KW - As-(m)CAS assay
KW - Bioremediation
KW - CAS assay
KW - Siderophore
LA - eng
IS - 1090-2414 (Electronic)
PT - Journal Article
TA - Ecotoxicol Environ Saf
YR - 2018
DATE- 20180424
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Ecotoxicology and environmental safety
EDAT- 20180402
STAT- In-Process
DOCNO- medline/29621709

75 - TOXLINE
TI - Speciation analysis of inorganic arsenic by magnetic solid phase
extraction on-line with inductively coupled mass spectrometry
determination.
AU - Montoro Leal P
AD - Department of Analytical Chemistry, Faculty of Sciences, University of
Malaga, Campus of Teatinos, 29071 M�laga, Spain.
AU - Vereda Alonso E
AD - Department of Analytical Chemistry, Faculty of Sciences, University of
Malaga, Campus of Teatinos, 29071 M�laga, Spain. Electronic address:
eivereda@uma.es.
AU - L�pez Guerrero MM
AD - Department of Analytical Chemistry, Faculty of Sciences, University of
Malaga, Campus of Teatinos, 29071 M�laga, Spain. Electronic address:
mmlopez@uma.es.
AU - Cordero MTS
AD - Department of Analytical Chemistry, Faculty of Sciences, University of
Malaga, Campus of Teatinos, 29071 M�laga, Spain.
AU - Cano Pav�n JM
AD - Department of Analytical Chemistry, Faculty of Sciences, University of
Malaga, Campus of Teatinos, 29071 M�laga, Spain.
AU - Garc�a de Torres A
AD - Department of Analytical Chemistry, Faculty of Sciences, University of
Malaga, Campus of Teatinos, 29071 M�laga, Spain.
SO - Talanta. 2018, Jul 01; 184:251-259. [Talanta]
AB - Arsenic, one of the main environmental pollutants and potent natural
poison, is a chemical element that is spread throughout the Earth's crust.
It is well known that the toxicity of arsenic is highly dependent on its
chemical forms. Generally, the inorganic species are more toxic than its
organics forms, and As(III) is 60 times more toxic than As(V). In
environmental waters, arsenic exists predominantly in two chemical forms:
As(III) and As(V). In view of these facts, fast, sensitive, accurate and
simple analytical methods for the speciation of inorganic arsenic in
environmental waters are required. In this work, a new magnetic solid
phase extraction with a hydride generation system was coupled on line with
inductively coupled plasma mass spectrometry (MSPE-HG-ICP-MS). The new
system was based on the retention of As(III) and As(V) in two knotted
reactors filled with (Fe3O4) magnetic nanoparticles functionalized with
[1,5-bis (2-pyridyl) 3-sulfophenylmethylene] thiocarbonohydrazide
(PSTH-MNPs). As(III) and total inorganic As were sequentially eluted in
different reduction conditions. The concentration of As(V) was obtained by
subtracting As(III) from total As. The system runs in a fully automated
way and the method has proved to have a wide linear range and to be
precise, sensitive and fast. The detection limits found were 2.7 and
3.2&#8239;ng/L for As(III) and total As, respectively; with relative
standard deviations (RSDs) of 2.5% and 2.7% and a sample throughput of
14.4&#8239;h-1. In order to validate the developed method, several
certified reference samples of environmental waters including sea water,
were analyzed and the determined values were in good agreement with the
certified values. The proposed method was successfully applied to the
speciation analysis of inorganic arsenic in well-water and sea water.
KW - Arsenic speciation
KW - Hydride generation
KW - ICP-MS
KW - Magnetic nanoparticles
KW - Solid phase extraction
LA - eng
IS - 1873-3573 (Electronic)
PT - Journal Article
TA - Talanta
YR - 2018
DATE- 20180427
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Talanta
EDAT- 20180308
STAT- PubMed-not-MEDLINE
DOCNO- medline/29674040

76 - TOXLINE
TI - Distribution of Arsenic and Risk Assessment of Activities on Soccer
Pitches Irrigated with Arsenic-Contaminated Water.
AU - Mart�nez-Villegas N
AD - IPICyT, Instituto Potosino de Investigacion Cientifica y Tecnologica,
Division de Geociencias Aplicadas, Camino a la Presa San Jose No. 2055, Col. Lomas
4a Sec., San Luis Potosi 78216, SLP, Mexico. nadia.martinez@ipicyt.edu.mx.
AU - Hern�ndez A
AD - IPICyT, Instituto Potosino de Investigacion Cientifica y Tecnologica,
Division de Geociencias Aplicadas, Camino a la Presa San Jose No. 2055, Col. Lomas
4a Sec., San Luis Potosi 78216, SLP, Mexico. abraham.hernandez@ipicyt.edu.mx.
AU - Meza-Figueroa D
AD - Departamento de Geolog�a, Universidad de Sonora, Rosales y Encinas s/n, Col.
Centro, Hermosillo 83000, Sonora, Mexico. dmeza@ciencias.uson.mx.
AU - Sen Gupta B
AD - School of Energy, Geoscience, Infrastructure &amp; Society, Institute for
Infrastructure and Environment, Water Academy, Heriot-Watt University, EGIS 2.02A
William Arrol Building, Scotland EH14 4AS, UK. B.SenGupta@hw.ac.uk.
SO - Int J Environ Res Public Health. 2018, May 24. [International journal of
environmental research and public health]
AB - The aim of this research was to estimate the risk of human exposure to
arsenic due to sporting activities in a private soccer club in Mexico,
where arsenic-contaminated water was regularly used for irrigation. For
this purpose, the total concentration in the topsoil was considered for
risk assessment. This was accomplished through three main objectives: (1)
measuring arsenic concentrations in irrigation water and irrigated soils,
(2) determining arsenic spatial distribution in shallow soils with
Geographical Information Systems (GIS) using geostatistical analysis, and
(3) collecting field and survey data to develop a risk assessment
calculation for soccer activities in the soccer club. The results showed
that the average arsenic concentrations in shallow soils (138.1 mg/kg)
were 6.2 times higher than the Mexican threshold for domestic soils (22
mg/kg). Furthermore, dermal contact between exposed users and contaminated
soils accounted for a maximum carcinogenic risk value of 1.8 &amp;times;
10&amp;minus;5, which is one order of magnitude higher than the
recommended risk value, while arsenic concentrations in the irrigation
water were higher (6 mg/L) than the WHO&amp;rsquo;s permissible threshold
in drinking water, explaining the contamination of soils after irrigation.
To the best of our knowledge, this is the first risk study regarding
dermal contact with arsenic following regular grass irrigation with
contaminated water in soccer pitches.
KW - arsenic
KW - irrigation
KW - risk characterization
KW - soccer fields
KW - soil
KW - water
LA - eng
IS - 1660-4601 (Electronic)
PT - Journal Article
TA - Int J Environ Res Public Health
YR - 2018
DATE- 20180608
CITO- NLM
CS - Switzerland
FJT - International journal of environmental research and public health
EDAT- 20180524
STAT- In-Data-Review
DOCNO- medline/29882913

77 - TOXLINE
TI - Arsenic removal by perilla leaf biochar in aqueous solutions and
groundwater: An integrated spectroscopic and microscopic examination.
AU - Niazi NK
AD - Institute of Soil and Environmental Sciences, University of Agriculture
Faisalabad, Faisalabad 38040, Pakistan; MARUM and Department of Geosciences,
University of Bremen, Bremen D-28359, Germany; Southern Cross GeoScience, Southern
Cross University, Lismore 2480 NSW, Australia. Electronic address:
nabeelkniazi@gmail.com.
AU - Bibi I
AD - Institute of Soil and Environmental Sciences, University of Agriculture
Faisalabad, Faisalabad 38040, Pakistan; MARUM and Department of Geosciences,
University of Bremen, Bremen D-28359, Germany.
AU - Shahid M
AD - Department of Environmental Sciences, COMSATS Institute of Information
Technology, Vehari, Pakistan.
AU - Ok YS
AD - Korea Biochar Research Center, O-Jeong Eco-Resilience Institute (OJERI) &amp;
Division of Environmental Science and Ecological Engineering, Korea University,
Seoul 02841, Republic of Korea.
AU - Burton ED
AD - Southern Cross GeoScience, Southern Cross University, Lismore 2480 NSW,
Australia.
AU - Wang H
AD - Key Laboratory of Soil Contamination Bioremediation of Zhejiang Province,
Zhejiang A &amp; F University, Lin'an, Hangzhou 311300, China; School of
Environment and Chemical Engineering, Foshan University, Foshan 528000, China.
AU - Shaheen SM
AD - University of Kafrelsheikh, Faculty of Agriculture, Department of Soil and
Water Sciences, 33 516 Kafr El-Sheikh, Egypt; University of Wuppertal, School of
Architecture and Civil Engineering, Institute of Foundation Engineering, Water- and
Waste-Management, Soil- and Groundwater-Management, Pauluskirchstra&szlig;e 7,
42285 Wuppertal, Germany.
AU - Rinklebe J
AD - University of Wuppertal, School of Architecture and Civil Engineering,
Institute of Foundation Engineering, Water- and Waste-Management, Soil- and
Groundwater-Management, Pauluskirchstra&szlig;e 7, 42285 Wuppertal, Germany;
Department of Environment and Energy, Sejong University, 98 Gunja-Dong, Guangjin-
Gu, Seoul, South Korea.
AU - L�ttge A
AD - MARUM and Department of Geosciences, University of Bremen, Bremen D-28359,
Germany.
SO - Environ Pollut. 2018, Jan; 232:31-41. [Environmental pollution (Barking,
Essex : 1987)]
AB - In this study, we examined the removal of arsenite (As(III)) and arsenate
(As(V)) by perilla leaf-derived biochars produced at 300 and
700 &deg;C (referred as BC300 and BC700) in aqueous environments.
Results revealed that the Langmuir isotherm model provided the best fit
for As(III) and As(V) sorption, with the sorption affinity following the
order:
BC700-As(III) > BC700-As(V) > BC300-As(III)
> BC300-As(V)
(QL = 3.85-11.01 mg g-1). In general, As removal
decreased (76-60%) with increasing pH from 7 to 10 except for the
BC700-As(III) system, where notably higher As removal (88-90%) occurred at
pH from 7 to 9. Surface functional moieties contributed to As
sequestration by the biochars examined here. However, significantly higher
surface area and aromaticity of BC700 favored a greater As removal
compared to BC300, suggesting that surface complexation/precipitation
dominated As removal by BC700. Arsenic K-edge X-ray absorption near edge
structure (XANES) spectroscopy demonstrated that up to 64% of the added
As(V) was reduced to As(III) in BC700- and BC300-As(V) sorption
experiments, and in As(III) sorption experiments, partial oxidation of
As(III) to As(V) occurred (37-39%). However, XANES spectroscopy was
limited to precisely quantify As binding with sulfur species as As2S3-like
phase. Both biochars efficiently removed As from natural As-contaminated
groundwater (As: 23-190 &mu;g L-1; n = 12) despite in
the presence of co-occurring anions (e.g., CO32-, PO43-, SO42-) with the
highest levels of As removal observed for BC700 (97-100%). Overall, this
study highlights that perilla leaf biochars, notably BC700, possessed the
greatest ability to remove As from solution and groundwater (drinking
water). Significantly, the integrated spectroscopic techniques advanced
our understanding to examine complex redox transformation of As(III)/As(V)
with biochar, which are crucial to determine fate of As on biochar in
aquatic environments.
KW - Arsenic toxicity
KW - Drinking water
KW - Groundwater remediation
KW - Sorbent
KW - Water filtration
KW - XANES
RN - 16291-96-6
RN - N5509X556J
RN - N712M78A8G
RN - N7CIZ75ZPN
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180208
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Environmental pollution (Barking, Essex : 1987)
EDAT- 20170929
STAT- MEDLINE
DOCNO- medline/28966026

78 - TOXLINE
TI - Combination of HPLC with organic and inorganic mass spectrometry to study
the metabolic response of the clam Scrobicularia plana to arsenic
exposure.
AU - Rodr�guez-Moro G
AD - Research Center of Health and Environment (CYSMA). University of Huelva,
Huelva, Spain.
AU - Garc�a-Barrera T
AD - Research Center of Health and Environment (CYSMA). University of Huelva,
Huelva, Spain.
AU - Trombini C
AD - Institute for Marine Sciences of Andaluc�a (ICMAN), Ciudad Real, Spain.
AU - Blasco J
AD - Institute for Marine Sciences of Andaluc�a (ICMAN), Ciudad Real, Spain.
AU - G�mez-Ariza JL
AD - Research Center of Health and Environment (CYSMA). University of Huelva,
Huelva, Spain.
SO - Electrophoresis. 2018, Feb; 39(4):635-644. [Electrophoresis]
AB - Arsenic is a toxic element extensively studied in the marine environment
due to differential toxicological effects of inorganic and organic
species. In the present work, the bivalve Scrobicularia plana was exposed
to AsV (10 and 100 &mu;g/L) for 14 days to evaluate the metabolic
perturbations caused by this element. Arsenic speciation and metabolomic
analysis were performed in the digestive gland of the bivalve using two
complementary analytical platforms based on inorganic and organic mass
spectrometry. It has been observed the greater presence of the innocuous
specie arsenobetaine produced in this organism as defense mechanism
against arsenic toxicity, although significant concentrations of
methylated and inorganic arsenic were also present, depending on the level
of arsenic in aqueous media. Complementarily, a metabolomic study based on
mass spectrometry and statistical discriminant analysis allows a good
classification of samples associated to low and high As(V) exposure in
relation to controls. About 15 metabolites suffer significant changes of
expression by the presence of As(V): amino acids, nucleotides,
energy-related metabolites, free fatty acids, phospholipids and
triacylglycerides, which can be related to membrane structural and
functional damage. In addition, perturbation of the methylation cycle,
associated with the increase of homocysteine and methionine was observed,
which enhance the methylation of toxic inorganic arsenic to less toxic
dimethylarsenic.
KW - Arsenic speciation
KW - DI-ESI-Qq-TOF-MS
KW - HPLC-ICP-MS
KW - Metabolomics
KW - Scrobicularia plana
LA - eng
IS - 1522-2683 (Electronic)
PT - Journal Article
TA - Electrophoresis
YR - 2018
DATE- 20180214
CI - &copy; 2017 WILEY-VCH Verlag GmbH &amp; Co. KGaA, Weinheim.
CITO- NLM
CS - Germany
FJT - Electrophoresis
EDAT- 20171211
STAT- In-Data-Review
DOCNO- medline/29125650

79 - TOXLINE
TI - PI3K/Akt/mTOR Signaling Pathway and the Biphasic Effect of Arsenic in
Carcinogenesis.
AU - Chen QY
AD - Department of Environmental Medicine, New York University School of Medicine,
Tuxedo, New York.
AU - Costa M
AD - Department of Environmental Medicine, New York University School of Medicine,
Tuxedo, New York Max.Costa@nyumc.org.
SO - Mol Pharmacol. 2018, Jul; 94(1):784-792. [Molecular pharmacology]
AB - Arsenic is a naturally occurring, ubiquitous metalloid found in the
Earth's crust. In its inorganic form, arsenic is highly toxic and
carcinogenic and is widely found across the globe and throughout the
environment. As an International Agency for Research on Cancer-defined
class 1 human carcinogen, arsenic can cause multiple human cancers,
including liver, lung, urinary bladder, skin, kidney, and prostate.
Mechanisms of arsenic-induced carcinogenesis remain elusive, and this
review focuses specifically on the role of the PI3K/AKT/mTOR pathway in
promoting cancer development. In addition to exerting potent carcinogenic
responses, arsenic is also known for its therapeutic effects against acute
promyelocytic leukemia. Current literature suggests that arsenic can
achieve both therapeutic as well as carcinogenic effects, and this review
serves to examine the paradoxical effects of arsenic, specifically through
the PI3K/AKT/mTOR pathway. Furthermore, a comprehensive review of current
literature reveals an imperative need for future studies to establish and
pinpoint the exact conditions for which arsenic can, and through what
mechanisms it is able to, differentially regulate the PI3K/AKT/mTOR
pathway to maximize the therapeutic and minimize the carcinogenic
properties of arsenic.
LA - eng
IS - 1521-0111 (Electronic)
PT - Journal Article
TA - Mol Pharmacol
YR - 2018
DATE- 20180616
CI - Copyright &copy; 2018 by The Author(s).
CITO- NLM
CS - United States
FJT - Molecular pharmacology
EDAT- 20180516
STAT- In-Data-Review
DOCNO- medline/29769245

80 - TOXLINE
TI - Reduction of arsenic toxicity in two rice cultivar seedlings by different
nanoparticles.
AU - Huang Q
AD - Agro-Environmental Protection Institute, Ministry of Agriculture, Tianjin
300191, China; School of Land and Environmental, Shenyang Agriculture University,
Shenyang 110000, China.
AU - Liu Q
AD - Geophysical Exploration Academy of China Metallurgical Geology Bureau,
Baoding 071051, China.
AU - Lin L
AD - School of Land and Environmental, Shenyang Agriculture University, Shenyang
110000, China.
AU - Li FJ
AD - Agro-Environmental Protection Institute, Ministry of Agriculture, Tianjin
300191, China.
AU - Han Y
AD - Geophysical Exploration Academy of China Metallurgical Geology Bureau,
Baoding 071051, China.
AU - Song ZG
AD - Agro-Environmental Protection Institute, Ministry of Agriculture, Tianjin
300191, China. Electronic address: forestman1218@163.com.
SO - Ecotoxicol Environ Saf. 2018, Sep 15; 159:261-271. [Ecotoxicology and
environmental safety]
AB - In this study, we investigated arsenic uptake and enzymatic activities in
rice seedlings after the addition of nanoparticles. Hydroponic experiments
were conducted to investigate the effects of different nanomaterials
(high-quality graphene oxide, multilayer graphene oxide, 20&#8239;nm
hydroxyapatite (HA20), 40&#8239;nm hydroxyapatite (HA40), nano-Fe3O4
(nFe3O4) and nano-zerovalent iron [nFe]) on the biomass, arsenic uptake,
and enzyme activities in seedlings of the rice cultivars T705 and X24.
Compared with the control, the addition of different nanomaterials
increased seedling growth, with X24 rice growing better than T705 rice.
Nanomaterials effectively reduced arsenic uptake in T705 rice seedlings
under low and high arsenic concentrations; however, they were only
effective at lower arsenic concentrations in X24 seedlings. nFe3O4 and nFe
performed better than other nanomaterials in preventing arsenic from being
transported to the aboveground parts of the rice seedlings. Different
nanomaterials obviously influenced enzyme activities in the T705 seedlings
at low arsenic concentrations (&le; 0.8&#8239;mg&#8239;L-1). High-quality
and multilayer graphene oxide decreased enzyme activities in the
aboveground parts of the T705 seedlings, whereas, HA20 and HA40 increased
the enzyme activities. nFe3O4 and nFe also reduced the effect of
antioxidants in the aboveground parts of the T705 seedlings. Nanomaterials
effectively reduced the arsenic uptake of T705 and X24 rice seedlings at
low arsenic concentrations.
KW - Arsenic
KW - Enzyme activity
KW - Nanomaterial
KW - Rice cultivar
KW - Uptake
LA - eng
IS - 1090-2414 (Electronic)
PT - Journal Article
TA - Ecotoxicol Environ Saf
YR - 2018
DATE- 20180527
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Ecotoxicology and environmental safety
EDAT- 20180521
STAT- In-Process
DOCNO- medline/29753827

81 - TOXLINE
TI - Effect of nutritional status on arsenic and smokeless tobacco induced
genotoxicity, sperm abnormality and oxidative stress in mice in vivo.
AU - Das S
AD - Department of Life Science and Bioinformatics, Molecular and Cell Biology
Laboratory, Assam University, Silchar, 788011, India.
AU - Langthasa P
AD - Department of Life Science and Bioinformatics, Molecular and Cell Biology
Laboratory, Assam University, Silchar, 788011, India.
AU - Barhoi D
AD - Department of Life Science and Bioinformatics, Molecular and Cell Biology
Laboratory, Assam University, Silchar, 788011, India.
AU - Upadhaya P
AD - Department of Life Science and Bioinformatics, Molecular and Cell Biology
Laboratory, Assam University, Silchar, 788011, India.
AU - Giri S
AD - Department of Life Science and Bioinformatics, Molecular and Cell Biology
Laboratory, Assam University, Silchar, 788011, India.
SO - Environ Mol Mutagen. 2018, Mar 22. [Environmental and molecular
mutagenesis]
AB - BACKGROUND: Recently, high concentrations of arsenic have been documented
in ground waters of Southern Assam, India. Indiscriminate smokeless
tobacco consumption is a common practice in this region. Correlation
between nutritional status and arsenic and smokeless tobacco-induced
health effects has not been taken up in humans or other test systems.
AB - METHODS: Mice were divided into groups based on protein (casein) content
in the diet: High protein (40%), optimum protein (20%), and low protein
(5%). Simultaneous chronic exposure (90 days) to arsenic and smokeless
tobacco (sadagura) orally was given to evaluate the extent of the
cytological and genotoxicological damage. Micronucleus assay and Comet
assay of the femur bone marrow cells were conducted. Germ cell toxicity
was evaluated by recording the sperm head abnormalities and total sperm
count. Cell cycle analysis was performed in femur bone marrow cells using
flow cytometer. Hepatic, renal, and intestinal tissues were analyzed for
various oxidative stress evaluations. Histological examination of liver
and kidney was performed.
AB - RESULTS: Notably, high protein diet groups had lower arsenic and sadagura
induced genotoxicity, germ cell abnormalities and oxidative stress as
compared to optimum protein and low protein diet counterparts.
AB - CONCLUSION: Our study indicates that sufficient levels of dietary protein
appear to reduce the long-term arsenic and smokeless tobacco-induced
toxicity in mice test system, as compared to lower or deficient amount of
protein in the diet. This observation has implications and invites further
studies especially epidemiological studies in the human population exposed
to arsenic in South East Asian countries. Environ. Mol. Mutagen., 2018.
&copy; 2018 Wiley Periodicals, Inc.
KW - arsenic
KW - comet assay
KW - diet protein
KW - oxidative damage
KW - smokeless tobacco
KW - sperm head abnormality assay
LA - eng
IS - 1098-2280 (Electronic)
PT - Journal Article
TA - Environ Mol Mutagen
YR - 2018
DATE- 20180323
CI - &copy; 2018 Wiley Periodicals, Inc.
CITO- NLM
CS - United States
FJT - Environmental and molecular mutagenesis
EDAT- 20180322
STAT- Publisher
DOCNO- medline/29569270

82 - TOXLINE
TI - Arsenic-induced carcinogenesis: the impact of miRNA dysregulation.
AU - Cardoso APF
AD - Department of Pharmacology and Toxicology, University of Louisville,
Louisville, KY, 40202, U.S.A.
AU - Al-Eryani L
AD - DNA Repair Section, Laboratory of Cancer Biology and Genetics, Center for
Cancer Research, National Cancer Institute, National Institutes of Health, 37
Convent Drive, Room 4002, Bethesda, MD 20892-4262, U.S.A.
AU - States JC
AD - Department of Pharmacology and Toxicology, University of Louisville,
Louisville, KY, 40202, U.S.A.
SO - Toxicol Sci. 2018, May 28. [Toxicological sciences : an official journal
of the Society of Toxicology]
AB - Arsenic is a toxic metalloid widely present in the earth's crust, and is a
proven human carcinogen. Chronic arsenic exposure mainly through drinking
water causes skin, lung and urinary bladder cancers, and is associated
with liver, prostate and kidney cancers, cardiovascular and neurological
disorders, and diabetes. Several modes of action have been suggested in
arsenic carcinogenesis. However, the molecular etiology of arsenic induced
cancer remains unclear. Recent evidence clearly indicates that gene
expression modifications induced by arsenic may involve epigenetic
alterations, including miRNA dysregulation. Many miRNAs have been
implicated in different human cancers as a consequence of losses and or
gains of miRNA function that contribute to cancer development. Progress in
identifying miRNA dysregulation induced by arsenic has been made using
different approaches and models. The present review discusses the recent
data regarding dysregulated expression of miRNA in arsenic-induced
malignant transformation in vitro, gaps in current understanding and
deficiencies in current models for arsenic-induced carcinogenesis, and
future directions of research that would improve our knowledge regarding
the mechanisms involved in arsenic-induced carcinogenesis.
LA - eng
IS - 1096-0929 (Electronic)
PT - Journal Article
TA - Toxicol Sci
YR - 2018
DATE- 20180530
CITO- NLM
CS - United States
FJT - Toxicological sciences : an official journal of the Society of Toxicology
EDAT- 20180528
STAT- Publisher
DOCNO- medline/29846715

83 - TOXLINE
TI - Effects of arsenic toxicity beyond epigenetic modifications.
AU - Bj�rklund G
AD - Council for Nutritional and Environmental Medicine, Toften 24, 8610, Mo i
Rana, Norway. bjorklund@conem.org.
AU - Aaseth J
AD - Innlandet Hospital Trust and Inland Norway University of Applied Sciences,
Elverum, Norway.
AU - Chirumbolo S
AD - Department of Neurological and Movement Sciences, University of Verona,
Verona, Italy.
AU - Urbina MA
AD - Departamento de Zoolog�a, Facultad de Ciencias Naturales y Oceanogr�ficas,
Universidad de Concepci�n, Casilla 160-C, Concepci�n, Chile.
AU - Uddin R
AD - Department of Pharmacy, Stamford University Bangladesh, Dhaka, Bangladesh.
SO - Environ Geochem Health. 2018, Jun; 40(3):955-965. [Environmental
geochemistry and health]
AB - Worldwide chronic arsenic (As) poisoning by arsenic-contaminated
groundwater is one of the most threatening public health problems. Chronic
inorganic As (inAs) exposure has been associated with various forms of
cancers and numerous other pathological effects in humans, collectively
known as arsenicosis. Over the past decade, evidence indicated that
As-induced epigenetic modifications have a role in the adverse effects on
human health. The main objective of this article is to review the evidence
on epigenetic modifications induced by arsenicals. The epigenetic
components play a crucial role in the regulation of gene expression, at
both transcriptional and posttranscriptional levels. We synthesized the
large body of existing research on arsenic exposure and epigenetic
mechanisms of health outcomes with an emphasis on recent publications.
Changes in patterns of DNA methylation, histone posttranslational
modifications, and microRNAs have been repeatedly observed after inAs
exposure in laboratory studies and in studies of human populations. Such
alterations have the potential to disturb cellular homeostasis, resulting
in the modulation of key pathways in the As-induced carcinogenesis. The
present article reviews recent data on As-induced epigenetic effects and
concludes that it is time for heightened awareness of pathogenic arsenic
exposure, particularly for pregnant women and children, given the
potential for a long-lasting disturbed cellular homeostasis.
KW - Arsenic
KW - Arsenic health effects
KW - Cancer
KW - Chronic arsenic exposure
KW - Drinking water
KW - Human development
KW - Skin lesions
LA - eng
IS - 1573-2983 (Electronic)
PT - Journal Article
PT - Review
TA - Environ Geochem Health
YR - 2018
DATE- 20180525
CITO- NLM
CS - Netherlands
FJT - Environmental geochemistry and health
EDAT- 20170508
STAT- In-Process
CM - Cites: Cancer Lett. 2008 Sep 18;268(2):325-30 (medline /18513855)
CM - Cites: Cancer Epidemiol Biomarkers Prev. 2012 Dec;21(12):2252-60 (medline
/23064002)
CM - Cites: Environ Health Perspect. 2013 Aug;121(8):971-7 (medline /23757598)
CM - Cites: Sci Total Environ. 2015 Jun 1;517:232-45 (medline /25748724)
CM - Cites: Food Chem Toxicol. 2010 Apr;48(4):1032-9 (medline /20096321)
CM - Cites: Nat Rev Cancer. 2004 Feb;4(2):143-53 (medline /14732866)
CM - Cites: Cancer Res. 2006 Nov 15;66(22):10843-8 (medline /17108120)
CM - Cites: Epigenomics. 2010 Feb;2(1):87-104 (medline /20514360)
CM - Cites: Arch Toxicol. 2014 May;88(5):1043-67 (medline /24691704)
CM - Cites: Nature. 2007 May 24;447(7143):433-40 (medline /17522677)
CM - Cites: Sci Total Environ. 2006 Nov 1;370(2-3):294-301 (medline /16875714)
CM - Cites: Environ Sci Technol. 2001 Jul 1;35(13):2621-6 (medline /11452583)
CM - Cites: Am J Epidemiol. 2001 Mar 1;153(5):411-8 (medline /11226969)
CM - Cites: Environ Mol Mutagen. 2014 Apr;55(3):196-208 (medline /24327377)
CM - Cites: Toxicol Appl Pharmacol. 2009 Mar 15;235(3):338-50 (medline
/19168087)
CM - Cites: Toxicol Appl Pharmacol. 2009 Dec 15;241(3):294-302 (medline
/19732783)
CM - Cites: Biomed Res Int. 2015;2015:892579 (medline /26295053)
CM - Cites: J Pharmacol Exp Ther. 1997 Jul;282(1):192-200 (medline /9223554)
CM - Cites: Metallomics. 2012 Jan;4(1):91-100 (medline /22028001)
CM - Cites: Environ Toxicol Pharmacol. 2013 Jul;36(1):73-9 (medline /23619517)
CM - Cites: Arch Toxicol. 2011 Jun;85(6):653-61 (medline /20978746)
CM - Cites: Nucleic Acids Res. 1983 Mar 11;11(5):1389-404 (medline /6402762)
CM - Cites: Environ Health Perspect. 2012 Jul;120(7):1061-6 (medline /22466225)
CM - Cites: Hypertension. 1999 Jan;33(1):74-8 (medline /9931084)
CM - Cites: Sci Prog. 1947 Jul;35(139):396-416 (medline /20256237)
CM - Cites: Sci Total Environ. 2012 Jul 1;429:2-35 (medline /21959248)
CM - Cites: Cell. 1999 Oct 29;99(3):247-57 (medline /10555141)
CM - Cites: Am J Clin Nutr. 2007 Oct;86(4):1179-86 (medline /17921400)
CM - Cites: Mol Biol Int. 2011;2011:718974 (medline /22091411)
CM - Cites: J Trace Elem Med Biol. 2015;31:260-6 (medline /25457281)
CM - Cites: Environ Int. 2009 Apr;35(3):466-72 (medline /18809211)
CM - Cites: Folia Biol (Praha). 2010;56(3):83-96 (medline /20653993)
CM - Cites: Arch Toxicol. 2005 Apr;79(4):183-91 (medline /15526190)
CM - Cites: J Trace Elem Med Biol. 2015;31:237-48 (medline /25660323)
CM - Cites: Bull World Health Organ. 2012 Nov 1;90(11):839-46 (medline
/23226896)
CM - Cites: Environ Geochem Health. 2016 Apr;38(2):339-51 (medline /26169729)
CM - Cites: Sci Total Environ. 2014 Aug 1;488-489:562-9 (medline /24262873)
CM - Cites: Virchows Arch. 2008 Jan;452(1):1-10 (medline /18040713)
CM - Cites: J Can Res Updates. 2012 Aug 21;1:57-68 (medline /23487506)
CM - Cites: Toxicol Appl Pharmacol. 2010 Mar 15;243(3):292-9 (medline
/19932709)
CM - Cites: Genome Biol. 2006;7(5):217 (medline /16689998)
CM - Cites: Toxicol Appl Pharmacol. 2004 Aug 1;198(3):268-71 (medline
/15276405)
CM - Cites: Environ Sci Technol. 2016 Jun 21;50(12 ):6556-64 (medline
/27223406)
CM - Cites: Cancer Epidemiol Biomarkers Prev. 2007 Jun;16(6):1270-8 (medline
/17548696)
CM - Cites: Toxicol Appl Pharmacol. 2008 Jul 1;230(1):33-40 (medline /18387645)
CM - Cites: Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):16916-21 (medline
/12481029)
CM - Cites: Environ Health Perspect. 2011 May;119(5):719-24 (medline /21147604)
CM - Cites: Int J Mol Sci. 2011;12(4):2351-82 (medline /21731446)
CM - Cites: Nihon Eiseigaku Zasshi. 2015;70(3):186-96 (medline /26411936)
CM - Cites: Toxicol Sci. 2011 May;121(1):110-22 (medline /21292642)
CM - Cites: Genome Res. 2009 Jan;19(1):92-105 (medline /18955434)
CM - Cites: J Biochem Mol Toxicol. 2013 Feb;27(2):106-15 (medline /23315758)
CM - Cites: Oman Med J. 2011 May;26(3):207 (medline /22043419)
CM - Cites: Saudi J Kidney Dis Transpl. 2015 May-Jun;26(3):611-2 (medline
/26022042)
CM - Cites: Epigenetics. 2013 May;8(5):464-76 (medline /23644490)
CM - Cites: Eur Respir J. 2012 May;39(5):1076-83 (medline /22088973)
CM - Cites: J Toxicol Clin Toxicol. 2001;39(7):683-700 (medline /11778666)
CM - Cites: Cancer Causes Control. 2008 Oct;19(8):829-39 (medline /18351295)
CM - Cites: Environ Mol Mutagen. 2015 Jan;56(1):60-9 (medline /25156000)
CM - Cites: Cell. 2007 Feb 23;128(4):693-705 (medline /17320507)
CM - Cites: Toxicology. 2003 Apr 15;186(1-2):33-50 (medline /12604169)
CM - Cites: Toxicol Appl Pharmacol. 2014 Oct 1;280(1):53-9 (medline /25062773)
CM - Cites: Toxicol Appl Pharmacol. 2010 Feb 1;242(3):352-62 (medline
/19914269)
CM - Cites: Metallomics. 2012 Nov;4(11):1167-75 (medline /23073540)
CM - Cites: Chem Res Toxicol. 2011 Feb 18;24(2):165-7 (medline /21291286)
CM - Cites: Biomed Res Int. 2014;2014:683124 (medline /24949461)
CM - Cites: Water Res. 2013 Oct 1;47(15):5801-18 (medline /23899878)
CM - Cites: Environ Pollut. 2006 Jan;139(1):95-106 (medline /16009476)
CM - Cites: Environ Int. 2014 Aug;69:148-58 (medline /24853282)
CM - Cites: J Occup Environ Med. 2003 Mar;45(3):241-8 (medline /12661181)
CM - Cites: Genes Dev. 2011 May 15;25(10):1010-22 (medline /21576262)
CM - Cites: Environ Health Perspect. 2011 Jan;119(1):113-8 (medline /21205583)
CM - Cites: Epidemiology. 2005 Jan;16(1):82-6 (medline /15613949)
CM - Cites: N Engl J Med. 1998 Nov 5;339(19):1341-8 (medline /9801394)
CM - Cites: J Environ Pathol Toxicol Oncol. 2015;34(1):63-84 (medline
/25746832)
CM - Cites: Am J Epidemiol. 1998 Jul 15;148(2):198-203 (medline /9676702)
CM - Cites: Environ Health Perspect. 2005 Mar;113(3):250-4 (medline /15743710)
CM - Cites: J Biol Chem. 2003 Apr 11;278(15):13183-91 (medline /12547826)
CM - Cites: Chem Res Toxicol. 2001 Apr;14(4):371-8 (medline /11304125)
CM - Cites: Environ Health Perspect. 2005 Dec;113(12):1683-8 (medline
/16330347)
CM - Cites: Lancet. 2010 Jul 24;376(9737):252-8 (medline /20646756)
CM - Cites: Sci Total Environ. 2007 Jan 1;372(2-3):413-25 (medline /17081593)
CM - Cites: Toxicol Appl Pharmacol. 2009 Apr 15;236(2):131-41 (medline
/19371612)
CM - Cites: Mamm Genome. 2009 Sep-Oct;20(9-10):573-80 (medline /19697081)
CM - Cites: J Trace Elem Med Biol. 2015;31:209-13 (medline /24837610)
CM - Cites: Epigenetics. 2014 May;9(5):774-82 (medline /24525453)
CM - Cites: Toxicol Appl Pharmacol. 2005 Aug 15;206(3):299-308 (medline
/16039941)
CM -Cites: Environ Int. 2004 May;30(3):383-7 (medline /14987870)
CM -Cites: Oncogene. 2001 May 28;20(24):3166-73 (medline /11420733)
CM -Cites: Rev Environ Health. 2010 Jul-Sep;25(3):193-220 (medline /21038756)
CM -Cites: Environ Int. 2015 Aug;81:8-17 (medline /25898228)
CM -Cites: Int J Environ Res Public Health. 2012 Dec 07;9(12):4522-36 (medline
/23222207)
CM - Cites: Environ Health Perspect. 2015 May;123(5):451-7 (medline /25575156)
CM - Cites: Sci Rep. 2013;3:2195 (medline /23873074)
CM - Cites: Environ Health Perspect. 2011 Jun;119(6):771-7 (medline /21193388)
DOCNO- medline/28484874

84 - TOXLINE
TI - Isolation and identification of the native population bacteria for
bioremediation of high levels of arsenic from water resources.
AU - Jebelli MA
AD - Department of Environmental Health Engineering, Environmental Health Research
Center, Kurdistan University of Medical Sciences, Sanandaj, Iran.
AU - Maleki A
AD - Department of Environmental Health Engineering, Environmental Health Research
Center, Kurdistan University of Medical Sciences, Sanandaj, Iran. Electronic
address: maleki43@yahoo.com.
AU - Amoozegar MA
AD - Extremophiles Laboratory, Department of Microbiology, Faculty of Biology and
Center of Excellence in Phylogeny of Living Organisms, College of Science,
University of Tehran, Iran.
AU - Kalantar E
AD - Dietary Supplement and Probiotic Research Center, Alborz University of
Medical Sciences, Karaj, Iran. Electronic address: enayat.kalantar66@gmail.com.
AU - Gharibi F
AD - Department of Environmental Health Engineering, Environmental Health Research
Center, Kurdistan University of Medical Sciences, Sanandaj, Iran.
AU - Darvish N
AD - Graduate School of Environment and Energy, Science and Research Branch,
Islamic Azad University,Tehran, Iran.
AU - Tashayoe H
AD - Department of Environmental Health Engineering, Faculty of Health, Water
Purification Research Center, Tehran Medical Sciences Branch Islamic Azad
University, Tehran, Iran.
SO - J Environ Manage. 2018, Apr 15; 212:39-45. [Journal of environmental
management]
AB - Health of millions of people is threatened by the risk of drinking
arsenic-contaminated water worldwide. Arsenic naturally conflicts with the
concept of life, but recent studies showed that some microorganisms use
toxic minerals as the source of energy. Hence, the researchers should
consider the development of cost-effective and highly productive
procedures to remove arsenic. The current study was conducted on a native
bacterial population of Seyed-Jalaleddin Spring Kurdistan, Iran.
Accordingly, the arsenic amount in water samples was measured
> 500&#8239;&mu;g/L by the two field and in vitro methods. Water
samples were transferred to laboratory and cultured on chemically defined
medium (CDM) with arsenic salts. A total of 14 native arsenic-resistant
bacterial strains were isolated and after providing pure culture and
performing biochemical tests, the isolates were identified using
polymerase chain reaction (PCR) and 16s rRNA genomic sequencing. The
potential of bacterial strains for the biotransformation of arsenic was
assessed by the qualitative assessment of AgNO3 method and efficiency of
arsenic speciation was determined for the first time by silver
diethyldithiocarbamate (SDDC) method with an error of less than 5%. Among
the isolated strains, only strain As-11 and strain As-12 showed arsenic
transformation characteristics and were registered in NCBI database by the
access numbers KY119262 and KY119261, respectively. Results of the current
study indicated that strain As-11 had the potential of biotransformation
of As(V) to As(III) and vice versa with the efficiency of 78% and 48%,
respectively. On the other hand, strain As-12 had the potential for
biotransformation of As(V) to As(III) and vice versa with the efficiency
of 28% and 45%, respectively.
KW - Arsenic
KW - Biotransformation
KW - SDDC
KW - Water resource
LA - eng
IS - 1095-8630 (Electronic)
PT - Journal Article
TA - J Environ Manage
YR - 2018
DATE- 20180309
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Journal of environmental management
EDAT- 20180222
STAT- In-Process
DOCNO- medline/29427940

85 - TOXLINE
TI - Two facets of world arsenic problem solution: crop poisoning restriction
and enforcement of phytoremediation.
AU - Kofro&#328;ov� M
AD - Department of Experimental Plant Biology, Faculty of Science, Charles
University, Vini&#269;n� 5, 128 43, Prague 2, Czech Republic.
AU - Ma&scaron;kov� P
AD - Department of Experimental Plant Biology, Faculty of Science, Charles
University, Vini&#269;n� 5, 128 43, Prague 2, Czech Republic.
petra.maskova@natur.cuni.cz.
AU - Lipavsk� H
AD - Department of Experimental Plant Biology, Faculty of Science, Charles
University, Vini&#269;n� 5, 128 43, Prague 2, Czech Republic.
SO - Planta. 2018, May 07. [Planta]
AB - MAIN CONCLUSION: This review provides insights into As toxicity in plants
with focus on photosynthesis and sugar metabolism as important arsenic
targets and simultaneously defence tools against accompanying oxidative
stress. Heavy metal contamination is a great problem all over the world.
Arsenic, a metalloid occurring naturally in the Earth's crust, also
massively spreads out in the environment by human activities. Its
accumulation in crops poses a severe health risk to humans and animals.
Besides the restriction of human-caused contamination, there are two basic
ways how to cope with the problem: first, to limit arsenic accumulation in
harvestable parts of the crops; second, to make use of some arsenic
hyperaccumulating plants for phytoremediation of contaminated soils and
waters. Progress in the use of both strategies depends strongly on the
level of our knowledge on the physiological and morphological processes
resulting from arsenic exposure. Arsenic uptake is mediated preferentially
by P and Si transporters and its accumulation substantially impairs plant
metabolism at numerous levels including damages through oxidative stress.
Rice is a predominantly studied crop where substantial progress has been
made in understanding of the mechanisms of arsenic uptake, distribution,
and detoxification, though many questions still remain. Full exploitation
of plant potential for soil and water phytoremediations also requires deep
understanding of the plant response to this toxic metalloid. The aim of
this review is to summarize data regarding the effect of arsenic on plant
physiology with a focus on mechanisms providing increased arsenic
tolerance and/or hyperaccumulation. The emphasis is placed on the topic
unjustifiably neglected in the previous reviews - i.e.,
carbohydrate metabolism, tightly connected to photosynthesis, and beside
others involved in plant ability to cope with arsenic-induced oxidative
and nitrosative stresses.
KW - Antioxidant
KW - Arsenic
KW - Carbohydrates
KW - Nitrosative stress
KW - Oxidative stress
KW - Phytoremediation
LA - eng
IS - 1432-2048 (Electronic)
PT - Journal Article
PT - Review
TA - Planta
YR - 2018
DATE- 20180619
CITO- NLM
CS - Germany
FJT - Planta
EDAT- 20180507
STAT- Publisher
CM - Cites: J Proteomics. 2014 Jun 13;105:46-57 (medline /24508335)
CM - Cites: Proc Natl Acad Sci U S A. 2008 Jul 22;105(29):9931-5 (medline
/18626020)
CM - Cites: Ecotoxicol Environ Saf. 2009 Feb;72(2):626-34 (medline /18262648)
CM - Cites: New Phytol. 2007;174(2):311-21 (medline /17388894)
CM - Cites: Curr Opin Plant Biol. 2009 Jun;12(3):364-72 (medline /19501016)
CM - Cites: New Phytol. 2014 Mar;201(4):1251-62 (medline /24206613)
CM - Cites: ISME J. 2016 Jan;10 (1):197-209 (medline /26151644)
CM - Cites: J Exp Bot. 2013 Jan;64(1):303-15 (medline /23162117)
CM - Cites: Plant Physiol. 2000 Apr;122(4):1171-7 (medline /10759512)
CM - Cites: J Hazard Mater. 2010 Mar 15;175(1-3):896-914 (medline /19944530)
CM - Cites: Plant Cell. 2010 Jun;22(6):2045-57 (medline /20530755)
CM - Cites: Plant Physiol. 1993 Aug;102(4):1163-1169 (medline /12231893)
CM - Cites: Protoplasma. 2011 Jul;248(3):565-77 (medline /20857150)
CM - Cites: Annu Rev Plant Physiol Plant Mol Biol. 1998 Jun;49:643-668 (medline
/15012249)
CM - Cites: Plant J. 2006 Mar;45(6):917-29 (medline /16507083)
CM - Cites: Chemosphere. 2005 Oct;61(2):293-301 (medline /16168752)
CM - Cites: PLoS One. 2017 Mar 15;12 (3):e0173681 (medline /28296918)
CM - Cites: Protoplasma. 2011 Oct;248(4):805-15 (medline /21188438)
CM - Cites: Annu Rev Plant Biol. 2010;61:535-59 (medline /20192735)
CM - Cites: Chemosphere. 2009 Feb;74(5):688-702 (medline /18996570)
CM - Cites: Plant Physiol. 2002 Nov;130(3):1552-61 (medline /12428020)
CM - Cites: Biol Trace Elem Res. 2012 Jun;146(3):360-8 (medline /22124861)
CM - Cites: Environ Pollut. 2009 Mar;157(3):887-94 (medline /19073356)
CM - Cites: Talanta. 2002 Aug 16;58(1):181-8 (medline /18968744)
CM - Cites: Physiol Plant. 2016 Jun;157(2):135-46 (medline /26853807)
CM - Cites: Nat Plants. 2015 Dec 21;2(1):15202 (medline /27004129)
CM - Cites: Chemosphere. 2007 Apr;67(6):1072-9 (medline /17239924)
CM - Cites: Environ Sci Pollut Res Int. 2011 Aug;19(7):3046-53 (medline
/22367495)
CM - Cites: Plant Physiol. 2004 Oct;136(2):3198-208 (medline /15448194)
CM - Cites: Plant Physiol Biochem. 2016 Jan;98:119-27 (medline /26686284)
CM - Cites: J Exp Bot. 2013 Apr;64(6):1439-49 (medline /23564957)
CM - Cites: Plant Physiol. 2011 Sep;157(1):498-508 (medline /21715673)
CM - Cites: J Exp Bot. 2009;60(1):9-18 (medline /19036839)
CM - Cites: Trends Plant Sci. 2012 Mar;17(3):155-62 (medline /22257759)
CM - Cites: Plant Cell Rep. 2007 Nov;26(11):2027-38 (medline /17653721)
CM - Cites: Environ Pollut. 2017 Apr;223:230-237 (medline /28108165)
CM - Cites: Front Plant Sci. 2014 Nov 04;5:592 (medline /25408694)
CM - Cites: Plant Physiol Biochem. 2013 Oct;71:307-14 (medline /24007815)
CM - Cites: Proc Natl Acad Sci U S A. 2006 Apr 4;103(14 ):5413-8 (medline
/16567632)
CM - Cites: Environ Pollut. 2017 May;224:125-135 (medline /28214191)
CM - Cites: J Biol Chem. 2009 Jan 23;284(4):2114-20 (medline /19029297)
CM - Cites: Proc Natl Acad Sci U S A. 2014 Nov 4;111(44):15699-704 (medline
/25331872)
CM - Cites: Ann Bot. 2003 Jan;91 Spec No:179-94 (medline /12509339)
CM - Cites: Front Plant Sci. 2016 Jun 14;7:817 (medline /27379117)
CM - Cites: New Phytol. 2016 Jan;209(2):762-72 (medline /26010225)
CM - Cites: Ecotoxicol Environ Saf. 2001 Jun;49(2):111-21 (medline /11386724)
CM - Cites: Cell Mol Life Sci. 2009 Jul;66(14):2329-39 (medline /19350206)
CM - Cites: Anal Chim Acta. 2010 Jan 11;657(2):83-99 (medline /20005319)
CM - Cites: New Phytol. 2009 Mar;181(4):777-94 (medline /19207683)
CM - Cites: Planta. 2015 May;241(5):1109-18 (medline /25600998)
CM - Cites: Ecotoxicol Environ Saf. 2017 May;139:344-351 (medline /28187398)
CM - Cites: J Environ Sci (China). 2007;19(6):725-32 (medline /17969647)
CM - Cites: Protoplasma. 2012 Jul;249(3):725-36 (medline /21901307)
CM - Cites: Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):16113-8 (medline
/14671332)
CM - Cites: Plant Cell Environ. 2017 Apr;40(4):462-472 (medline /26754426)
CM - Cites: Plant Physiol. 2010 Jan;152(1):309-19 (medline /19880610)
CM - Cites: Plant Physiol. 2008 Jul;147(3):1251-63 (medline /18502973)
CM - Cites: Ecotoxicol Environ Saf. 2017 Apr;138:199-205 (medline /28061413)
CM - Cites: Biochemistry. 2012 Jul 10;51(27):5476-85 (medline /22712827)
CM - Cites: Plant Physiol Biochem. 2017 Mar;112:74-86 (medline /28049059)
CM - Cites: Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2075-80 (medline
/16452170)
CM - Cites: Plant Physiol. 2009 Aug;150(4):2071-80 (medline /19542298)
CM - Cites: New Phytol. 2016 Jan;209(2):746-61 (medline /26372374)
CM - Cites: J Exp Bot. 2013 Feb;64(4):1025-38 (medline /23349141)
CM - Cites: J Hazard Mater. 2013 Nov 15;262:1123-31 (medline /22917495)
CM - Cites: J Mol Model. 2012 Sep;18(9):4249-62 (medline /22562211)
CM - Cites: J Plant Physiol. 2004 Jul;161(7):867-72 (medline /15310076)
CM - Cites: J Biotechnol. 2002 Nov 13;99(3):259-78 (medline /12385714)
CM - Cites: Front Plant Sci. 2017 Apr 19;8:516 (medline /28469622)
CM - Cites: Protoplasma. 2015 Sep;252(5):1217-29 (medline /25586108)
CM - Cites: Plant Cell. 2007 Mar;19(3):1123-33 (medline /17400898)
CM - Cites: Plant Cell. 2013 Aug;25(8):2944-57 (medline /23922208)
CM - Cites: Environ Pollut. 2016 Sep;216:215-222 (medline /27263113)
CM - Cites: Plant Physiol. 2010 Nov;154(3):1505-13 (medline /20870777)
CM - Cites: Environ Pollut. 2017 Aug;227:569-577 (medline /28501771)
CM - Cites: Ecotoxicol Environ Saf. 2009 May;72(4):1102-10 (medline /19013643)
CM - Cites: J Hazard Mater. 2017 May 15;330:68-75 (medline /28212511)
CM - Cites: Ecotoxicol Environ Saf. 2013 Apr;90:28-34 (medline /23321366)
CM - Cites: Mol Plant. 2015 May;8(5):722-33 (medline /25732589)
CM - Cites: Trends Biotechnol. 2007 Apr;25(4):158-65 (medline /17306392)
CM - Cites: PLoS One. 2012;7(8):e42408 (medline /22879969)
CM - Cites: Annu Rev Plant Physiol Plant Mol Biol. 1998 Jun;49:249-279 (medline
/15012235)
CM - Cites: Sci Total Environ. 2002 Feb 4;284(1-3):27-35 (medline /11846172)
CM -Cites: J Hazard Mater. 2017 Jun 5;331:246-256 (medline /28273574)
CM -Cites: Sci Rep. 2014 Jul 22;4:5784 (medline /25048298)
CM -Cites: Physiol Mol Biol Plants. 2015 Jul;21(3):453-8 (medline /26261411)
CM -Cites: Chemosphere. 2017 May;175:192-199 (medline /28222373)
CM -Cites: Nat Commun. 2014 Aug 07;5:4617 (medline /25099865)
CM -Cites: BMC Biol. 2008 Jun 10;6:26 (medline /18544156)
CM -Cites: Environ Sci Pollut Res Int. 2016 Jun;23 (12 ):11864-75 (medline
/26957429)
CM - Cites: J Hazard Mater. 2013 Nov 15;262:1230-6 (medline /22947180)
CM - Cites: Plant J. 2015 Jun;82(5):822-39 (medline /25891826)
CM - Cites: Plant Physiol. 2000 Jul;123(3):825-32 (medline /10889232)
CM - Cites: Environ Sci Technol. 2011 Jul 15;45(14):6080-7 (medline /21692537)
CM - Cites: Transgenic Res. 2012 Dec;21(6):1265-77 (medline /22350764)
CM - Cites: J Exp Bot. 2006;57(3):449-59 (medline /16397003)
CM - Cites: Environ Sci Technol. 2002 Mar 1;36(5):962-8 (medline /11918027)
CM - Cites: Front Plant Sci. 2017 Mar 01;8:268 (medline /28298917)
CM - Cites: Environ Sci Pollut Res Int. 2012 Sep;19(8):3506-15 (medline
/22529007)
CM - Cites: Chemosphere. 2011 Apr;83(5):633-46 (medline /21435676)
CM - Cites: Plant Signal Behav. 2009 Oct;4(10):920-3 (medline /19826215)
CM - Cites: New Phytol. 2011 Oct;192(1):87-98 (medline /21658183)
CM - Cites: Plant Physiol. 2006 Aug;141(4):1544-54 (medline /16766666)
CM - Cites: Proc Natl Acad Sci U S A. 2010 Dec 7;107(49):21187-92 (medline
/21078981)
CM - Cites: Ecotoxicol Environ Saf. 2017 Apr;138:47-55 (medline /28006731)
CM - Cites: Plant J. 2004 Aug;39(4):629-42 (medline /15272879)
CM - Cites: Plant Cell Physiol. 2009 Feb;50(2):265-79 (medline /19112080)
CM - Cites: Plant Cell Environ. 2009 Jul;32(7):851-8 (medline /19236608)
CM - Cites: Environ Sci Technol. 2006 Aug 15;40(16):5010-4 (medline /16955900)
CM - Cites: PLoS Biol. 2014 Dec 02;12(12):e1002009 (medline /25464340)
CM - Cites: Nature. 2001 Feb 1;409(6820):579 (medline /11214308)
CM - Cites: Biosci Biotechnol Biochem. 2011;75(3):522-30 (medline /21389618)
CM - Cites: Environ Sci Technol. 2017 Feb 7;51(3):1224-1230 (medline /28076949)
CM - Cites: Environ Pollut. 2012 Jul;166:136-43 (medline /22504427)
DOCNO- medline/29736625

86 - TOXLINE
TI - Arsenic Induces Thioredoxin 1 and Apoptosis in Human Liver HHL-5 Cells.
AU - Li Y
AD - Center for Endemic Disease Control, Chinese Center for Disease Control and
Prevention, Key Laboratory of Etiologic Epidemiology of Education Bureau of
Heilongjiang Province and Ministry of Health, Harbin Medical University, Harbin,
150081, China.
AU - Zhang Y
AD - Center for Endemic Disease Control, Chinese Center for Disease Control and
Prevention, Key Laboratory of Etiologic Epidemiology of Education Bureau of
Heilongjiang Province and Ministry of Health, Harbin Medical University, Harbin,
150081, China.
AU - Gao Y
AD - Center for Endemic Disease Control, Chinese Center for Disease Control and
Prevention, Key Laboratory of Etiologic Epidemiology of Education Bureau of
Heilongjiang Province and Ministry of Health, Harbin Medical University, Harbin,
150081, China.
AU - Zhang W
AD - Center for Endemic Disease Control, Chinese Center for Disease Control and
Prevention, Key Laboratory of Etiologic Epidemiology of Education Bureau of
Heilongjiang Province and Ministry of Health, Harbin Medical University, Harbin,
150081, China.
AU - Cui X
AD - Advanced Institute for Medical Sciences, Dalian Medical University, Dalian,
116044, China.
AU - Liu J
AD - Center for Endemic Disease Control, Chinese Center for Disease Control and
Prevention, Key Laboratory of Etiologic Epidemiology of Education Bureau of
Heilongjiang Province and Ministry of Health, Harbin Medical University, Harbin,
150081, China.
AU - Wei Y
AD - Department of Community Medicine, Mercer University School of Medicine,
Macon, GA, 31207, USA. wei_yd@mercer.edu.
SO - Biol Trace Elem Res. 2018, Feb; 181(2):234-241. [Biological trace element
research]
AB - To further characterize the mechanisms underlying liver toxicity induced
by arsenic, we examined in this study the effect of arsenic on thioredoxin
(Trx) and the apoptotic signaling pathways in human liver HHL-5 cells. The
cells were treated with 0, 2, 5, and 10 &mu;M of sodium arsenite for
24 h, and the changes of Trx1 and thioredoxin reductase (TrxR1) as
well as intracellular ROS and apoptosis were examined. A
concentration-dependent increase in mRNA and protein levels of Trx1 and
TrxR1 was observed in arsenic-treated cells. Intracellular ROS levels and
apoptosis were also significantly increased in a concentration-dependent
manner. In line with this, protein levels of Bax and cytochrome C were
increased and Bcl-2 was decreased by arsenic treatments. Increases in
caspase 3 activity were observed. These results indicate that Trx is
involved in arsenic-induced liver cell injury, probably through the
apoptotic signaling pathway. However, further studies are needed to
elucidate on these findings.
KW - Apoptosis
KW - Arsenic
KW - HHL-5 liver cells
KW - Liver injury
KW - Oxidative stress
KW - Thioredoxin
LA - eng
IS - 1559-0720 (Electronic)
PT - Journal Article
TA - Biol Trace Elem Res
YR - 2018
DATE- 20180114
CITO- NLM
CS - United States
FJT - Biological trace element research
EDAT- 20170517
STAT- In-Process
DOCNO- medline/28512695

87 - TOXLINE
TI - Improved biotransformation of arsenic by arsenite oxidase - Chitosan
nanoparticle conjugates.
AU - Pandey N
AD - Department of Biotechnology, Guru Ghasidas Vishwavidyalaya (A Central
University), Bilaspur, Chhattisgarh 495009, India.
AU - Bhatt R
AD - Department of Biotechnology, Guru Ghasidas Vishwavidyalaya (A Central
University), Bilaspur, Chhattisgarh 495009, India. Electronic address:
dr.renubhatt@yahoo.com.
SO - Int J Biol Macromol. 2018, Jan; 106:258-265. [International journal of
biological macromolecules]
AB - Recent developments in the potential use of nanoparticles as carriers of
enzyme have attracted great attention. In the present study, arsenite
oxidase (AOase) enzyme capable of transforming the more toxic arsenite
[As(III)] to the less toxic arsenate [As(V)] was extracted from an arsenic
resistant bacterium (Exiguobacterium sp. As-9) and partially purified.
Chitosan nanoparticles were prepared on the basis of ionic gelation of
chitosan with tripolyphosphate (TPP) anions. The purified AOase was
immobilized efficiently by physical adsorption on to chitosan
nanoparticles and were characterized for particle size, morphology, zeta
potential, AOase loading efficiency and in vitro transformation assay. The
chitosan nanoparticles were spherical in shape with the average diameter
of 100nm which increased to 294nm upon successful loading of AOase. Under
optimized conditions, the loading capacity of the chitosan nanoparticle
was determined to be 71% for AOase. Further, immobilization also increased
the stability of AOase at varying temperature (4-37&deg;C) and pH (5-10)
for a period of 30days with the increased enzymatic activity
(159.57Uml-1). It also facilitated increased biotransformation (89%) of
As(III) to As(V). A conceptual understanding of biological responses to
AOase loaded chitosan nanoparticles is needed for the development of novel
methods of drug delivery.
KW - Arsenic
KW - Arsenite oxidase
KW - Biotransformation
KW - Chitosan
KW - Nanoparticles
LA - eng
IS - 1879-0003 (Electronic)
PT - Journal Article
TA - Int J Biol Macromol
YR - 2018
DATE- 20171128
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - International journal of biological macromolecules
EDAT- 20170811
STAT- In-Process
DOCNO- medline/28803973

88 - TOXLINE
TI - Cellular and Molecular Effects of Prolonged Low-Level Sodium Arsenite
Exposure on Human Hepatic HepaRG Cells.
AU - Dreval K
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, Jefferson, Arkansas 72079.
AU - Tryndyak V
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, Jefferson, Arkansas 72079.
AU - Kindrat I
AD - Department of Biological and Medical Chemistry, Ivano-Frankivsk National
Medical University, Ivano-Frankivsk, Ukraine.
AU - Twaddle NC
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, Jefferson, Arkansas 72079.
AU - Orisakwe OE
AD - Department of Experimental Pharmacology and Toxicology, University of Port-
Harcourt, Rivers State, Nigeria.
AU - Mudalige TK
AD - Office of Regulatory Affairs, Arkansas Regional Laboratory, U.S. Food and
Drug Administration, Jefferson, Arkansas 72079.
AU - Beland FA
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, Jefferson, Arkansas 72079.
AU - Doerge DR
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, Jefferson, Arkansas 72079.
AU - Pogribny IP
AD - Division of Biochemical Toxicology, National Center for Toxicological
Research, Jefferson, Arkansas 72079.
SO - Toxicol Sci. 2018, Apr 01; 162(2):676-687. [Toxicological sciences : an
official journal of the Society of Toxicology]
AB - Inorganic arsenic is a human carcinogen associated with several types of
cancers, including liver cancer. Inorganic arsenic has been postulated to
target stem cells, causing their oncogenic transformation. This is
proposed to be one of the key events in arsenic-associated carcinogenesis;
however, the underlying mechanisms for this process remain largely
unknown. To address this question, human hepatic HepaRG cells, at
progenitor and differentiated states, were continuously treated with a
noncytotoxic concentration of 1 &mu;M sodium arsenite (NaAsO2). The HepaRG
cells demonstrated active intracellular arsenite metabolism that shared
important characteristic with primary human hepatocytes. Treatment of
proliferating progenitor-like HepaRG cells with NaAsO2 inhibited their
differentiation into mature hepatocyte-like cells, up-regulated genes
involved in cell growth, proliferation, and survival, and down-regulated
genes involved in cell death. In contrast, treatment of differentiated
hepatocyte-like HepaRG cells with NaAsO2 resulted in enhanced cell death
of mature hepatocyte-like cells, overexpression of cell death-related
genes, and down-regulation of genes in the cell proliferation pathway,
while biliary-like cells remained largely unaffected. Mechanistically, the
cytotoxic effect of arsenic on mature hepatocyte-like HepaRG cells may be
attributed to arsenic-induced dysregulation of cellular iron metabolism.
The inhibitory effect of NaAsO2 on the differentiation of progenitor
cells, the resistance of biliary-like cells to cell death, and the
enhanced cell death of functional hepatocyte-like cells resulted in
stem-cell activation. These effects favored the proliferation of liver
progenitor cells that can serve as a source of initiation and driving
force of arsenic-mediated liver carcinogenesis.
LA - eng
IS - 1096-0929 (Electronic)
PT - Journal Article
TA - Toxicol Sci
YR - 2018
DATE- 20180412
CITO- NLM
CS - United States
FJT - Toxicological sciences : an official journal of the Society of Toxicology
STAT- In-Data-Review
CM - Cites: Int J Cancer. 2015 Mar 1;136(5):E359-86 (medline /25220842)
CM - Cites: Cancer Epidemiol Biomarkers Prev. 2013 Nov;22(11):1944-53 (medline
/23800676)
CM - Cites: Food Chem Toxicol. 2018 Jan;111:482-493 (medline /29217265)
CM - Cites: IARC Monogr Eval Carcinog Risks Hum. 2004;84:1-477 (medline
/15645577)
CM - Cites: Biochim Biophys Acta. 2015 May;1853(5):1130-44 (medline /25661197)
CM - Cites: J Natl Cancer Inst. 2010 May 5;102(9):638-49 (medline /20339138)
CM - Cites: Chem Res Toxicol. 2013 Jan 18;26(1):96-105 (medline /23137061)
CM - Cites: Inorg Chem. 2005 Apr 18;44(8):2964-72 (medline /15819584)
CM - Cites: Environ Health Perspect. 2011 Jan;119(1):11-9 (medline /20682481)
CM - Cites: Crit Rev Toxicol. 2010 Nov;40(10):912-27 (medline /20812815)
CM -Cites: Toxicol Sci. 2011 Jan;119(1):73-83 (medline /20937726)
CM -Cites: Toxicol Sci. 2011 Mar;120 Suppl 1:S192-203 (medline /21071725)
CM -Cites: Arch Toxicol. 2014 Aug;88(8):1619-29 (medline /25005685)
CM -Cites: Nat Protoc. 2008;3(6):1101-8 (medline /18546601)
CM -Cites: Gastroenterology. 2004 Apr;126(4):1147-56 (medline /15057753)
CM -Cites: Exp Cell Res. 2013 Apr 1;319(6):875-87 (medline /23219847)
CM -Cites: Nat Rev Cancer. 2015 Nov;15(11):653-67 (medline /26493646)
CM -Cites: Acta Pharm Sin B. 2016 Sep;6(5):426-429 (medline /27709011)
CM -Cites: Exp Cell Res. 2013 Jan 15;319(2):126-32 (medline /22999864)
CM -Cites: IARC Monogr Eval Carcinog Risk Chem Hum. 1980;23:1-415 (medline
/6933135)
CM - Cites: Toxicol Appl Pharmacol. 2010 May 15;245(1):47-56 (medline
/20138079)
CM - Cites: Exp Biol Med (Maywood). 2016 Sep;241(15):1653-62 (medline
/27390263)
CM - Cites: Methods Mol Biol. 2009;563:379-98 (medline /19597796)
CM - Cites: Sci Rep. 2015 Oct 08;5:14993 (medline /26447599)
CM - Cites: Hepatology. 2011 Dec;54(6):2159-72 (medline /21809358)
CM - Cites: Chem Res Toxicol. 2006 Aug;19(8):1010-8 (medline /16918239)
CM - Cites: Toxicol Appl Pharmacol. 2004 Aug 1;198(3):366-76 (medline
/15276416)
CM - Cites: Cancer Epidemiol Biomarkers Prev. 2008 Aug;17(8):1982-7 (medline
/18708388)
CM - Cites: Crit Rev Clin Lab Sci. 2007;44(5-6):413-59 (medline /17943492)
CM - Cites: Nature. 2017 Jul 20;547(7663):350-354 (medline /28700576)
CM - Cites: Toxicol Appl Pharmacol. 2011 Feb 15;251(1):59-69 (medline
/21134390)
CM - Cites: IARC Monogr Eval Carcinog Risks Hum. 2012;100(Pt C):11-465 (medline
/23189751)
CM - Cites: Chem Res Toxicol. 2014 Nov 17;27(11):1979-89 (medline /25325836)
CM - Cites: Antioxid Redox Signal. 2002 Oct;4(5):749-58 (medline /12470502)
CM - Cites: Environ Health Perspect. 2013 Mar;121(3):295-302 (medline
/23458756)
CM - Cites: J Cell Biochem. 2013 Jul;114(7):1575-83 (medline /23334867)
CM - Cites: Environ Res. 2014 Nov;135:120-5 (medline /25262084)
CM - Cites: Toxicol Sci. 2011 Oct;123(2):305-32 (medline /21750349)
CM - Cites: Biofabrication. 2017 Jun 30;9(3):035001 (medline /28664876)
CM - Cites: Hepatology. 2007 Apr;45(4):957-67 (medline /17393521)
DOCNO- medline/29301061

89 - TOXLINE
TI - Arsenic speciation in food in Belgium. Part 2: Cereals and cereal
products.
AU - Ruttens A
AD - CODA-CERVA-VAR Veterinary and Agrochemical Research Centre, Leuvensesteenweg
17, B-3080 Tervuren, Belgium. Electronic address: ann.ruttens@coda-cerva.be.
AU - Cheyns K
AD - CODA-CERVA-VAR Veterinary and Agrochemical Research Centre, Leuvensesteenweg
17, B-3080 Tervuren, Belgium.
AU - Blanpain AC
AD - CODA-CERVA-VAR Veterinary and Agrochemical Research Centre, Leuvensesteenweg
17, B-3080 Tervuren, Belgium.
AU - De Temmerman L
AD - CODA-CERVA-VAR Veterinary and Agrochemical Research Centre, Leuvensesteenweg
17, B-3080 Tervuren, Belgium.
AU - Waegeneers N
AD - CODA-CERVA-VAR Veterinary and Agrochemical Research Centre, Leuvensesteenweg
17, B-3080 Tervuren, Belgium.
SO - Food Chem Toxicol. 2018, Apr 22; 118:32-41. [Food and chemical toxicology
: an international journal published for the British Industrial Biological
Research Association]
AB - This study reports results of total arsenic (Astot) and various As species
in 75 samples of cereals and cereal products bought on the Belgian market.
In addition to rice, the samples were wheat, pasta, bread and some
breakfast cereals. The inorganic species arsenite (AsIII) and arsenate
(AsV), and the organic As compounds dimethyl arsinate (DMA) and monomethyl
arsonate (MA) were the only As species detected. Mean Astot was
0.150&#8239;&plusmn;&#8239;0.089&#8239;mg&#8239;kg-1 in rice and
0.012&#8239;&plusmn;&#8239;0.008&#8239;mg kg- in the non-rice cereals. The
inorganic arsenic fraction (Asi&#8239;=&#8239;AsIII + AsV)
dominated in all samples and was in the range 55%-100%. Significantly
higher Astot and Asi concentrations were observed in white rice and brown
rice compared to Basmati rice. Within the group of non-rice cereals bread
and pasta showed significantly lower concentrations compared to wheat. All
30 rice samples were conform to the European maximum limits for Asi, laid
down in Commission Regulation (EU) 2015/1006. Although regulatory limits
certainly can help to protect consumer health, our results suggest that
the currently fixed European maximum levels are, in Belgium, not expected
to have any impact on the human exposure to Asi, which is a known
carcinogenic substance.
KW - Dietary exposure
KW - European maximum limit
KW - Inorganic arsenic
KW - Rice
KW - Rice products
KW - Wheat
LA - eng
IS - 1873-6351 (Electronic)
PT - Journal Article
TA - Food Chem Toxicol
YR - 2018
DATE- 20180619
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Food and chemical toxicology : an international journal published for the
British Industrial Biological Research Association
EDAT- 20180422
STAT- Publisher
DOCNO- medline/29689359

90 - TOXLINE
TI - Role of arsenic exposure in adipose tissue dysfunction and its possible
implication in diabetes pathophysiology.
AU - Renu K
AD - Department of Biomedical Sciences, School of Biosciences and Technology, VIT
University, Vellore, Tamil Nadu- 632014, India.
AU - Madhyastha H
AD - Department of Applied Physiology, Faculty of Medicine, University of
Miyazaki, Miyazaki 889 1692, Japan.
AU - Madhyastha R
AD - Department of Applied Physiology, Faculty of Medicine, University of
Miyazaki, Miyazaki 889 1692, Japan.
AU - Maruyama M
AD - Department of Applied Physiology, Faculty of Medicine, University of
Miyazaki, Miyazaki 889 1692, Japan.
AU - Arunachlam S
AD - Department of Biotechnology, Kalasalingam University, Krishnankoil-626126,
Tamil Nadu, India.
AU - V G A
AD - Department of Biomedical Sciences, School of Biosciences and Technology, VIT
University, Vellore, Tamil Nadu- 632014, India. Electronic address:
abilash.vg@vit.ac.in.
SO - Toxicol Lett. 2018, Mar 01; 284:86-95. [Toxicology letters]
AB - Exposure to arsenic in drinking water can stimulate a diverse number of
diseases that originate from impaired lipid metabolism in adipose and
glucose metabolism, leading to insulin resistance. Arsenic inhibits
differentiation of adipocyte and mediates insulin resistance with
diminutive information on arsenicosis on lipid storage and lipolysis. This
review focused on different mechanisms and pathways involved in
adipogenesis and lipolysis in adipose tissue during arsenic-induced
diabetes. Though arsenic is known to cause type2 diabetes through
different mechanisms, the role of adipose tissue in causing type2 diabetes
is still unclear. With the existing literature, this review exhibits the
effect of arsenic on adipose tissue and its signalling events such as
SIRT3- FOXO3a signalling pathway, Ras -MAP -AP-1 cascade, PI(3)-K-Akt
pathway, endoplasmic reticulum stress protein, C/EBP homologous protein
(CHOP10) and GPCR pathway with role of adipokines. There is a need to
elucidate the different types of adipokines which are involved in
arsenic-induced diabetes. The exhibited information brings to light that
arsenic has negative effects on a white adipose tissue (WAT) by decreasing
adipogenesis and enhancing lipolysis. Some of the epidemiological studies
show that arsenic would causes obesity. Few studies indicate that arsenic
might induces lipodystrophy condition. Further research is needed to
evaluate the mechanistic link between arsenic and adipose tissue
dysfunction which leads to insulin resistance.
KW - Adipogenesis
KW - Adipose tissue pathophysiology
KW - Arsenic
KW - Diabetes
KW - Lipolysis
LA - eng
IS - 1879-3169 (Electronic)
PT - Journal Article
PT - Review
TA - Toxicol Lett
YR - 2018
DATE- 20180207
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Toxicology letters
EDAT- 20171201
STAT- In-Process
DOCNO- medline/29198881

91 - TOXLINE
TI - Associations between urinary total arsenic levels, fetal development, and
neonatal birth outcomes: A cohort study in Taiwan.
AU - Liao KW
AD - Institute of Environmental and Occupational Health Sciences, School of
Medicine, National Yang Ming University, Taipei, Taiwan.
AU - Chang CH
AD - Institute of Environmental and Occupational Health Sciences, School of
Medicine, National Yang Ming University, Taipei, Taiwan.
AU - Tsai MS
AD - Department of Obstetrics and Gynecology, Cathay General Hospital, Taipei,
Taiwan; School of Medicine, Fu Jen Catholic University, Taipei, Taiwan; School of
Medicine, Taipei Medical University, Taipei, Taiwan.
AU - Chien LC
AD - School of Public Health, Taipei Medical University, Taipei, Taiwan.
AU - Chung MY
AD - Department of Life Sciences, Institute of Genome Sciences, National Yang Ming
University, Taipei, Taiwan.
AU - Mao IF
AD - Department of Occupational Safety and Health, Chung Shan Medical University,
Taichung, Taiwan.
AU - Tsai YA
AD - Institute of Environmental and Occupational Health Sciences, School of
Medicine, National Yang Ming University, Taipei, Taiwan.
AU - Chen ML
AD - Institute of Environmental and Occupational Health Sciences, School of
Medicine, National Yang Ming University, Taipei, Taiwan. Electronic address:
mlchen@ym.edu.tw.
SO - Sci Total Environ. 2018, Jan 15; 612:1373-1379. [The Science of the total
environment]
AB - BACKGROUND: Arsenic exposure is a global health concern. Several studies
have focused on chronic arsenic exposure in adults; however, limited data
are available regarding the potential adverse effects of prenatal exposure
on fetuses and neonates.
AB - OBJECTIVES: To assess which time point maternal arsenic exposure may
influence the fetus during pregnancy and birth outcomes.
AB - METHODS: In this study, total arsenic concentrations were analyzed in
urine samples collected from 130 women with singleton pregnancies
(22-45years old) in Taiwan from March to December of 2010. All fetal
biometric measurements in each trimester period and birth outcomes at
delivery were obtained. We applied a generalized estimating equation model
and multivariate regression models to evaluate the associations between
maternal urinary total arsenic (UtAs) exposure during pregnancy, fetal
biometric measurements, and neonatal birth outcomes.
AB - RESULTS: We observed statistically significant correlations between
maternal UtAs levels and the fetal biparietal diameter over all three
trimesters (&beta;=-1.046mm, p < 0.05). Multiple regression analyses
showed a negative association between maternal UtAs levels and chest
circumference in the first trimester (&beta;=-0.721cm, p < 0.05), and
second-trimester UtAs exposure was associated with decreases in birth
weight (&beta;=-173.26g, p < 0.01), head circumference (&beta;=-0.611cm,
p < 0.05), and chest circumference (&beta;=-0.654cm, p < 0.05).
Dose-response relationships were also observed for maternal UtAs exposure
and birth outcomes.
AB - CONCLUSIONS: We identified a negative relationship between maternal UtAs
levels during pregnancy, fetal development, and neonatal birth outcomes.
These findings should be confirmed in future studies with large sample
sizes.
KW - Birth outcomes
KW - Cohort study
KW - Fetal development
KW - Maternal exposure
KW - Urinary total arsenic
LA - eng
IS - 1879-1026 (Electronic)
PT - Journal Article
TA - Sci Total Environ
YR - 2018
DATE- 20180103
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - The Science of the total environment
EDAT- 20170925
STAT- In-Process
DOCNO- medline/28898944

92 - TOXLINE
TI - Associations of arsenic exposure with telomere length and na�ve T
cells in childhood- A birth cohort study.
AU - Mannan T
AD - Department of Immunology, Bangladesh University of Health Sciences, Dhaka-
1216, Bangladesh.
AU - Ahmed S
AD - Infectious Diseases Division, icddr,b, Dhaka-1212, Bangladesh.
AU - Akhtar E
AD - Infectious Diseases Division, icddr,b, Dhaka-1212, Bangladesh.
AU - Ahsan KB
AD - Infectious Diseases Division, icddr,b, Dhaka-1212, Bangladesh.
AU - Haq A
AD - Infectious Diseases Division, icddr,b, Dhaka-1212, Bangladesh.
AU - Kippler M
AD - Institute of Environmental Medicine, Karolinska Institutet, SE- 171 77
Stockholm, Sweden.
AU - Vahter M
AD - Institute of Environmental Medicine, Karolinska Institutet, SE- 171 77
Stockholm, Sweden.
AU - Raqib R
AD - Infectious Diseases Division, icddr,b, Dhaka-1212, Bangladesh.
SO - Toxicol Sci. 2018, May 10. [Toxicological sciences : an official journal
of the Society of Toxicology]
AB - There is limited knowledge of association between arsenic exposure and
telomere length (TL) and signal joint T-cell receptor excision circle
(sjTREC) that are potential biomarkers of immune senescence and disease
susceptibility. We aimed to clarify whether long-term inorganic arsenic
exposure influences TL and sjTRECs in childhood. Children born in a
longitudinal mother-child cohort were followed-up at 4.5 (n=275) and 9
years (n=351) of age. Arsenic exposure was assessed by metabolite
concentrations in urine (U-As) from mothers at gestational week 8
(prenatal) and their children at 4.5 and 9 years. TL and sjTRECs were
determined in blood cells using quantitative PCR. The oxidative DNA damage
marker 8-hydroxy-2'-deoxyguanosine (8-OHdG) in plasma was measured by
ELISA. In multivariable-adjusted spline regression analyses, both prenatal
and childhood arsenic exposure above U-As of 45&micro;g/L were
significantly inversely associated with TL and sjTRECs at 9years. Fraction
of monomethylarsonic acid (MMA) above spline knot 7% were significantly
inversely associated with both TL and sjTRECs reflecting increased
toxicity due to less-efficient arsenic metabolism in 9 years old children.
Prenatal and childhood arsenic exposure were positively associated with
8-OHdG at 9 years which in turn was inversely associated with sjTRECs at 9
years. However, adjustment with 8-OHdG did not change the estimates of the
association of U-As with sjTRECs reflecting little contribution from
8-OHdG-induced oxidative stress. Our findings suggest that chronic arsenic
exposure from early life can result in TL attrition and lower production
of na�ve T cells potentially leading to immunosenescence and
immunodeficiency.
LA - eng
IS - 1096-0929 (Electronic)
PT - Journal Article
TA - Toxicol Sci
YR - 2018
DATE- 20180514
CITO- NLM
CS - United States
FJT - Toxicological sciences : an official journal of the Society of Toxicology
EDAT- 20180510
STAT- Publisher
DOCNO- medline/29757418

93 - TOXLINE
TI - Estimating the risk of bladder and kidney cancer from exposure to
low-levels of arsenic in drinking water, Nova Scotia, Canada.
AU - Saint-Jacques N
AD - Nova Scotia Cancer Care Program, Nova Scotia Health Authority, 1276 South
Park Street, Room 560 Bethune Building, Halifax B3H 2Y9, Nova Scotia, Canada.
Electronic address: nathalie.st-jacques@nshealth.ca.
AU - Brown P
AD - Centre for Global Health Research, St. Michael's Hospital, 30 Bond Street,
Toronto M5B 1W8, Ontario, Canada. Electronic address: patrick.brown@utoronto.ca.
AU - Nauta L
AD - Population Cancer Research Program, Dalhousie University, 1494 Carlton
Street, PO Box 15000, Halifax B3H 4R2, Nova Scotia, Canada. Electronic address:
lnauta@dal.ca.
AU - Boxall J
AD - GIS Centre Killam Library, Dalhousie University, 6225 University Avenue,
Halifax B3H 4R2, Nova Scotia, Canada. Electronic address: james.boxall@dal.ca.
AU - Parker L
AD - Department of Pediatrics and Population Cancer Research Program, Dalhousie
University, 1494 Carlton Street, PO Box 15000, Halifax B3H 4R2, Nova Scotia,
Canada. Electronic address: louise.parker@dal.ca.
AU - Dummer TJB
AD - The University of British Columbia, Centre for Excellence in Cancer
Prevention, School of Population and Public Health, 2206 East Mall, Vancouver V6T
1Z3, British Columbia, Canada. Electronic address: trevor.dummer@ubc.ca.
SO - Environ Int. 2018, 01; 110:95-104. [Environment international]
AB - Arsenic in drinking water impacts health. Highest levels of arsenic have
been historically observed in Taiwan and Bangladesh but the contaminant
has been affecting the health of people globally. Strong associations have
been confirmed between exposure to high-levels of arsenic in drinking
water and a wide range of diseases, including cancer. However, at lower
levels of exposure, especially near the current World Health Organization
regulatory limit (10&mu;g/L), this association is inconsistent as the
effects are mostly extrapolated from high exposure studies. This
ecological study used Bayesian inference to model the relative risk of
bladder and kidney cancer at these lower concentrations-0-2&mu;g/L;
2-5&mu;g/L and; &ge;5&mu;g/L of arsenic-in 864 bladder and 525 kidney
cancers diagnosed in the study area, Nova Scotia, Canada between 1998 and
2010. The model included proxy measures of lifestyle (e.g. smoking) and
accounted for spatial dependencies. Overall, bladder cancer risk was 16%
(2-5&mu;g/L) and 18% (&ge;5&mu;g/L) greater than that of the referent
group ( < 2&mu;g/L), with posterior probabilities of 88% and 93% for
these risks being above 1. Effect sizes for kidney cancer were 5%
(2-5&mu;g/L) and 14% (&ge;5&mu;g/L) above that of the referent group
( < 2&mu;g/L), with probabilities of 61% and 84%. High-risk areas were
common in southwestern areas, where higher arsenic-levels are associated
with the local geology. The study suggests an increased bladder cancer,
and potentially kidney cancer, risk from exposure to drinking water
arsenic-levels within the current the World Health Organization maximum
acceptable concentration.
KW - *Arsenic
KW - *BYM model
KW - *Bladder and kidney cancer
KW - *Drinking water
KW - *Geostatistical analysis
KW - *Small-area disease mapping
RN - N712M78A8G
LA - eng
IS - 1873-6750 (Electronic)
PT - Journal Article
PT - Research Support, Non-U.S. Gov't
TA - Environ Int
YR - 2018
DATE- 20180420
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Environment international
EDAT- 20171031
STAT- MEDLINE
DOCNO- medline/29089168

94 - TOXLINE
TI - NF-&kappa;B-regulated miR-155, via repression of QKI, contributes to the
acquisition of CSC-like phenotype during the neoplastic transformation of
hepatic cells induced by arsenite.
AU - Chen C
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu, People's Republic of
China.
AU - Luo F
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu, People's Republic of
China.
AU - Yang Q
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu, People's Republic of
China.
AU - Wang D
AD - The Key Laboratory of Environmental Pollution Monitoring and Disease Control,
Ministry of Education, School of Public Health, Guizhou Medical University,
Guiyang, Guizhou, People's Republic of China.
AU - Yang P
AD - The School of Public Health, Institute for Chemical Carcinogenesis, Guangzhou
Medical University, Guangzhou, Guangdong, People's Republic China.
AU - Xue J
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu, People's Republic of
China.
AU - Dai X
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu, People's Republic of
China.
AU - Liu X
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu, People's Republic of
China.
AU - Xu H
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu, People's Republic of
China.
AU - Lu J
AD - The School of Public Health, Institute for Chemical Carcinogenesis, Guangzhou
Medical University, Guangzhou, Guangdong, People's Republic China.
AU - Zhang A
AD - The Key Laboratory of Environmental Pollution Monitoring and Disease Control,
Ministry of Education, School of Public Health, Guizhou Medical University,
Guiyang, Guizhou, People's Republic of China.
AU - Liu Q
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu, People's Republic of
China.
SO - Mol Carcinog. 2018, Apr; 57(4):483-493. [Molecular carcinogenesis]
AB - Chronic exposure to arsenite can cause various human tumors. For the
initiation and recurrence of human liver cancer, the acquisition of
CSC-like properties is essential. In various cancers, microRNAs (miRNAs)
act as regulators in induction of CSC-like properties. Liver cancers
over-express miR-155, but the mechanism relating miR-155 and
arsenite-induced liver cancer is unknown. Here, we show that long-term
exposure of L-02 cells to arsenite increases miR-155 levels by activation
of NF-&kappa;B and leads to the acquisition of CSC-like properties. In
spheroids formed from arsenite-transformed L-02 cells, the levels of
miR-155 positively relate to the levels of CD90, EpCAM, and OCT4.
Inhibition of miR-155, by reduction of SOX2 and OCT4, results in
suppression of spheroid formation. Luciferase reporter assays indicate
that QKI is a target of miR-155. Inhibition of QKI expression by miR-155
promotes arsenite-induced acquisition of CSC-like properties, whereas QKI
over-expression has the opposite effect. Collectively, the findings
demonstrate that miR-155, driven by NF-&kappa;B, reduces QKI expression
and is involved in acquisition of the CSC-like phenotype during neoplastic
transformation of hepatic cells induced by arsenite.
KW - NF-κB
KW - QKI
KW - arsenite
KW - cancer stem cells (CSCs)
KW - miR-155
LA - eng
IS - 1098-2744 (Electronic)
PT - Journal Article
TA - Mol Carcinog
YR - 2018
DATE- 20180301
CI - &copy; 2017 Wiley Periodicals, Inc.
CITO- NLM
CS - United States
FJT - Molecular carcinogenesis
EDAT- 20171229
STAT- In-Data-Review
DOCNO- medline/29240254

95 - TOXLINE
TI - PI3K/Akt/GSK3&beta; induced CREB activation ameliorates arsenic mediated
alterations in NMDA receptors and associated signaling in rat hippocampus:
Neuroprotective role of curcumin.
AU - Srivastava P
AD - Developmental Toxicology and NeuroToxicology Laboratory, Systems Toxicology
and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research
(CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow, 226 001, UP,
India; School of Pharmacy, Babu Banarsi Das University, Faizabad Road, Lucknow, 226
028, UP, India.
AU - Dhuriya YK
AD - Developmental Toxicology and NeuroToxicology Laboratory, Systems Toxicology
and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research
(CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow, 226 001, UP,
India.
AU - Kumar V
AD - Human Genome and Stem-Cell Research Center, Institute of Biosciences,
University of S�o Paulo, Brazil.
AU - Srivastava A
AD - Developmental Toxicology and NeuroToxicology Laboratory, Systems Toxicology
and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research
(CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow, 226 001, UP,
India.
AU - Gupta R
AD - Developmental Toxicology and NeuroToxicology Laboratory, Systems Toxicology
and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research
(CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow, 226 001, UP,
India; School of Pharmacy, Babu Banarsi Das University, Faizabad Road, Lucknow, 226
028, UP, India.
AU - Shukla RK
AD - Developmental Toxicology and NeuroToxicology Laboratory, Systems Toxicology
and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research
(CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow, 226 001, UP,
India.
AU - Yadav RS
AD - Department of Criminology and Forensic Science, Dr. Harisingh Gour Central
University, Sagar, 470003, MP, India.
AU - Dwivedi HN
AD - School of Pharmacy, Babu Banarsi Das University, Faizabad Road, Lucknow, 226
028, UP, India.
AU - Pant AB
AD - Developmental Toxicology and NeuroToxicology Laboratory, Systems Toxicology
and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research
(CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow, 226 001, UP,
India. Electronic address: abpant@iitr.res.in.
AU - Khanna VK
AD - Developmental Toxicology and NeuroToxicology Laboratory, Systems Toxicology
and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research
(CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow, 226 001, UP,
India. Electronic address: vkkhanna1@iitr.res.in.
SO - Neurotoxicology. 2018, Apr 30; 67:190-205. [Neurotoxicology]
AB - Protective efficacy of curcumin in arsenic induced NMDA receptor
dysfunctions and PI3K/Akt/ GSK3&beta; signalling in hippocampus has been
investigated in vivo and in vitro. Exposure to sodium arsenite (in vivo -
20&#8239;mg/kg, body weight p.o. for 28 days; in vitro - 10&#8239;&mu;M
for 24&#8239;h) and curcumin (in vivo - 100&#8239;mg/kg body weight p.o.
for 28 days; in vitro - 20&#8239;&mu;M for 24&#8239;h) was carried out
alone or simultaneously. Treatment with curcumin ameliorated sodium
arsenite induced alterations in the levels of NMDA receptors, its receptor
subunits and synaptic proteins - pCaMKII&alpha;, PSD-95 and SynGAP both in
vivo and in vitro. Decreased levels of BDNF, pAkt, pERK1/2, pGSK3&beta;
and pCREB on sodium arsenite exposure were also protected by curcumin.
Curcumin was found to decrease sodium arsenite induced changes in
hippocampus by modulating PI3K/Akt/GSK3&beta; neuronal survival pathway,
known to regulate various cellular events. Treatment of hippocampal
cultures with pharmacological inhibitors for ERK1/2, GSK3&beta; and Akt
individually inhibited levels of CREB and proteins associated with
PI3K/Akt/GSK3&beta; pathway. Simultaneous treatment with curcumin was
found to improve sodium arsenite induced learning and memory deficits in
rats assessed by water maze and Y-maze. The results provide evidence that
curcumin exercises its neuroprotective effect involving PI3K/Akt pathway
which may affect NMDA receptors and downstream signalling through
TrK&beta; and BDNF in arsenic induced cognitive deficits in hippocampus.
KW - Curcumin
KW - Hippocampus
KW - Learning and memory
KW - NMDA receptors
KW - PI3K/Akt/GSK3β signalling
KW - Sodium arsenite
LA - eng
IS - 1872-9711 (Electronic)
PT - Journal Article
TA - Neurotoxicology
YR - 2018
DATE- 20180616
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Neurotoxicology
EDAT- 20180430
STAT- Publisher
DOCNO- medline/29723552

96 - TOXLINE
TI - Rethinking anaerobic As(III) oxidation in filters: Effect of indigenous
nitrate respirers.
AU - Cui J
AD - State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing,
100085, PR China.
AU - Du J
AD - State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing,
100085, PR China; University of Chinese Academy of Sciences, Beijing, 100049,
China.
AU - Tian H
AD - State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing,
100085, PR China.
AU - Chan T
AD - National Synchrotron Radiation Research Center, HsinChu, 300, Taiwan, ROC.
Electronic address: chan.ts@nsrrc.org.tw.
AU - Jing C
AD - State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research
Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing,
100085, PR China; University of Chinese Academy of Sciences, Beijing, 100049,
China. Electronic address: cyjing@rcees.ac.cn.
SO - Chemosphere. 2018, Apr; 196:223-230. [Chemosphere]
AB - Microorganisms play a key role in the redox transformation of arsenic (As)
in aquifers. In this study, the impact of indigenous bacteria, especially
the prevailing nitrate respirers, on arsenite (As(III)) oxidation was
explored during groundwater filtration using granular TiO2 and subsequent
spent TiO2 anaerobic landfill. X-ray absorption near edge structure
spectroscopy analysis showed As(III) oxidation (46% in 10 days) in the
presence of nitrate in the simulated anaerobic landfills. Meanwhile, iron
(Fe) species on the spent TiO2 were dominated by amorphous ferric
arsenate, ferrihydrite and goethite. The Fe phase showed no change during
the anaerobic landfill incubation. Batch incubation experiments implied
that the indigenous bacteria completely oxidized As(III) to arsenate
(As(V)) in 10 days using nitrate as the terminal electron acceptor under
anaerobic conditions. The bacterial community analysis indicated that
various kinds of microbial species exist in groundwater matrix.
Phylogenetic tree analysis revealed that Proteobacteria was the dominant
phylum, with Hydrogenophaga (34%), Limnohabitans (16%), and Simplicispira
(7%) as the major bacterial genera. The nitrate respirers especially from
the Hydrogenophaga genus anaerobically oxidized As(III) using nitrate as
an electron acceptor instead of oxygen. Our study implied that microbes
can facilitate the groundwater As oxidation using nitrate on the
adsorptive media.
KW - Anaerobic As(III) oxidation
KW - Bacterial diversity
KW - Groundwater filtration
KW - Landfill incubation
KW - Nitrate respirers
RN - 1310-14-1
RN - 87PZU03K0K
RN - E1UOL152H7
RN - N5509X556J
RN - N712M78A8G
RN - N7CIZ75ZPN
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180517
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171227
STAT- MEDLINE
DOCNO- medline/29304460

97 - TOXLINE
TI - Organic Arsenicals as Functional Motifs in Polymer and Biomaterials
Science.
AU - Tanaka J
AD - Department of Chemistry, University of Warwick, Coventry, CV4 7AL, UK.
AU - Davis TP
AD - ARC Centre of Excellence in Convergent Bio-Nano Science and Technology,
Monash Institute of Pharmaceutical Sciences, Monash University (Parkville Campus),
399 Royal Parade, Parkville, Victoria, 3152, Australia.
AU - Wilson P
AD - ARC Centre of Excellence in Convergent Bio-Nano Science and Technology,
Monash Institute of Pharmaceutical Sciences, Monash University (Parkville Campus),
399 Royal Parade, Parkville, Victoria, 3152, Australia.
SO - Macromol Rapid Commun. 2018, May 28:e1800205. [Macromolecular rapid
communications]
AB - Arsenic (As) exhibits diverse (bio)chemical reactivity and biological
activity depending upon its oxidation state. However, this distinctive
reactivity has been largely overlooked across many fields owing to
concerns regarding the toxicity of arsenic. Recently, a clinical
renaissance in the use of arsenicals, including organic arsenicals that
are known to be less toxic than inorganic arsenicals, alludes to the
possibility of broader acceptance and application in the field of polymer
and biomaterials science. Here, current examples of
polymeric/macromolecular arsenicals are reported to stimulate interest and
highlight their potential as a novel platform for functional, responsive,
and bioactive materials.
KW - biomaterials
KW - drug delivery systems
KW - imaging
KW - nanoparticles
KW - polymerization
LA - eng
IS - 1521-3927 (Electronic)
PT - Journal Article
PT - Review
TA - Macromol Rapid Commun
YR - 2018
DATE- 20180528
CI - &copy; 2018 WILEY-VCH Verlag GmbH &amp; Co. KGaA, Weinheim.
CITO- NLM
CS - Germany
FJT - Macromolecular rapid communications
EDAT- 20180528
STAT- Publisher
DOCNO- medline/29806240

98 - TOXLINE
TI - Carcinogenic and non-carcinogenic risk assessments of arsenic
contamination in drinking water of Ardabil city in the Northwest of Iran.
AU - Sadeghi F
AD - a Center for Water Quality Research (CWQR) , Institute for Environmental
Research (IER), Tehran University of Medical Sciences , Tehran , Iran.
AU - Nasseri S
AD - b Department of Environmental Health Engineering , School of Public Health,
Tehran University of Medical Sciences , Tehran , Iran.
AU - Yunesian M
AD - c Center for Air Pollution Research (CAPR) , Institute for Environmental
Research (IER), Tehran University of Medical Sciences , Tehran , Iran.
AU - Nabizadeh R
AD - c Center for Air Pollution Research (CAPR) , Institute for Environmental
Research (IER), Tehran University of Medical Sciences , Tehran , Iran.
AU - Mosaferi M
AD - d Tabriz Health Services Management Research Center , Tabriz University of
Medical Sciences , Tabriz , Iran.
AU - Mesdaghinia A
AD - b Department of Environmental Health Engineering , School of Public Health,
Tehran University of Medical Sciences , Tehran , Iran.
SO - J Environ Sci Health A Tox Hazard Subst Environ Eng. 2018, Apr 16;
53(5):421-429. [Journal of environmental science and health. Part A,
Toxic/hazardous substances & environmental engineering]
AB - Based on the environmental health assessment framework of the United State
Environmental Protection Agency, a quantitative health risk assessment of
arsenic in contaminated drinking water in a city in the northwest of Iran
has been carried out. In the exposure assessment step, arsenic
concentrations in drinking water were determined during four seasons. In
addition, the water ingestion rate for different age groups in this region
was determined. The concentration of arsenic in 163 collected samples from
different locations during four seasons ranged from 0 to 99 &mu;g
L-1. Furthermore, a high percentage of the samples manifested higher
levels than the permissible limit of 10 &mu;g L-1. The total daily
water intake rates of four age groups 1 to < 2 (group 1), 2 to < 6
(group 2), 6 to < 16 (group 3), and &ge;16 years (group 4) were
estimated as 0.86, 1.49, 2.00, and 2.33 L day-1, respectively.
Calculating the lifetime average daily dose of arsenic indicated that
adults (group 4) had the highest and children (group 1) had the lowest
daily intake of arsenic in their entire life. The results of risk
characteristic showed that the order of excess lifetime cancer risk via
arsenic exposure in the four groups was 4 > 3 > 2 > 1. The
estimated risks for all age groups were higher than the acceptable range
(1E-6 to 1E-4). The hazard quotient values for all of the classified
groups were lower than the recommended limit values ( < 1), but it cannot
be concluded that potential non-carcinogenicity risks are non-existent
since the possible exposure to arsenic via food and skin may also pose the
risk.
KW - Arsenic
KW - carcinogenic risk assessment
KW - drinking water
KW - non-carcinogenic risk assessment
RN - N712M78A8G
LA - eng
IS - 1532-4117 (Electronic)
PT - Journal Article
TA - J Environ Sci Health A Tox Hazard Subst Environ Eng
YR - 2018
DATE- 20180525
CITO- NLM
CS - England
CSET- IM
FJT - Journal of environmental science and health. Part A, Toxic/hazardous
substances &amp; environmental engineering
EDAT- 20171226
STAT- MEDLINE
DOCNO- medline/29278989

99 - TOXLINE
TI - Arsenic accumulation in rice (Oryza sativa L.) is influenced by
environment and genetic factors.
AU - Kumarathilaka P
AD - School of Civil Engineering and Surveying, Faculty of Health, Engineering and
Sciences, University of Southern Queensland, West Street, Toowoomba, Queensland
4350, Australia.
AU - Seneweera S
AD - Center for Crop Health, Faculty of Health, Engineering and Sciences,
University of Southern Queensland, West Street, Toowoomba, Queensland 4350,
Australia.
AU - Meharg A
AD - Queen's University Belfast, Institute for Global Food Security, David Keir
Building, Malone Road, Belfast BT9 5BN, United Kingdom.
AU - Bundschuh J
AD - School of Civil Engineering and Surveying, Faculty of Health, Engineering and
Sciences, University of Southern Queensland, West Street, Toowoomba, Queensland
4350, Australia; UNESCO Chair on Groundwater Arsenic within the 2030 Agenda for
Sustainable Development University of Southern Queensland, West Street, Toowoomba,
Queensland 4350, Australia. Electronic address: jochen.bundschuh@usq.edu.au.
SO - Sci Total Environ. 2018, Jun 13; 642:485-496. [The Science of the total
environment]
AB - Arsenic (As) elevation in paddy soils will have a negative impact on both
the yield and grain quality of rice (Oryza sativa L.). The mechanistic
understanding of As uptake, translocation, and grain filling is an
important aspect to produce rice grains with low As concentrations through
agronomical, physico-chemical, and breeding approaches. A range of factors
(i.e. physico-chemical, biological, and environmental) govern the
speciation and mobility of As in paddy soil-water systems. Major As uptake
transporters in rice roots, such as phosphate and aquaglyceroporins,
assimilate both inorganic (As(III) and As(V)) and organic As (DMA(V) and
MMA(V)) species from the rice rhizosphere. A number of metabolic pathways
(i.e. As (V) reduction, As(III) efflux, and As(III)-thiol complexation and
subsequent sequestration) are likely to play a key role in determining the
translocation and substantial accumulation of As species in rice tissues.
The order of translocation efficiency (caryopsis-to-root) for different As
species in rice plants is comprehensively evaluated as follows:
DMA(V)&#8239; > &#8239;MMA(V)&#8239; > &#8239;inorganic As species. The
loading patterns of both inorganic and organic As species into the rice
grains are largely dependent on the genetic makeup and maturity stage of
the rice plants together with environmental interactions. The knowledge of
As metabolism in rice plants and how it is affected by plant genetics and
environmental factors would pave the way to develop adaptive strategies to
minimize the accumulation of As in rice grains.
KW - Arsenic metabolism
KW - Arsenic speciation
KW - Arsenic toxicity
KW - Arsenic transporters
KW - Detoxification
KW - Grain filling
LA - eng
IS - 1879-1026 (Electronic)
PT - Journal Article
PT - Review
TA - Sci Total Environ
YR - 2018
DATE- 20180619
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - The Science of the total environment
EDAT- 20180613
STAT- Publisher
DOCNO- medline/29908507

100 - TOXLINE
TI - Protective Effect of Curcumin by Modulating BDNF/DARPP32/CREB in
Arsenic-Induced Alterations in Dopaminergic Signaling in Rat Corpus
Striatum.
AU - Srivastava P
AD - School of Pharmacy, Babu Banarasi Das University, BBD City, Faizabad Road,
Lucknow, 227 015, India.
AU - Dhuriya YK
AD - Developmental Toxicology Laboratory, Systems Toxicology and Health Risk
Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR),
Vishvigyan Bhawan; 31, Mahatma Gandhi Marg, Lucknow, Uttar Pradesh, 226 001, India.
AU - Gupta R
AD - School of Pharmacy, Babu Banarasi Das University, BBD City, Faizabad Road,
Lucknow, 227 015, India.
AU - Shukla RK
AD - Developmental Toxicology Laboratory, Systems Toxicology and Health Risk
Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR),
Vishvigyan Bhawan; 31, Mahatma Gandhi Marg, Lucknow, Uttar Pradesh, 226 001, India.
AU - Yadav RS
AD - Department of Criminology and Forensic Science, School of Applied Sciences,
Dr. Harisingh Gour Central University, Sagar, Madhya Pradesh, 470 003, India.
AU - Dwivedi HN
AD - School of Pharmacy, Babu Banarasi Das University, BBD City, Faizabad Road,
Lucknow, 227 015, India.
AU - Pant AB
AD - Developmental Toxicology Laboratory, Systems Toxicology and Health Risk
Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR),
Vishvigyan Bhawan; 31, Mahatma Gandhi Marg, Lucknow, Uttar Pradesh, 226 001, India.
AU - Khanna VK
AD - Developmental Toxicology Laboratory, Systems Toxicology and Health Risk
Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR),
Vishvigyan Bhawan; 31, Mahatma Gandhi Marg, Lucknow, Uttar Pradesh, 226 001, India.
vkkhanna1@iitr.res.in.
SO - Mol Neurobiol. 2018, Jan; 55(1):445-461. [Molecular neurobiology]
AB - Earlier, protective role of curcumin in arsenic-induced dopamine (DA)-D2
receptor dysfunctions in corpus striatum has been demonstrated by us. In
continuation to that, the present study is focused to decipher the
molecular mechanisms associated with alterations in dopaminergic signaling
on arsenic exposure in corpus striatum and assess the protective efficacy
of curcumin. Exposure to arsenic (20 mg/kg, body weight p.o. for
28 days) in rats resulted to decrease the expression of presynaptic
proteins-tyrosine hydroxylase and VMAT2 while no effect was observed on
the expression of DAT in comparison to controls. A significant decrease in
the expression of DA-D2 receptors associated with alterations in the
expression of PKA, pDARPP32 (Thr 34), and PP1 &alpha; was clearly evident
on arsenic exposure. Expression of BDNF and pGSK3&beta; in corpus striatum
was found decreased in arsenic-exposed rats. Simultaneous treatment with
curcumin (100 mg/kg, body weight p.o. for 28 days) resulted to
protect arsenic-induced alterations in the expression of DA-D2 receptors,
PKA, pDARPP32, pCREB, and pPP1&alpha;. Neuroprotective efficacy of
curcumin can possibly be attributed to its antioxidant potential which
significantly protected arsenic-induced mitochondrial dysfunctions by
modulating the ROS generation and apoptosis. Modulation in the expression
of BDNF and pGSK3&beta; in corpus striatum by curcumin exhibits the
importance of neuronal survival pathway in arsenic-induced dopaminergic
dysfunctions. Interestingly, curcumin was also found to protect
arsenic-induced ultrastructural changes in corpus striatum. The results
exhibit that curcumin modulates BDNF/DARPP32/CREB in arsenic-induced
alterations in dopaminergic signaling in rat corpus striatum.
KW - Arsenic
KW - BDNF
KW - CREB
KW - Corpus striatum
KW - Curcumin
KW - DARPP32
KW - Dopamine
LA - eng
IS - 1559-1182 (Electronic)
PT - Journal Article
TA - Mol Neurobiol
YR - 2018
DATE- 20180219
CITO- NLM
CS - United States
FJT - Molecular neurobiology
EDAT- 20161213
STAT- In-Data-Review
CM - Cites: Neurotoxicol Teratol. 2010 Nov-Dec;32(6):640-7 (medline /20699118)
CM - Cites: Environ Int. 2007 Aug;33(6):805-11 (medline /17481731)
CM - Cites: Nature. 2001 Mar 15;410(6826):376-80 (medline /11268215)
CM - Cites: Free Radic Res. 2008 Jun;42(6):574-81 (medline /18569015)
CM - Cites: Food Chem Toxicol. 1997 Oct-Nov;35(10-11):1107-30 (medline
/9463546)
CM - Cites: Methods Enzymol. 1978;53:3-4 (medline /713841)
CM - Cites: Biochem Pharmacol. 2008 Sep 1;76(5):569-81 (medline /18555207)
CM - Cites: J Agric Food Chem. 2007 Feb 7;55(3):1039-44 (medline /17263510)
CM - Cites: Phytother Res. 2016 Feb;30(2):175-83 (medline /26610378)
CM - Cites: Toxicol Appl Pharmacol. 2009 Sep 1;239(2):169-77 (medline
/19121333)
CM - Cites: J Neurosci. 2004 Apr 28;24(17):4250-8 (medline /15115821)
CM - Cites: J Expo Sci Environ Epidemiol. 2016 Sep;26(5):464-70 (medline
/27072426)
CM - Cites: Toxicol Lett. 2002 Jul 7;133(1):1-16 (medline /12076506)
CM - Cites: Altern Ther Health Med. 2014 Winter;20 Suppl 1:18-25 (medline
/24473982)
CM - Cites: Curr Environ Health Rep. 2016 Mar;3(1):1-12 (medline /26875182)
CM - Cites: Toxicol Lett. 1990 Dec;54(2-3):345-53 (medline /2260129)
CM - Cites: Toxicol Lett. 2000 Sep 30;117(1-2):61-7 (medline /11033234)
CM - Cites: Toxicol Appl Pharmacol. 2014 Sep 15;279(3):428-40 (medline
/24952339)
CM - Cites: Environ Health Perspect. 2007 Sep;115(9):1371-5 (medline /17805430)
CM - Cites: Int J Dev Neurosci. 2014 May;34:60-75 (medline /24517892)
CM - Cites: J Biomed Sci. 2010 May 31;17:43 (medline /20513244)
CM - Cites: Toxicol Appl Pharmacol. 2011 Nov 1;256(3):241-8 (medline /21513725)
CM - Cites: Transl Neurodegener. 2012 Aug 20;1(1):16 (medline /23210631)
CM - Cites: Neurosci Lett. 1993 Oct 29;161(2):223-6 (medline /7903803)
CM - Cites: J Neurochem. 2011 Jan;116(1):1-9 (medline /21044077)
CM - Cites: Eur Rev Med Pharmacol Sci. 2013 May;17 (10 ):1360-8 (medline
/23740450)
CM - Cites: PLoS One. 2015 Sep 14;10 (9):e0137810 (medline /26368803)
CM - Cites: Indian J Pharm Sci. 2010 Mar;72(2):149-54 (medline /20838516)
CM - Cites: Rejuvenation Res. 2010 Feb;13(1):55-64 (medline /20230279)
CM - Cites: Toxicology. 2015 Feb 3;328:75-81 (medline /25496994)
CM - Cites: Biol Trace Elem Res. 2014 Dec;162(1-3):175-80 (medline /25319007)
CM - Cites: Toxicol Appl Pharmacol. 2009 Nov 1;240(3):367-76 (medline
/19631675)
CM - Cites: Br J Nutr. 2010 Jun;103(11):1545-57 (medline /20100380)
CM - Cites: Pharmacol Rev. 2011 Mar;63(1):182-217 (medline /21303898)
CM - Cites: Neuron. 1999 Jul;23(3):435-47 (medline /10433257)
CM - Cites: J Clin Psychopharmacol. 2015 Aug;35(4):406-10 (medline /26066335)
CM - Cites: Neurotoxicology. 2011 Dec;32(6):760-8 (medline /21839772)
CM - Cites: Food Chem Toxicol. 2013 Sep;59:739-47 (medline /23871787)
CM - Cites: PLoS One. 2012;7(3):e33057 (medline /22427945)
CM - Cites: Biochim Biophys Acta. 2012 Aug;1822(8):1207-15 (medline /22561904)
CM - Cites: Brain Res. 2009 Jul 28;1282:133-41 (medline /19445907)
CM - Cites: Front Cell Neurosci. 2014 Aug 28;8:254 (medline /25221473)
CM - Cites: Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1856-60 (medline
/10677546)
CM - Cites: Toxicology. 2014 Sep 2;323:78-94 (medline /24953689)
CM - Cites: Environ Sci Technol. 2003 Jan 15;37(2):229-34 (medline /12564892)
CM - Cites: Br J Nutr. 2016 Feb 14;115(3):449-65 (medline /26652155)
CM - Cites: Prog Neuropsychopharmacol Biol Psychiatry. 2010 Feb 1;34(1):147-53
(medline /19879308)
CM - Cites: Arch Toxicol. 2010 Jul;84(7):521-40 (medline /20224926)
CM -Cites: Appl Physiol Nutr Metab. 2014 Feb;39(2):211-8 (medline /24476477)
CM -Cites: Brain Res Bull. 2001 May 15;55(2):301-8 (medline /11470331)
CM -Cites: Neurotoxicology. 2010 Sep;31(5):533-9 (medline /20466022)
CM -Cites: PLoS One. 2013;8(3):e59843 (medline /23555802)
CM -Cites: Pharmacol Biochem Behav. 2016 Nov - Dec;150-151:39-47 (medline
/27619637)
CM - Cites: Toxicology. 2013 Aug 9;310:73-83 (medline /23702354)
CM - Cites: Curr Environ Health Rep. 2014 Mar 21;1:132-147 (medline /24860722)
CM - Cites: Sci Total Environ. 2000 Apr 17;249(1-3):297-312 (medline /10813460)
CM - Cites: Trends Mol Med. 2007 Aug;13(8):353-61 (medline /17644431)
CM - Cites: Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2012 Feb;30(2):85-8
(medline /22801079)
CM - Cites: Mol Neurodegener. 2012 Apr 04;7:12 (medline /22475209)
CM - Cites: Eur Neuropsychopharmacol. 2015 Jan;25(1):38-50 (medline /25523883)
CM - Cites: Free Radic Res. 2005 Oct;39(10):1119-25 (medline /16298737)
CM - Cites: Transl Neurodegener. 2012 Jan 13;1(1):3 (medline /23210978)
CM - Cites: Neurotoxicology. 2014 Dec;45:159-67 (medline /25451969)
CM - Cites: Curr Opin Pharmacol. 2009 Feb;9(1):53-8 (medline /19138563)
CM - Cites: Biochem Pharmacol. 1966 Jul;15(7):977-87 (medline /5967909)
CM - Cites: Environ Health Perspect. 2013 Mar;121(3):295-302 (medline
/23458756)
CM - Cites: Neurosci Bull. 2012 Jun;28(3):253-8 (medline /22622825)
CM - Cites: Int J Epidemiol. 2011 Dec;40(6):1593-604 (medline /22158669)
CM - Cites: Nature. 2010 Dec 2;468(7324):696-700 (medline /21068725)
CM - Cites: Toxicol In Vitro. 2007 Sep;21(6):1104-12 (medline /17553662)
CM - Cites: Sci Total Environ. 2015 Sep 15;527-528:540-51 (medline /26004539)
CM - Cites: Free Radic Biol Med. 2008 Mar 1;44(5):907-17 (medline /18166164)
CM - Cites: Environ Res. 2015 Feb;137:329-37 (medline /25601736)
CM - Cites: J Health Popul Nutr. 2006 Jun;24(2):142-63 (medline /17195556)
CM - Cites: Neurotoxicology. 2003 Aug;24(4-5):747-53 (medline /12900089)
CM - Cites: Arch Toxicol. 2011 Feb;85(2):119-25 (medline /20571777)
CM - Cites: Cell Biochem Biophys. 2014 Nov;70(2):1433-8 (medline /24989681)
CM - Cites: Exp Neurol. 1999 Jan;155(1):109-17 (medline /9918710)
CM - Cites: Life Sci. 2006 Sep 13;79(16):1514-22 (medline /16737717)
DOCNO- medline/27966075

101 - TOXLINE
TI - Thiolated arsenic in natural systems: What is current, what is new and
what needs to be known.
AU - Herath I
AD - School of Civil Engineering and Surveying, Faculty of Health, Engineering and
Sciences, University of Southern Queensland, West Street, 4350 Toowoomba,
Queensland, Australia.
AU - Vithanage M
AD - International Centre for Applied Climate Science, University of Southern
Queensland, West Street, Toowoomba, 4350, Queensland, Australia; Faculty of Applied
Sciences, University of Sri Jayewardenepura, Nugegoda 10250, Sri Lanka.
AU - Seneweera S
AD - Plant Stress Biology Research Group, Centre for Crop Health, University of
Southern Queensland, West Street, Toowoomba, 4350, Queensland, Australia.
AU - Bundschuh J
AD - School of Civil Engineering and Surveying, Faculty of Health, Engineering and
Sciences, University of Southern Queensland, West Street, 4350 Toowoomba,
Queensland, Australia; UNESCO Chair on Groundwater Arsenic within the 2030 Agenda
for Sustainable Development, University of Southern Queensland, West Street, 4350
Toowoomba, Queensland, Australia. Electronic address: Jochen.Bundschuh@usq.edu.au.
SO - Environ Int. 2018, Jun; 115:370-386. [Environment international]
AB - Thiolated arsenic compounds are the sulfur analogous substructures of
oxo-arsenicals as the arsinoyl (As&#8239;=&#8239;O) is substituted by an
arsinothioyl (As&#8239;=&#8239;S) group. Relatively brief history of
thioarsenic research, mostly in the current decade has endeavored to
understand their consequences in the natural environment. However,
thioarsenic related aspects have by far not attached much research concern
on global scale compared to other arsenic species. This review attempts to
provide a critical overview for the first time on formation mechanisms of
thioarsenicals, their chemistry, speciation and analytical methodologies
in order to provide a rational assessment of what is new, what is current,
what needs to be known or what should be done in future research.
Thioarsenic compounds play a vital role in determining the biogeochemistry
of arsenic in sulfidic environments under reducing conditions. Thioarsenic
species are widely immobilized by naturally occurring processes such as
the adsorption on iron (oxyhydr)oxides and precipitation on iron sulfide
minerals. Accurate measurement of thioarsenic species is a challenging
task due to their instability upon pH, temperature, redox potential, and
concentrations of oxygen, sulfur and iron. Assessment of direct and
indirect effects of toxic thioarsenic species on global population those
who frequently get exposed to high levels of arsenic is an urgent
necessity. Dimethylmonothioarsinic acid (DMMTAV) is the most cytotoxic
arsenic metabolite having similar toxicological effects as
dimethylarsinous acid (DMAIII) in human and animal tissues. The formation
and chemical analysis of thioarsenicals in soil and sediments are highly
unknown. Therefore, future research needs to be more inclined towards in
determining the molecular structure of unknown thioarsenic complexes in
various environmental suites. Contemporary approaches hyphenated to
existing technologies would pave the way to overcome critical challenges
of thioarsenic speciation such as standards synthesis, structural
determination, quantification and sample preservation in future research.
KW - Arsenic
KW - Kinetics
KW - Speciation
KW - Thermodynamics
KW - Thioarsenicals
KW - Thiolation
LA - eng
IS - 1873-6750 (Electronic)
PT - Journal Article
PT - Review
TA - Environ Int
YR - 2018
DATE- 20180525
CI - Crown Copyright &copy; 2018. Published by Elsevier Ltd. All rights
reserved.
CITO- NLM
CS - Netherlands
FJT - Environment international
EDAT- 20180502
STAT- In-Data-Review
DOCNO- medline/29705693

102 - TOXLINE
TI - Effects of arsenolipids on in vitro blood-brain barrier model.
AU - M�ller SM
AD - Heinrich-Stockmeyer Foundation, Parkstra&szlig;e 44-46, 49214, Bad
Rothenfelde, Germany.
AU - Ebert F
AD - Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-
Allee 114-116, 14558, Nuthetal, Germany.
AU - Raber G
AD - Institute of Chemistry, NAWI Graz, University of Graz, Universitaetsplatz 1,
8010, Graz, Austria.
AU - Meyer S
AD - Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-
Allee 114-116, 14558, Nuthetal, Germany.
AU - Bornhorst J
AD - Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-
Allee 114-116, 14558, Nuthetal, Germany.
AU - H�wel S
AD - Institute of Biochemistry, University of M�nster, Wilhelm-Klemm-Str. 2,
48149, M�nster, Germany.
AU - Galla HJ
AD - Institute of Biochemistry, University of M�nster, Wilhelm-Klemm-Str. 2,
48149, M�nster, Germany.
AU - Francesconi KA
AD - Institute of Chemistry, NAWI Graz, University of Graz, Universitaetsplatz 1,
8010, Graz, Austria.
AU - Schwerdtle T
AD - Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-
Allee 114-116, 14558, Nuthetal, Germany. tanja.schwerdtle@uni-potsdam.de.
SO - Arch Toxicol. 2018, Feb; 92(2):823-832. [Archives of toxicology]
AB - Arsenic-containing hydrocarbons (AsHCs), a subgroup of arsenolipids (AsLs)
occurring in fish and edible algae, possess a substantial neurotoxic
potential in fully differentiated human brain cells. Previous in vivo
studies indicating that AsHCs cross the blood-brain barrier of the fruit
fly Drosophila melanogaster raised the question whether AsLs could also
cross the vertebrate blood-brain barrier (BBB). In the present study, we
investigated the impact of several representatives of AsLs (AsHC 332, AsHC
360, AsHC 444, and two arsenic-containing fatty acids, AsFA 362 and AsFA
388) as well as of their metabolites (thio/oxo-dimethylpropionic acid,
dimethylarsinic acid) on porcine brain capillary endothelial cells
(PBCECs, in vitro model for the blood-brain barrier). AsHCs exerted the
strongest cytotoxic effects of all investigated arsenicals as they were up
to fivefold more potent than the toxic reference species arsenite
(iAsIII). In our in vitro BBB-model, we observed a slight transfer of AsHC
332 across the BBB after 6 h at concentrations that do not affect the
barrier integrity. Furthermore, incubation with AsHCs for 72 h led to
a disruption of the barrier at sub-cytotoxic concentrations. The
subsequent immunocytochemical staining of three tight junction proteins
revealed a significant impact on the cell membrane. Because AsHCs enhance
the permeability of the in vitro blood-brain barrier, a similar behavior
in an in vivo system cannot be excluded. Consequently, AsHCs might
facilitate the transfer of accompanying foodborne toxicants into the
brain.
KW - Arsenic-containing fatty acids
KW - Arsenic-containing hydrocarbons
KW - Arsenolipids
KW - In vitro blood–brain barrier model
LA - eng
IS - 1432-0738 (Electronic)
PT - Journal Article
TA - Arch Toxicol
YR - 2018
DATE- 20180220
CITO- NLM
CS - Germany
FJT - Archives of toxicology
EDAT- 20171020
STAT- In-Data-Review
DOCNO- medline/29058019

103 - TOXLINE
TI - Influence of operating parameters on arsenic transformation during
municipal sewage sludge incineration with cotton stalk.
AU - Zhao Y
AD - Institute of Engineering Thermophysics, Chinese Academy of Sciences, Beijing,
100190, China; University of Chinese Academy of Sciences, Beijing, 100049, China.
AU - Ren Q
AD - Institute of Engineering Thermophysics, Chinese Academy of Sciences, Beijing,
100190, China; University of Chinese Academy of Sciences, Beijing, 100049, China.
Electronic address: renqiangqiang@iet.cn.
AU - Na Y
AD - Institute of Engineering Thermophysics, Chinese Academy of Sciences, Beijing,
100190, China; University of Chinese Academy of Sciences, Beijing, 100049, China.
SO - Chemosphere. 2018, Feb; 193:951-957. [Chemosphere]
AB - Addition of cotton stalk (CS) has been proved to promote dramatically the
transformation of toxic As3+ to less toxic As5+ in the fly ash during
municipal sewage sludge (MSS) incineration. However, the fate of arsenic
during co-firing of MSS and CS in different operating parameters was still
unclear. In the present study, the effects of incineration temperatures
and O2 content in the flue gas on speciation transformation of arsenic
during MSS and 70% MSS/30% CS incineration were investigated in a bubbling
fluidized bed. The results show that less arsenic is distributed in bottom
ash whereas more arsenic is migrated to the fly ash and flue gas, with the
temperature increasing from 800 &deg;C to 950 &deg;C. The
arsenic capture in fly ash is facilitated predominantly by the
condensation and/or physical adsorption of As2O3(g) at the temperatures
from 800 &deg;C to 900 &deg;C. The chemical oxidation of
As2O3(g) is favored by forming various arsenates (As5+) at
950 &deg;C. At low O2 content from 1% to 5%, some arsenic compounds
in MSS such as As2S3 can react with O2 to produce As2O3(g), and then more
As2O3(g) is captured in the fly ash by the inherent mineral compounds like
CaO through the condensation and/or physical adsorption. Further
increasing O2 content especially to 9% stimulates significantly the
oxidation of As3+ to As5+ in the fly ash, which is mainly attributed to
the chemical reactions between As2O3(g), various mineral compounds and
sufficient O2.
KW - Arsenic speciation transformation
KW - Cotton stalk
KW - Flue gas
KW - Incineration temperature
KW - Municipal sewage sludge
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180607
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Chemosphere
EDAT- 20171123
STAT- In-Process
DOCNO- medline/29874771

104 - TOXLINE
TI - Arsenic, cadmium, lead, and chromium in well water, rice, and human urine
in Sri Lanka in relation to chronic kidney disease of unknown etiology.
AU - S Herath HMA
AD - Department of Environmental Engineering, Faculty of Engineering, Toyama
Prefectural University, 5180 Kurokawa, Imizu-city, Toyama 939-0398, Japan E-mail:
sunaliherath@gmail.com.
AU - Kawakami T
AD - Department of Environmental Engineering, Faculty of Engineering, Toyama
Prefectural University, 5180 Kurokawa, Imizu-city, Toyama 939-0398, Japan E-mail:
sunaliherath@gmail.com.
AU - Nagasawa S
AD - Department of Environmental Engineering, Faculty of Engineering, Toyama
Prefectural University, 5180 Kurokawa, Imizu-city, Toyama 939-0398, Japan E-mail:
sunaliherath@gmail.com.
AU - Serikawa Y
AD - Department of Environmental Engineering, Faculty of Engineering, Toyama
Prefectural University, 5180 Kurokawa, Imizu-city, Toyama 939-0398, Japan E-mail:
sunaliherath@gmail.com.
AU - Motoyama A
AD - Graduate School of Gifu University, 1-1 Yanagido, Gifu City 501-1193, Japan.
AU - Chaminda GGT
AD - Department of Civil &amp; Environmental Engineering, Faculty of Engineering,
University of Ruhuna, Hapugala, Galle, Sri Lanka.
AU - Weragoda SK
AD - National Water Supply and Drainage Board, Sri Lanka.
AU - Yatigammana SK
AD - Department of Zoology, Faculty of Science, University of Peradeniya,
Peradeniya, Sri Lanka.
AU - Amarasooriya AAGD
AD - Department of Environmental Engineering, Faculty of Engineering, Toyama
Prefectural University, 5180 Kurokawa, Imizu-city, Toyama 939-0398, Japan E-mail:
sunaliherath@gmail.com.
SO - J Water Health. 2018, Apr; 16(2):212-222. [Journal of water and health]
AB - Chronic kidney disease of unknown etiology (CKDu) is spreading gradually
in Sri Lanka. In the current research, 1,435 well water samples from all
25 districts of Sri Lanka, 91 rice samples, and 84 human urine samples
from both CKDu-endemic and non-endemic areas in Sri Lanka were analyzed
for arsenic, cadmium, lead, and chromium to detect whether toxic elements
could be a cause of CKDu. The liver-type fatty acid binding protein
(L-FABP) concentration and arsenic, cadmium, lead, and chromium
concentrations of the urine samples were analyzed to determine the
relation of L-FABP with arsenic, cadmium, lead, and chromium. High
concentrations of arsenic, cadmium, lead, and chromium were not detected
in the well water samples from CKDu-endemic areas. Arsenic, cadmium, and
lead contents in the rice samples from both CKDu-endemic and non-endemic
areas were well below the Codex standard. There were no relationships
between the L-FABP concentration and concentrations of arsenic, cadmium,
lead, and chromium in urine. In addition, arsenic, cadmium, lead, and
chromium concentrations in human urine samples from CKDu-endemic areas
were not significantly different from those from non-endemic areas. These
findings indicated that arsenic, cadmium, lead, and chromium could not
cause CKDu.
LA - eng
IS - 1477-8920 (Print)
PT - Journal Article
TA - J Water Health
YR - 2018
DATE- 20180420
CITO- NLM
CS - England
FJT - Journal of water and health
STAT- In-Data-Review
DOCNO- medline/29676757

105 - TOXLINE
TI - Lead, cadmium and arsenic in human milk and their socio-demographic and
lifestyle determinants in Lebanon.
AU - Bassil M
AD - Department of Natural Sciences, School of Arts and Sciences, Lebanese
American University, Beirut, 1102-2801, Lebanon.
AU - Daou F
AD - Department of Laboratory Science and Technology, American University of
Science and Technology, Achrafieh, 16-6452, Lebanon.
AU - Hassan H
AD - Department of Natural Sciences, School of Arts and Sciences, Lebanese
American University, Beirut, 1102-2801, Lebanon.
AU - Yamani O
AD - Department of Laboratory Science and Technology, American University of
Science and Technology, Achrafieh, 16-6452, Lebanon.
AU - Kharma JA
AD - Department of Natural Sciences, School of Arts and Sciences, Lebanese
American University, Beirut, 1102-2801, Lebanon.
AU - Attieh Z
AD - Department of Laboratory Science and Technology, American University of
Science and Technology, Achrafieh, 16-6452, Lebanon.
AU - Elaridi J
AD - Department of Natural Sciences, School of Arts and Sciences, Lebanese
American University, Beirut, 1102-2801, Lebanon. Electronic address:
Jomana.aridi@lau.edu.lb.
SO - Chemosphere. 2018, Jan; 191:911-921. [Chemosphere]
AB - INTRODUCTION: Exposure of newborns to toxic metals is of special interest
due to their reported contamination in breast milk and potential harm. The
aim of this study was to assess the occurrence and factors associated with
lead, cadmium and arsenic contamination in breast milk collected from
lactating mothers in Lebanon.
AB - METHODS: A total of 74 breast milk samples were collected from primaparas
according to guidelines set by the World Health Organization. A survey was
administered to determine the demographic and anthropometric
characteristics of participating lactating mothers. Dietary habits were
assessed using a semi-quantitative food frequency questionnaire. The milk
samples were analyzed for the presence of arsenic, cadmium and lead using
microwave-assisted digestion and atomic absorption spectrophotometry.
AB - RESULTS: Arsenic contamination was found in 63.51% of breast milk samples
(mean 2.36 &plusmn; 1.95 &mu;g/L) whereas cadmium and lead
were detected in 40.54% and 67.61% of samples respectively (means
0.87 &plusmn; 1.18 &mu;g/L and
18.18 &plusmn; 13.31 &mu;g/L). Regression analysis
indicated that arsenic contamination was associated with cereal and fish
intake (p = 0.013 and p = 0.042 respectively).
Residence near cultivation activities (p = 0.008), smoking
status before pregnancy (p = 0.046), potato consumption
(p = 0.046) and education level (p = 0.041) were
associated with lead contamination. Cadmium contamination was
significantly associated with random smoke exposure (p = 0.002).
AB - CONCLUSION: Our study is the first in Lebanon to report toxic metal
contamination in breast milk. Although estimated weekly infant intake of
these metals from breast milk was found to be lower than the limit set by
international guidelines, our results highlight the need for developing
strategies to protect infants from exposure to these hazardous substances.
KW - Arsenic
KW - Breast milk
KW - Cadmium
KW - Determinants
KW - Lead
KW - Lebanon
RN - 00BH33GNGH
RN - 2P299V784P
RN - N712M78A8G
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180321
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171027
STAT- MEDLINE
DOCNO- medline/29145136

106 - TOXLINE
TI - Differentially Expressed mRNA Targets of Differentially Expressed miRNAs
Predict Changes in the TP53 Axis and Carcinogenesis-Related Pathways in
Human Keratinocytes Chronically Exposed to Arsenic.
AU - Al-Eryani L
AD - Department of Pharmacology and Toxicology.
AU - Waigel S
AD - Department of Medicine.
AU - Tyagi A
AD - Department of Urology, University of Louisville, Louisville, Kentucky 40202.
AU - Peremarti J
AD - Universitat Aut�noma de Barcelona, 08193 Bellaterra, Spain.
AU - Jenkins SF
AD - Department of Pharmacology and Toxicology.
AU - Damodaran C
AD - Department of Urology, University of Louisville, Louisville, Kentucky 40202.
AU - States JC
AD - Department of Pharmacology and Toxicology.
SO - Toxicol Sci. 2018, Apr 01; 162(2):645-654. [Toxicological sciences : an
official journal of the Society of Toxicology]
AB - Arsenic is a widely distributed toxic natural element. Chronic arsenic
ingestion causes several cancers, especially skin cancer. Arsenic-induced
cancer mechanisms are not well defined, but several studies indicate that
mutation is not the driving force and that microRNA expression changes
play a role. Chronic low arsenite exposure malignantly transforms
immortalized human keratinocytes (HaCaT), serving as a model for
arsenic-induced skin carcinogenesis. Early changes in miRNA expression in
HaCaT cells chronically exposed to arsenite will reveal early steps in
transformation. HaCaT cells were maintained with 0/100&thinsp;nM NaAsO2
for 3 and 7&thinsp;weeks. Total RNA was purified. miRNA and mRNA
expression was assayed using Affymetrix microarrays. Targets of
differentially expressed miRNAs were collected from TargetScan 6.2,
intersected with differentially expressed mRNAs using Partek Genomic Suite
software, and mapped to their pathways using MetaCore software. MDM2,
HMGB1 and TP53 mRNA, and protein levels were assayed by RT-qPCR and
Western blot. Numerous miRNAs and mRNAs involved in carcinogenesis
pathways in other systems were differentially expressed at 3 and
7&thinsp;weeks. A TP53 regulatory network including MDM2 and HMGB1 was
predicted by the miRNA and mRNA networks. Total TP53 and
TP53-S15-phosphorylation were induced. However, TP53-K382-hypoacetylation
suggested that the induced TP53 is inactive in arsenic exposed cells. Our
data provide strong evidence that early changes in miRNAs and target mRNAs
may contribute to arsenic-induced carcinogenesis.
LA - eng
IS - 1096-0929 (Electronic)
PT - Journal Article
TA - Toxicol Sci
YR - 2018
DATE- 20180518
CITO- NLM
CS - United States
FJT - Toxicological sciences : an official journal of the Society of Toxicology
STAT- In-Data-Review
CM - Cites: Cancer Res. 2008 Nov 15;68(22):9131-6 (medline /19010883)
CM - Cites: Toxicol Lett. 2014 Jun 5;227(2):91-8 (medline /24704393)
CM - Cites: Comp Med. 2011 Feb;61(1):39-44 (medline /21819680)
CM - Cites: J Biol Chem. 2009 Apr 24;284(17 ):11171-83 (medline /19265193)
CM - Cites: Cancer Res. 2001 Apr 1;61(7):3212-9 (medline /11306511)
CM - Cites: Cancer Cell. 2002 Jul;2(1):9-15 (medline /12150820)
CM - Cites: Oncotarget. 2012 Feb;3(2):132-43 (medline /22361592)
CM - Cites: Toxicol Sci. 2007 Sep;99(1):126-40 (medline /17567589)
CM - Cites: PLoS One. 2013 Aug 09;8(8):e71730 (medline /23951231)
CM - Cites: Curr Drug Targets. 2013 Sep;14(10):1128-34 (medline /23834148)
CM - Cites: Cell Mol Biol (Noisy-le-grand). 2016 Sep 30;62(11):13-20 (medline
/27755946)
CM - Cites: J Genet Genomics. 2009 Aug;36(8):447-54 (medline /19683667)
CM - Cites: Mol Cell. 2010 Apr 9;38(1):140-53 (medline /20385095)
CM - Cites: Clin Cancer Res. 2008 Sep 1;14 (17 ):5318-24 (medline /18765522)
CM - Cites: Rev Diabet Stud. 2012 Spring;9(1):6-22 (medline /22972441)
CM - Cites: J Cutan Pathol. 1998 Oct;25(9):457-62 (medline /9821074)
CM - Cites: Proc Natl Acad Sci U S A. 2004 Feb 24;101(8):2259-64 (medline
/14982997)
CM - Cites: Cancer Invest. 2008 Oct;26(8):843-51 (medline /18798064)
CM - Cites: Mol Cell Biochem. 2007 Oct;304(1-2):219-26 (medline /17530187)
CM - Cites: Mol Med Rep. 2014 Oct;10(4):1663-70 (medline /25069581)
CM - Cites: Oncol Lett. 2013 Mar;5(3):884-888 (medline /23426143)
CM - Cites: J Biol Chem. 2002 Mar 1;277(9):7157-64 (medline /11748232)
CM - Cites: Front Genet. 2012 Jan 09;2:91 (medline /22303385)
CM - Cites: J Cell Physiol. 2014 Nov;229(11):1630-8 (medline /24610393)
CM - Cites: Int J Cancer. 2001 May 20;95(3):168-75 (medline /11307150)
CM - Cites: Toxicology. 2009 Aug 3;262(2):162-70 (medline /19524636)
CM - Cites: Curr Genomics. 2010 Nov;11(7):537-61 (medline /21532838)
CM - Cites: Biochim Biophys Acta. 2010 Jan-Feb;1799(1-2):131-40 (medline
/20123075)
CM - Cites: Oncol Lett. 2012 Aug;4(2):339-345 (medline /22844381)
CM - Cites: Clin Cancer Drugs. 2015;2(2):138-147 (medline /27054085)
CM - Cites: Int J Cancer. 2001 Jun 15;92 (6):790-6 (medline /11351297)
CM - Cites: Free Radic Biol Med. 2008 Sep 1;45(5):651-8 (medline /18572023)
CM - Cites: Mol Cancer Res. 2007 Apr;5(4):403-12 (medline /17426254)
CM - Cites: Mol Cancer Res. 2003 Dec;1(14 ):1001-8 (medline /14707283)
CM - Cites: Exp Dermatol. 2013 Jun;22(6):426-8 (medline /23711067)
CM - Cites: EMBO Mol Med. 2012 Mar;4(3):143-59 (medline /22351564)
CM - Cites: Mol Ther. 2007 Dec;15(12):2070-9 (medline /17878899)
CM - Cites: Br J Cancer. 1999 Jun;80(7):1080-6 (medline /10362120)
CM -Cites: Mol Cell Biol. 2014 Sep 15;34(18):3407-20 (medline /24980435)
CM -Cites: Cell. 1993 Dec 3;75(5):843-54 (medline /8252621)
CM -Cites: Annu Rev Public Health. 2009;30:107-22 (medline /19012537)
CM -Cites: Cancers (Basel). 2016 Jul 20;8(7):null (medline /27447672)
CM -Cites: J Thorac Oncol. 2011 Mar;6(3):482-8 (medline /21258252)
CM -Cites: Diabetes. 2013 Mar;62(3):789-800 (medline /22966074)
CM -Cites: Cancer Lett. 2014 Nov 28;354(2):211-9 (medline /25173797)
CM -Cites: FEBS Lett. 1997 Dec 22;420(1):25-7 (medline /9450543)
CM -Cites: Histopathology. 2015 Oct;67(4):491-500 (medline /25684546)
CM -Cites: Genes Dev. 1998 Sep 15;12(18):2831-41 (medline /9744860)
CM -Cites: Int J Clin Exp Pathol. 2015 Sep 01;8(9):11258-67 (medline
/26617850)
CM - Cites: Cold Spring Harb Perspect Biol. 2009 Aug;1(2):a002881 (medline
/20066091)
CM - Cites: FEBS J. 2011 May;278(10):1598-609 (medline /21395977)
CM - Cites: Nat Med. 1996 Aug;2(8):912-7 (medline /8705862)
CM - Cites: Cancer Res. 1998 Feb 15;58(4):609-13 (medline /9485008)
CM - Cites: IARC Monogr Eval Carcinog Risks Hum. 2012;100(Pt C):11-465 (medline
/23189751)
CM - Cites: Cell. 1997 Oct 31;91(3):325-34 (medline /9363941)
CM - Cites: Dermatol Surg. 1996 Mar;22(3):301-4 (medline /8599743)
CM - Cites: Proc Natl Acad Sci U S A. 1999 Apr 27;96(9):5117-22 (medline
/10220428)
CM - Cites: Int J Oncol. 2001 Sep;19(3):625-32 (medline /11494046)
CM - Cites: Science. 2001 Oct 26;294(5543):853-8 (medline /11679670)
CM - Cites: Hippokratia. 2010 Oct;14(4):236-40 (medline /21311629)
CM - Cites: Mol Cell Biol. 2003 Apr;23(8):2991-8 (medline /12665595)
CM - Cites: Proc Natl Acad Sci U S A. 1991 Nov 15;88(22):10124-8 (medline
/1946433)
CM - Cites: Environ Health Perspect. 2002 Oct;110 Suppl 5:883-6 (medline
/12426152)
CM - Cites: Environ Sci. 2005;12(5):283-92 (medline /16308561)
CM - Cites: Carcinogenesis. 1993 May;14(5):833-9 (medline /8504475)
CM - Cites: Cancer J. 2012 May-Jun;18(3):223-31 (medline /22647358)
CM - Cites: Oncol Res. 1998;10(9):475-82 (medline /10223623)
CM - Cites: J Cell Biol. 1988 Mar;106(3):761-71 (medline /2450098)
CM - Cites: Cell. 1997 Aug 22;90(4):595-606 (medline /9288740)
CM - Cites: Int J Clin Exp Pathol. 2015 Jun 01;8(6):6646-55 (medline /26261546)
CM - Cites: Nat Rev Cancer. 2012 Jan 19;12 (2):84-8 (medline /22257949)
CM - Cites: Biol Trace Elem Res. 2015 Jul;166(1):34-40 (medline /25796515)
CM - Cites: Biomark Insights. 2012;7:127-41 (medline /23115478)
CM - Cites: Cancer Cell Int. 2015 Sep 17;15:87 (medline /26388702)
CM - Cites: Nat Commun. 2013;4:2996 (medline /24356649)
CM - Cites: Asian Pac J Cancer Prev. 2007 Jan-Mar;8(1):13-23 (medline
/17477765)
DOCNO- medline/29319823

107 - TOXLINE
TI - Impact of prenatal arsenic exposure on chronic adult diseases.
AU - Young JL
AD - a Department of Pharmacology and Toxicology , University of Louisville ,
Louisville , KY , USA.
AU - Cai L
AD - b Departments of Pediatrics, Radiation Oncology and pharmacology and
Toxicology , Pediatric Research Institute, University of Louisville , Louisville ,
KY , USA.
AU - States JC
AD - a Department of Pharmacology and Toxicology , University of Louisville ,
Louisville , KY , USA.
SO - Syst Biol Reprod Med. 2018, Jun 06:1-15. [Systems biology in reproductive
medicine]
AB - Exposure to environmental stressors during susceptible windows of
development can result in negative health outcomes later in life, a
concept known as the Developmental Origins of Health and Disease (DOHaD).
There is a growing body of evidence that exposures to metals early in life
(in utero and postnatal) increase the risk of developing adult diseases
such as cancer, cardiovascular disease, non-alcoholic fatty liver disease,
and diabetes. Of particular concern is exposure to the metalloid arsenic,
a drinking water contaminant and worldwide health concern. Epidemiological
studies of areas with high levels of arsenic in the drinking water, such
as some regions in Chile and Bangladesh, indicate an association between
in utero arsenic exposure and the development of adult diseases.
Therefore, the need for experimental models to address the mechanism
underlining early onset of adult diseases have emerged including the in
utero and whole-life exposure models. This review will highlight the
epidemiological events and subsequent novel experimental models
implemented to study the impact of early life exposure to arsenic on the
development of adult diseases. In addition, current research using these
models will be discussed as well as possible underlying mechanism for the
early onset of disease.
AB - ABBREVIATIONS: ALT: alanine aminotransferase; AMI: acute myocardial
infarction; AST: aspartate aminotransferase; ATSDR: Agency for Toxic
Substances and Disease Registry; CVD: cardiovascular disease; DMA:
dimethylarsinate; DOHaD: Developmental Origins of Health and Disease; EPA:
U.S. Environmental Protection Agency; ER-&alpha;: estrogen receptor alpha;
HDL: high-density lipoprotein; HOMA-IR: homeostatic model assessment of
insulin resistance; iAs: inorganic arsenic; LDL: low-density lipoprotein;
MetS: metabolic syndrome; MMA: monomethylarsonate; NAFLD: non-alcoholic
fatty liver disease; PND: postnatal day; ppb: parts per billion; ppm:
parts per million; SAM: S-adenosylmethionine; USFDA: United States Food
and Drug Administration.
KW - Arsenic
KW - cancer
KW - cardiovascular disease
KW - chronic adult disease
KW - prenatal exposure
LA - eng
IS - 1939-6376 (Electronic)
PT - Journal Article
TA - Syst Biol Reprod Med
YR - 2018
DATE- 20180606
CITO- NLM
CS - England
FJT - Systems biology in reproductive medicine
EDAT- 20180606
STAT- Publisher
DOCNO- medline/29873257

108 - TOXLINE
TI - Melatonin attenuates arsenic induced nephropathy via the regulation of
oxidative stress and inflammatory signaling cascades in mice.
AU - Dutta S
AD - Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M,
Kolkata 700054, India.
AU - Saha S
AD - Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M,
Kolkata 700054, India.
AU - Mahalanobish S
AD - Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M,
Kolkata 700054, India.
AU - Sadhukhan P
AD - Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M,
Kolkata 700054, India.
AU - Sil PC
AD - Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M,
Kolkata 700054, India. Electronic address: parames@jcbose.ac.in.
SO - Food Chem Toxicol. 2018, May 12; 118:303-316. [Food and chemical
toxicology : an international journal published for the British Industrial
Biological Research Association]
AB - Arsenic is a potent inducer of several acute and chronic nephrotoxic
disorders. It promotes deleterious phenomenon like oxidative stress,
inflammation, cell death and altered glucose uptake leading to distorted
kidney homeostasis that end up in chronic kidney disease. This study
investigated the possible protective role of melatonin; a natural
antioxidant produced by the pineal gland, against arsenic induced
nephrotoxicity. Melatonin successfully ameliorated arsenic induced renal
toxicity both in in vitro and in vivo models. Elevated BUN, creatinine,
urine glucose and protein levels and altered renal histopathological
conditions were observed in arsenic intoxicated mice. Significant
oxidative stress induced damage of biomolecules along with downregulation
in antioxidant enzymes and thiols were also detected in the kidney tissues
of arsenic-intoxicated mice. These alterations along with mitochondrial
dysfunction ultimately triggered TNF&alpha; mediated inflammatory and cell
death cascades. Interestingly arsenic also led to disruption of glucose
uptake in the kidney. These findings suggest that melatonin protects the
kidney against toxic effect of arsenic, presumably through its
antioxidant, anti-inflammatory and antidiabetic properties by inhibiting
inflammatory outburst, apoptosis, necroptosis and stimulating glucose
uptake. As melatonin is a natural antioxidant molecule, detailed
pharmacokinetic and pharmacodynamic studies are expected to establish it
as an effective nephro-protective agent in future.
KW - Apoptosis
KW - Arsenic
KW - Glucose uptake
KW - Inflammation
KW - Kidney
KW - Melatonin
KW - Necroptosis
KW - Oxidative stress
LA - eng
IS - 1873-6351 (Electronic)
PT - Journal Article
TA - Food Chem Toxicol
YR - 2018
DATE- 20180619
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Food and chemical toxicology : an international journal published for the
British Industrial Biological Research Association
EDAT- 20180512
STAT- Publisher
DOCNO- medline/29763682

109 - TOXLINE
TI - Arsenic-gene interactions and beta-cell function in the Strong Heart
Family Study.
AU - Balakrishnan P
AD - Department of Environmental Health Sciences, Columbia University Mailman
School of Public Health, New York, NY, United States.
AU - Navas-Acien A
AD - Department of Environmental Health Sciences, Columbia University Mailman
School of Public Health, New York, NY, United States.
AU - Haack K
AD - Texas Biomedical Research Institute, San Antonio, TX, United States.
AU - Vaidya D
AD - Department of Epidemiology, Johns Hopkins University Bloomberg School of
Public Health, Baltimore, MD, United States; Clinical and Translational Research,
Johns Hopkins School of Medicine, Baltimore, MD, United States.
AU - Umans JG
AD - MedStar Health Research Institute, Hyattsville, MD, United States.
AU - Best LG
AD - Missouri Breaks Industries Research, Inc., Eagle Butte, SD, United States.
AU - Goessler W
AD - Institute of Chemistry, University of Graz, Graz, Austria.
AU - Francesconi KA
AD - Institute of Chemistry, University of Graz, Graz, Austria.
AU - Franceschini N
AD - Department of Epidemiology, University of North Carolina at Chapel Hill,
Chapel Hill, NC, United States.
AU - North KE
AD - Department of Epidemiology, University of North Carolina at Chapel Hill,
Chapel Hill, NC, United States.
AU - Cole SA
AD - Texas Biomedical Research Institute, San Antonio, TX, United States.
AU - Voruganti VS
AD - Department of Nutrition and UNC Nutrition Research Institute, University of
North Carolina at Chapel Hill, Kannapolis, NC, United States.
AU - Gribble MO
AD - Department of Environmental Health, Emory University Rollins School of Public
Health, Atlanta, GA, United States; Department of Epidemiology, Emory University
Rollins School of Public Health, Atlanta, GA, United States. Electronic address:
matt.gribble@emory.edu.
SO - Toxicol Appl Pharmacol. 2018, Jun 01; 348:123-129. [Toxicology and applied
pharmacology]
AB - We explored arsenic-gene interactions influencing pancreatic beta-cell
activity in the Strong Heart Family Study (SHFS). We considered 42
variants selected for associations with either beta-cell function (31
variants) or arsenic metabolism (11 variants) in the SHFS. Beta-cell
function was calculated as homeostatic model - beta corrected for insulin
resistance (cHOMA-B) by regressing homeostatic model - insulin resistance
(HOMA-IR) on HOMA-B and adding mean HOMA-B. Arsenic exposure was
dichotomized at the median of the sum of creatinine-corrected inorganic
and organic arsenic species measured by high performance liquid
chromatography-inductively coupled plasma mass spectrometry (HPLC-ICPMS).
Additive GxE models for cHOMA-B were adjusted for age and ancestry, and
accounted for family relationships. Models were stratified by center
(Arizona, Oklahoma, North Dakota and South Dakota) and meta-analyzed. The
two interactions between higher vs. lower arsenic and SNPs for cHOMA-B
that were nominally significant at P&#8239; < &#8239;0.05 were with
rs10738708 (SNP overall effect -3.91, P&#8239;=&#8239;0.56; interaction
effect with arsenic -31.14, P&#8239;=&#8239;0.02) and rs4607517 (SNP
overall effect +16.61, P&#8239;=&#8239;0.03; interaction effect with
arsenic +27.02, P&#8239;=&#8239;0.03). The corresponding genes GCK and
TUSC1 suggest oxidative stress and apoptosis as possible mechanisms for
arsenic impacts on beta-cell function. No interactions were
Bonferroni-significant (1.16&#8239;&times;&#8239;10-3). Our findings are
suggestive of oligogenic moderation of arsenic impacts on pancreatic
&beta;-cell endocrine function, but were not Bonferroni-significant.
KW - Arsenicals
KW - Diabetes
KW - Environmental Epidemiology
KW - Genetic Epidemiology
KW - Pancreas
KW - Susceptibility
LA - eng
IS - 1096-0333 (Electronic)
PT - Journal Article
TA - Toxicol Appl Pharmacol
YR - 2018
DATE- 20180523
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - United States
FJT - Toxicology and applied pharmacology
EDAT- 20180403
STAT- In-Data-Review
CM - Cites: Trends Genet. 2017 Apr;33(4):244-255 (medline /28245910)
CM - Cites: PLoS Genet. 2012;8(8):e1002793 (medline /22876189)
CM - Cites: Environ Health Perspect. 2017 Jan;125(1):15-22 (medline /27352405)
CM - Cites: Diabetologia. 2011 Jun;54(6):1273-90 (medline /21442161)
CM - Cites: Diabetes Care. 2010 Nov;33(11):2370-7 (medline /20805255)
CM - Cites: Epigenomics. 2017 May;9(5):701-710 (medline /28470093)
CM - Cites: Environ Health Perspect. 2012 Dec;120(12 ):1658-70 (medline
/22889723)
CM - Cites: Am J Epidemiol. 1986 Jul;124(1):17-27 (medline /3521261)
CM - Cites: PLoS One. 2013 Jun 11;8(6):e66114 (medline /23776618)
CM - Cites: Hum Mutat. 2009 Nov;30(11):1512-26 (medline /19790256)
CM - Cites: Bioinformatics. 2010 Sep 1;26(17):2190-1 (medline /20616382)
CM - Cites: J Biol Chem. 2006 Mar 17;281(11):7364-73 (medline /16407288)
CM - Cites: Am J Epidemiol. 1990 Dec;132(6):1141-55 (medline /2260546)
CM - Cites: Curr Environ Health Rep. 2014 Jan 19;1:22-34 (medline /24860721)
CM - Cites: Nat Genet. 2002 Jan;30(1):97-101 (medline /11731797)
CM - Cites: Am J Hum Genet. 1998 May;62(5):1198-211 (medline /9545414)
CM - Cites: Nat Genet. 2012 May 13;44(6):659-69 (medline /22581228)
CM - Cites: Diabetes Technol Ther. 2010 Aug;12(8):599-604 (medline /20615100)
CM - Cites: Oncol Rep. 2014 Mar;31(3):1305-13 (medline /24366000)
CM - Cites: Anal Methods. 2012;4(2):406-413 (medline /22685491)
CM - Cites: Am J Epidemiol. 2003 Feb 15;157(4):303-14 (medline /12578801)
CM - Cites: Environ Health Perspect. 2017 Dec 20;125(12 ):127004 (medline
/29373862)
CM - Cites: Nat Genet. 2010 Feb;42(2):105-16 (medline /20081858)
CM - Cites: Diabetologia. 1985 Jul;28(7):412-9 (medline /3899825)
DOCNO- medline/29621497

110 - TOXLINE
TI - Chronic exposure to high fat diet exacerbates arsenic-induced lung damages
in male mice: Possible role for oxidative stress.
AU - Hemmati AA
AD - Ahvaz Jundishapur University of Medical Sciences. Hemmati.AA@yahoo.com.
AU - Alboghobeish S
AD - Ahvaz Jundishapur University of Medical Sciences. Hemmati.AA@yahoo.com.
AU - Ahangarpour A
AD - Ahvaz Jundishapur University of Medical Sciences. Hemmati.AA@yahoo.com.
SO - Monaldi Arch Chest Dis. 2018, Mar 23; 88(1):903. [Monaldi archives for
chest disease = Archivio Monaldi per le malattie del torace]
AB - Arsenic is a common environmental and occupational contaminant worldwide
which can influence the development of respiratory diseases. In recent
years, alteration in the lifestyle as well as food habits have led to
increased consumption of food containing high levels of fat. The present
study was designed to evaluate the effects of chronic exposure to a
high-fat diet (HFD) on arsenic-induced damages and oxidative stress in the
lung tissue of mice. This is the first study to reveal the effect of
diet-induced obesity on arsenic-induced lung damages. Seventy-two male
Naval Medical Research Institute (NMRI) mice were divided into six groups
and fed an HFD or standard diet (SD) while being exposed to 25 or 50 ppm
of arsenic through drinking water for 20 weeks. At the end of the
experiment, the lung weight to body weight ratio; oxidative stress
markers, nitrite level, and hydroxyproline content in the lung tissue; and
lung histology were evaluated. The results demonstrated that arsenic
exposure leads to a significant decrease in the glutathione level and
catalase enzyme activity, and significantly increased reactive oxygen
species, malondialdehyde, and nitrite level, but it did not affect the
superoxide dismutase activity and hydroxyproline content in the lung
tissue. Consequently, all the parameters studied aggravated when HFD was
consumed along with arsenic. These findings were confirmed by histological
examination. Our study showed that HFD increased arsenic-induced lung
damages through oxidative stress in mice. These findings could be
important for clinical research to protect against arsenic-induced
respiratory toxicity in humans.
KW - Lung
KW - arsenic
KW - high fat diet
KW - oxidative stress.
LA - eng
IS - 1122-0643 (Print)
PT - Journal Article
TA - Monaldi Arch Chest Dis
YR - 2018
DATE- 20180509
CITO- NLM
CS - Italy
FJT - Monaldi archives for chest disease = Archivio Monaldi per le malattie del
torace
EDAT- 20180323
STAT- PubMed-not-MEDLINE
DOCNO- medline/29741077

111 - TOXLINE
TI - Multidrug Resistance Protein 1 (MRP1/ABCC1)-mediated cellular protection
and transport of methylated arsenic metabolites differs between human cell
lines.
AU - Banerjee M
AD - University of Alberta.
AU - Kaur G
AD - University of Alberta.
AU - Whitlock BD
AD - University of Alberta.
AU - Carew MW
AD - University of Alberta.
AU - Le XC
AD - University of Alberta.
AU - Leslie EM
AD - University of Alberta eleslie@ualberta.ca.
SO - Drug Metab Dispos. 2018, May 11. [Drug metabolism and disposition: the
biological fate of chemicals]
AB - The ATP-binding cassette (ABC) transporter Multidrug Resistance Protein 1
(MRP1/ABCC1) is known to protect cells from the proven human carcinogen
arsenic through the cellular efflux of arsenic triglutathione [As(GS)3],
and the diglutathione conjugate of the highly toxic monomethylarsonous
acid (MMAIII) [MMA(GS)2]. Previously, differences in MRP1 phosphorylation
(at Y920/S921) and N-glycosylation (at N19/N23) were associated with
marked differences in As(GS)3 transport kinetics between HEK293 and HeLa
cell lines. The objectives of the current study were to determine if
differences in MRP1-mediated cellular protection and transport of other
arsenic metabolites exist between HEK293 and HeLa cells. MRP1 expressed in
HEK293 cells conferred protection against the major urinary arsenic
metabolite dimethylarsinic acid (DMAV) through high apparent affinity and
capacity transport (Km 0.19 &mu;M, Vmax 342 pmol mg-1 protein min-1). In
contrast, DMAV transport was not detected using HeLa-WT-MRP1 membrane
vesicles. MMA(GS)2 transport by HeLa-WT-MRP1 vesicles had a similar
apparent Km, but a greater than 3-fold higher Vmax, compared to
HEK-WT-MRP1 vesicles. Cell line differences in DMAV and MMA(GS)2 transport
were not explained by differences in phosphorylation at Y920/S921. DMAV
did not inhibit, while MMA(GS)2 was an uncompetitive inhibitor of As(GS)3
transport, suggesting that DMAV and MMA(GS)2 have non-identical binding
sites to As(GS)3 on MRP1. Detoxification of different arsenic metabolites
by MRP1 is likely influenced by multiple factors including cell and tissue
type. This could have implications for the influence of MRP1 on both
tissue specific susceptibility to arsenic-induced disease, and tumour
sensitivity to arsenic-based therapeutics.
KW - Transporter-mediated drug/metabolite disposition
KW - carcinogen metabolism
KW - efflux transporters (P-gp, BCRP, MRP, MATE, BSEP, etc)
KW - glutathione
KW - heavy metals
KW - toxicology
LA - eng
IS - 1521-009X (Electronic)
PT - Journal Article
TA - Drug Metab Dispos
YR - 2018
DATE- 20180512
CI - The American Society for Pharmacology and Experimental Therapeutics.
CITO- NLM
CS - United States
FJT - Drug metabolism and disposition: the biological fate of chemicals
EDAT- 20180511
STAT- Publisher
DOCNO- medline/29752257

112 - TOXLINE
TI - Long-term exposure of immortalized keratinocytes to arsenic induces EMT,
impairs differentiation in organotypic skin models and mimics aspects of
human skin derangements.
AU - Weinmuellner R
AD - Christian Doppler Laboratory on Biotechnology of Skin Aging, Department of
Biotechnology, BOKU - University of Natural Resources and Life Sciences Vienna,
Vienna, Austria.
AU - Kryeziu K
AD - Department of Medicine I, Institute of Cancer Research and Comprehensive
Cancer Center Vienna, Medical University of Vienna, Borschkegasse 8a, 1090, Vienna,
Austria.
AU - Zbiral B
AD - Christian Doppler Laboratory on Biotechnology of Skin Aging, Department of
Biotechnology, BOKU - University of Natural Resources and Life Sciences Vienna,
Vienna, Austria.
AU - Tav K
AD - Christian Doppler Laboratory on Biotechnology of Skin Aging, Department of
Biotechnology, BOKU - University of Natural Resources and Life Sciences Vienna,
Vienna, Austria.
AU - Schoenhacker-Alte B
AD - Department of Medicine I, Institute of Cancer Research and Comprehensive
Cancer Center Vienna, Medical University of Vienna, Borschkegasse 8a, 1090, Vienna,
Austria.
AU - Groza D
AD - Department of Medicine I, Institute of Cancer Research and Comprehensive
Cancer Center Vienna, Medical University of Vienna, Borschkegasse 8a, 1090, Vienna,
Austria.
AU - Wimmer L
AD - Department of Medicine I, Institute of Cancer Research and Comprehensive
Cancer Center Vienna, Medical University of Vienna, Borschkegasse 8a, 1090, Vienna,
Austria.
AU - Schosserer M
AD - Department of Biotechnology, BOKU - University of Natural Resources and Life
Sciences Vienna, Muthgasse 18, Haus B, 1190, Vienna, Austria.
AU - Nagelreiter F
AD - Department of Biotechnology, BOKU - University of Natural Resources and Life
Sciences Vienna, Muthgasse 18, Haus B, 1190, Vienna, Austria.
AU - R�singer S
AD - Christian Doppler Laboratory on Biotechnology of Skin Aging, Department of
Biotechnology, BOKU - University of Natural Resources and Life Sciences Vienna,
Vienna, Austria.
AU - Mildner M
AD - Department of Dermatology, Medical University of Vienna, Vienna, Austria.
AU - Tschachler E
AD - Department of Dermatology, Medical University of Vienna, Vienna, Austria.
AU - Grusch M
AD - Department of Medicine I, Institute of Cancer Research and Comprehensive
Cancer Center Vienna, Medical University of Vienna, Borschkegasse 8a, 1090, Vienna,
Austria.
AU - Grillari J
AD - Department of Biotechnology, BOKU - University of Natural Resources and Life
Sciences Vienna, Muthgasse 18, Haus B, 1190, Vienna, Austria.
johannes.grillari@boku.ac.at.
AU - Heffeter P
AD - Department of Medicine I, Institute of Cancer Research and Comprehensive
Cancer Center Vienna, Medical University of Vienna, Borschkegasse 8a, 1090, Vienna,
Austria. petra.heffeter@meduniwien.ac.at.
SO - Arch Toxicol. 2018, Jan; 92(1):181-194. [Archives of toxicology]
AB - Arsenic is one of the most important human carcinogens and environmental
pollutants. However, the evaluation of the underlying carcinogenic
mechanisms is challenging due to the lack of suitable in vivo and in vitro
models, as distinct interspecies differences in arsenic metabolism exist.
Thus, it is of high interest to develop new experimental models of
arsenic-induced skin tumorigenesis in humans. Consequently, aim of this
study was to establish an advanced 3D model for the investigation of
arsenic-induced skin derangements, namely skin equivalents, built from
immortalized human keratinocytes (NHEK/SVTERT3-5). In contrast to
spontaneously immortalized HACAT cells, NHEK/SVTERT3-5 cells more closely
resembled the differentiation pattern of primary keratinocytes. With
regard to arsenic, our results showed that while our new cell model was
widely unaffected by short-time treatment (72 h) with low, non-toxic
doses of ATO (0.05-0.25 &micro;M), chronic exposure (6 months)
resulted in distinct changes of several cell characteristics. Thus, we
observed an increase in the G2 fraction of the cell cycle accompanied by
increased nucleus size and uneven tubulin distribution. Moreover, cells
showed strong signs of de-differentiation and upregulation of several
epithelial-to-mesenchymal transition markers. In line with these effects,
chronic contact to arsenic resulted in impaired skin-forming capacities as
well as localization of ki67-positive (proliferating) cells at the upper
layers of the epidermis; a condition termed Bowen's disease. Finally,
chronically arsenic-exposed cells were characterized by an increased
tumorigenicity in SCID mice. Taken together, our study presents a new
model system for the investigation of mechanisms underlying the
tumor-promoting effects of chronic arsenic exposure.
KW - Arsenic
KW - EMT
KW - Immortalized keratinocytes
KW - Organotypic culture
KW - Skin equivalents
LA - eng
IS - 1432-0738 (Electronic)
PT - Journal Article
TA - Arch Toxicol
YR - 2018
DATE- 20180315
CITO- NLM
CS - Germany
FJT - Archives of toxicology
EDAT- 20170803
STAT- In-Data-Review
CM - Cites: J Clin Oncol. 2007 Jul 1;25(19):2735-40 (medline /17602078)
CM - Cites: Environ Health Perspect. 2007 Apr;115(4):513-8 (medline /17450217)
CM - Cites: Mutat Res. 1997 Jun;386(3):209-18 (medline /9219559)
CM - Cites: Toxicol Appl Pharmacol. 2013 Aug 15;271(1):20-9 (medline /23643801)
CM - Cites: Proteomics. 2017 Mar;17 (6):null (medline /28000977)
CM - Cites: PLoS One. 2013 Aug 30;8(8):e72457 (medline /24023619)
CM - Cites: Adv Drug Deliv Rev. 2014 Apr;69-70:81-102 (medline /24378581)
CM - Cites: Mol Biol Int. 2011;2011:718974 (medline /22091411)
CM - Cites: Am J Epidemiol. 2011 Feb 15;173(4):414-20 (medline /21190988)
CM - Cites: Cell. 2000 Jan 7;100(1):57-70 (medline /10647931)
CM - Cites: Bull World Health Organ. 2000;78(9):1093-103 (medline /11019458)
CM - Cites: Arch Toxicol. 2017 Nov;91(11):3507-3516 (medline /28470405)
CM - Cites: Kaohsiung J Med Sci. 2011 Sep;27(9):390-5 (medline /21914526)
CM - Cites: Science. 1988 Jul 1;241(4861):79-81 (medline /3388020)
CM - Cites: Chemosphere. 2016 Sep;158:37-49 (medline /27239969)
CM - Cites: Br J Dermatol. 2015 Aug;173(2):391-403 (medline /25939812)
CM - Cites: Crit Rev Toxicol. 2009;39(4):271-98 (medline /19235533)
CM - Cites: Cancer Lett. 2000 Apr 28;152(1):79-85 (medline /10754209)
CM - Cites: Arch Toxicol. 2013 Jun;87(6):991-1000 (medline /23069812)
CM - Cites: Cancer Lett. 2014 Nov 28;354(2):211-9 (medline /25173797)
CM - Cites: Biol Pharm Bull. 2001 May;24(5):510-4 (medline /11379771)
CM - Cites: Biochem Biophys Res Commun. 2006 Sep 15;348(1):76-82 (medline
/16875670)
CM - Cites: Biochem Pharmacol. 2007 Jun 15;73(12 ):1873-86 (medline /17445775)
CM - Cites: Arch Toxicol. 2016 Oct;90(10 ):2349-67 (medline /27353523)
CM - Cites: Environ Sci Pollut Res Int. 2017 Feb;24(6):5316-5325 (medline
/28013460)
CM - Cites: J Nutr Biochem. 2016 Dec;38:25-40 (medline /27723467)
CM -Cites: Methods Enzymol. 2016;569:287-308 (medline /26778564)
CM -Cites: ALTEX. 2014;31(4):441-77 (medline /25027500)
CM -Cites: Cancer Prev Res (Phila). 2015 Mar;8(3):208-21 (medline /25586904)
CM -Cites: Postgrad Med. 1964 May;35:503-11 (medline /14163260)
CM -Cites: Toxicol Appl Pharmacol. 2015 Jul 1;286(1):36-43 (medline /25804888)
CM -Cites: Int J Environ Res Public Health. 2017 Jan 14;14 (1): (medline
/28098817)
CM - Cites: Toxicol Appl Pharmacol. 2017 Sep 15;331:6-17 (medline /28336213)
CM - Cites: Toxicol Mech Methods. 2016 Oct;26(8):565-579 (medline /27580671)
CM - Cites: Environ Sci Technol. 2012 Apr 3;46(7):4142-8 (medline /22352724)
CM - Cites: Arch Toxicol. 2015 Dec;89(12 ):2229-41 (medline /25537191)
CM - Cites: BMJ. 2013 Jun 05;346:f3625 (medline /23741031)
CM - Cites: Int Immunol. 2015 Jun;27(6):269-80 (medline /25813515)
CM - Cites: Toxicol In Vitro. 1997 Feb-Apr;11(1-2):89-98 (medline /20654299)
DOCNO- medline/28776197

113 - TOXLINE
TI - Shielding effect of anethole against arsenic induced genotoxicity in
cultured human peripheral blood lymphocytes and effect of GSTO1
polymorphism.
AU - Bal S
AD - 1Department of Biotechnology, Kurukshetra University, Kurukshetra, Haryana
136119 India.
AU - Yadav A
AD - 1Department of Biotechnology, Kurukshetra University, Kurukshetra, Haryana
136119 India.
AU - Verma N
AD - 1Department of Biotechnology, Kurukshetra University, Kurukshetra, Haryana
136119 India.
AU - Gupta R
AD - 2Department of Biochemistry, Kurukshetra University, Kurukshetra, Haryana
136119 India.
AU - Aggarwal NK
AD - 3Department of Microbiology, Kurukshetra University, Kurukshetra, Haryana
136119 India.
SO - 3 Biotech. 2018, May; 8(5):232. []
AB - Chronic exposure of inorganic arsenic compounds is responsible for the
manifestation of various tumours as well as other diseases. The principal
mechanism behind arsenic toxicity is the induction of a strong oxidative
stress with production of free radicals in cells. The present study was
aimed to explore the shielding effect of anethole against oxidative damage
induced by arsenic in cultured human peripheral blood lymphocytes and the
effect of GSTO1 polymorphism. Sister chromatid exchange (SCE) frequency,
comet tail moment and lipid peroxidation levels were used as biomarkers to
assess the oxidative damage. Heparinised venous blood was collected from
healthy individuals and treated with sodium arsenite (50 &micro;M) in
the presence of anethole (25 and 50 &micro;M) for the analysis of
shielding effect of anethole. For the genotyping of GSTO1, PCR RFLP method
was adopted. A significant dose-dependent increase in the frequency of
SCEs, tail moment and lipid peroxidation levels, was observed when
lymphocytes were treated with sodium arsenite. Anethole in combination
with sodium arsenite has shown a dose-dependent significant decrease in
the frequency of SCEs, tail moment and lipid peroxidation levels. Genetic
polymorphism of GSTO1 was found to effect individual susceptibility
towards arsenic-mediated genotoxicity and was found insignificant when
antigenotoxic effect of anethole was considered. GSTO1 mutant genotypes
were found to have significant higher genotoxicity of sodium arsenite as
compared to wild-type genotype. The results of the present study suggest
ameliorative effects of anethole against arsenic-mediated genotoxic damage
in cultured human peripheral blood lymphocytes. A significant effect of
GSTO1 polymorphism was observed on genotoxicity of sodium arsenite.
COI - Compliance with ethical standardsThe authors declare that there is no
conflict of interest regarding the publication of the present work.
KW - Anethole
KW - Genotoxicity
KW - Oxidative stress
KW - Sodium arsenite
LA - eng
IS - 2190-572X (Print)
PT - Journal Article
TA - 3 Biotech
YR - 2018
DATE- 20180509
CITO- NLM
CS - Germany
FJT - 3 Biotech
EDAT- 20180430
STAT- PubMed-not-MEDLINE
CM - Cites: Mol Biotechnol. 2004 Mar;26(3):249-61 (medline /15004294)
CM - Cites: Chem Res Toxicol. 2001 Aug;14(8):1051-7 (medline /11511179)
CM - Cites: IARC Monogr Eval Carcinog Risks Hum. 2004;84:1-477 (medline
/15645577)
CM - Cites: Am J Epidemiol. 2013 Sep 1;178(5):813-8 (medline /23764934)
CM - Cites: Pharmacogenetics. 2003 Mar;13(3):131-44 (medline /12618591)
CM - Cites: Cancer Lett. 2006 May 18;236(2):276-81 (medline /15992993)
CM - Cites: Chemosphere. 2012 Jul;88(4):432-8 (medline /22440634)
CM - Cites: J Appl Toxicol. 2011 Mar;31(2):95-107 (medline /21321970)
CM - Cites: Planta Med. 2008 Oct;74(13):1560-9 (medline /18612945)
CM - Cites: Curr Environ Health Rep. 2014 Jun 1;1(2):148-162 (medline
/25013752)
CM - Cites: Exp Cell Res. 1960 Sep;20:613-6 (medline /13772379)
CM - Cites: J Korean Med Sci. 2002 Jun;17(3):316-21 (medline /12068133)
CM - Cites: Exp Cell Res. 1988 Mar;175(1):184-91 (medline /3345800)
CM - Cites: Free Radic Biol Med. 2011 Jul 15;51(2):257-81 (medline /21554949)
CM - Cites: Toxicol Mech Methods. 2009 Jan;19(1):59-65 (medline /19778234)
CM - Cites: Toxicol Ind Health. 2016 Mar;32(3):410-21 (medline /24105067)
CM - Cites: Toxicol Appl Pharmacol. 1987 Oct;91(1):65-74 (medline /3672518)
CM - Cites: Environ Health Perspect. 2015 Jul;123(7):A169 (medline /26132290)
CM - Cites: Environ Health Perspect. 2013 Jul;121(7):832-8 (medline /23665672)
CM - Cites: J Biomed Sci. 2011 Jul 29;18:51 (medline /21798077)
CM - Cites: Food Chem Toxicol. 2001 May;39(5):493-8 (medline /11313116)
CM - Cites: Toxicol Lett. 2012 Apr 5;210(1):100-6 (medline /22306368)
CM - Cites: Int J Environ Res Public Health. 2013 Apr 12;10(4):1527-46 (medline
/23583964)
CM - Cites: Methods Enzymol. 1978;52:302-10 (medline /672633)
CM - Cites: Environ Health Perspect. 2008 Aug;116(8):1056-62 (medline
/18709164)
CM - Cites: PLoS Genet. 2012;8(2):e1002522 (medline /22383894)
CM - Cites: Molecules. 2011 Feb 01;16(2):1366-77 (medline /21285921)
CM - Cites: J Med Biochem. 2016 Sep;35(3):302-311 (medline /28356881)
CM - Cites: Anal Biochem. 1979 Jun;95(2):351-8 (medline /36810)
CM - Cites: Food Chem Toxicol. 1999 Jul;37(7):789-811 (medline /10496381)
CM - Cites: Mol Cell Biol. 1999 Jul;19(7):5166-9 (medline /10373565)
CM - Cites: Ecotoxicol Environ Saf. 2009 Feb;72(2):635-8 (medline /18499251)
CM - Cites: Nature. 1974 Sep 13;251(5471):156-8 (medline /4138930)
CM - Cites: Environ Res. 2011 Aug;111(6):804-10 (medline /21605854)
CM - Cites: Mutat Res. 2008 Jul 31;654(2):101-7 (medline /18602860)
DOCNO- medline/29725571
114 - TOXLINE
TI - Inorganic arsenic contents in ready-to-eat rice products and various
Korean rice determined by a highly sensitive gas chromatography-tandem
mass spectrometry.
AU - Jung MY
AD - Department of Food and Biotechnology, Graduate School, Woosuk University,
Samnye-eup, Wanju-gun, Jeonbuk Province 565-701, Republic of Korea; Agricultural
and Food Product Safety Analysis Center, Woosuk University, Republic of Korea.
Electronic address: munjung@woosuk.ac.kr.
AU - Kang JH
AD - Department of Food and Biotechnology, Graduate School, Woosuk University,
Samnye-eup, Wanju-gun, Jeonbuk Province 565-701, Republic of Korea.
AU - Jung HJ
AD - Department of Food Science and Biotechnology, College of Food Science, Woosuk
University, Samnye-eup, Wanju-gun, Jeonbuk Province 565-701, Republic of Korea.
AU - Ma SY
AD - Department of Food Science and Biotechnology, College of Food Science, Woosuk
University, Samnye-eup, Wanju-gun, Jeonbuk Province 565-701, Republic of Korea;
Agricultural and Food Product Safety Analysis Center, Woosuk University, Republic
of Korea.
SO - Food Chem. 2018, Feb 01; 240:1179-1183. [Food chemistry]
AB - Rice and rice products have been reported to contain high contents of
toxic inorganic arsenic (iAs). The inorganic arsenic contents in
microwavable ready-to-eat rice products (n=30) and different types of
Korean rice (n=102) were determined by a gas chromatography-tandem mass
spectrometry (GC-MS/MS). The method showed low limit of detection
(0.015pg), high intra- and inter-day repeatability ( < 7.3%, RSD), and
recovery rates (90-117%). The mean iAs content in the ready-to-eat rice
products was 59&mu;gkg-1 (dry weight basis). The mean iAs contents in
polished white, brown, black, and waxy rice were 65, 109, 91, and
66&mu;gkg-1, respectively. The percentages of ready-to-eat rice products,
white, brown, black, and waxy rice containing iAs over the maximum level
(100&mu;gkg-1) set by EU for the infant foods were 17, 4, 70, 36 and 0%,
respectively.
KW - Black rice
KW - British Anti-Lewisite
KW - Brown rice
KW - Derivatization
KW - Method validation
KW - Polished rice
KW - Safety
KW - Waxy rice
RN - N712M78A8G
LA - eng
IS - 0308-8146 (Print)
PT - Journal Article
TA - Food Chem
YR - 2018
DATE- 20171102
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Food chemistry
EDAT- 20170818
STAT- MEDLINE
DOCNO- medline/28946240
115 - TOXLINE
TI - Enhancing arsenic removal from arsenic-contaminated water by Echinodorus
cordifolius-endophytic Arthrobacter creatinolyticus interactions.
AU - Prum C
AD - School of Bioresources and Technology, King Mongkut's University of
Technology Thonburi, Bangkok 10150, Thailand.
AU - Dolphen R
AD - Pilot Plant Development and Training Institute, King Mongkut's University of
Technology Thonburi, Bangkok 10150, Thailand.
AU - Thiravetyan P
AD - School of Bioresources and Technology, King Mongkut's University of
Technology Thonburi, Bangkok 10150, Thailand. Electronic address:
paitip.thi@kmutt.ac.th.
SO - J Environ Manage. 2018, May 01; 213:11-19. [Journal of environmental
management]
AB - In this study, Echinodorus cordifolius was the best plant for arsenic
removal compared to Cyperus alternifolius, Acrostichum aureum and
Colocasia esculenta. Under arsenic stress, the combination of
E. cordifolius with microbes (Bacillus subtilis and Arthrobacter
creatinolyticus) was investigated. It was found that
A. creatinolyticus, a native microbe, can endure arsenic toxicity,
produce higher indole-3 acetic acid (IAA) and ammonium production better
than B. subtilis. Interestingly, E. cordifolius-endophytic
A. creatinolyticus interactions showed that dipping plant roots in
A. creatinolyticus suspension for 5&#8239;min had the highest arsenic
removal efficiency compared to dipping plant roots in
A. creatinolyticus suspension for 2&#8239;h and inoculating
A. creatinolyticus with E. cordifolius directly. Our findings
indicated that under this inoculation condition, the inoculum could
colonize from the roots to the shoots of the host tissues in order to
avoid arsenic toxicity and favored arsenic removal by the host through
plant growth-promoting traits, such as IAA production. Highest levels of
IAA were found in plant tissues and the plants exhibited higher root
elongation than other conditions. Moreover, low level of reactive oxygen
species (ROS) was related to low arsenic stress. In addition, dipping
E. cordifolius roots in A. creatinolyticus for 5&#8239;min was
applied in a constructed wetland, the result showed higher arsenic removal
than conventional method. Therefore, this knowledge can be applied at a
real site for improving plant tolerance stress, plant growth stimulation,
and enhancing arsenic remediation.
KW - Arsenic
KW - Arthrobacter creatinolyticus
KW - Constructed wetland
KW - Echinodorus cordifolius
KW - Reactive oxygen species (ROS)
KW - indole−3−acetic acid (IAA)
LA - eng
IS - 1095-8630 (Electronic)
PT - Journal Article
TA - J Environ Manage
YR - 2018
DATE- 20180313
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Journal of environmental management
EDAT- 20180222
STAT- In-Process
DOCNO- medline/29477846
116 - TOXLINE
TI - N6-methyladenosine mediates the cellular proliferation and apoptosis via
microRNAs in arsenite-transformed cells.
AU - Gu S
AD - Department of Environmental and Occupational Health, West China School of
Public Health, Sichuan University, Chengdu, Sichuan, People's Republic of China.
AU - Sun D
AD - Department of Environmental and Occupational Health, West China School of
Public Health, Sichuan University, Chengdu, Sichuan, People's Republic of China.
AU - Dai H
AD - Department of Environmental and Occupational Health, West China School of
Public Health, Sichuan University, Chengdu, Sichuan, People's Republic of China.
AU - Zhang Z
AD - Department of Environmental and Occupational Health, West China School of
Public Health, Sichuan University, Chengdu, Sichuan, People's Republic of China.
Electronic address: zhangzunzhen@163.com.
SO - Toxicol Lett. 2018, Aug; 292:1-11. [Toxicology letters]
AB - N6-methyladenosine (m6A) modification is implicated to play an important
role in cellular biological processes, but its regulatory mechanisms in
arsenite-induced carcinogenesis are largely unknown. Here, human bronchial
epithelial (HBE) cells were chronically treated with 2.5&#8239;&mu;M
arsenite sodium (NaAsO2) for about 13 weeks and these cells were
identified with malignant phenotype which was demonstrated by increased
levels of cellular proliferation, percentages of plate colony formation
and soft agar clone formation, and high potential of resistance to
apoptotic induction. Our results firstly demonstrated that m6A
modification on RNA was significantly increased in arsenite-transformed
cells and this modification may be synergistically regulated by
methyltransferase-like 3 (METTL3), methyltransferase-like 14 (METTL14),
Wilms tumor 1-associated protein (WTAP) and Fat mass and
obesity-associated protein (FTO). In addition, knocking down of METTL3 in
arsenite-transformed cells can dramatically reverse the malignant
phenotype, which was manifested by lower percentages of clone and colony
formation as well as higher rates of apoptotic induction. Given the
critical roles of miRNAs in cellular proliferation and apoptosis, miRNAs
regulated by m6A in arsenite-transformed cells were analyzed by Venn
diagram and KEGG pathway in this study. The results showed that these
m6A-mediated miRNAs can regulate pathways which are closely associated
with cellular proliferation and apoptosis, implicating that these miRNAs
may be the critical bridge by which m6A mediates dysregulation of cell
survival and apoptosis in arsenite-transformed cells. Taken together, our
results firstly demonstrated the significant role of m6A in the prevention
of tumor occurrence and progression induced by arsenite.
KW - Apoptosis
KW - Arsenite
KW - Cellular proliferation
KW - MicroRNA
KW - N(6)-methyladenosine
RN - 1867-73-8
RN - 48OVY2OC72
RN - EC 1.14.11.33
RN - EC 1.14.11.33
RN - EC 2.1.1.-
RN - EC 2.1.1.-
RN - EC 2.1.1.62
RN - K72T3FS567
LA - eng
IS - 1879-3169 (Electronic)
PT - Journal Article
TA - Toxicol Lett
YR - 2018
DATE- 20180612
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Toxicology letters
EDAT- 20180420
STAT- MEDLINE
DOCNO- medline/29680375

117 - TOXLINE
TI - The possible neuroprotective effect of ellagic acid on sodium
arsenate-induced neurotoxicity in rats.
AU - Goudarzi M
AD - Medicinal Plant Research Center, Ahvaz Jundishapur University of Medical
Sciences, Ahvaz, Iran; Student Research Committee, Ahvaz Jundishapur University of
Medical Sciences, Ahvaz, Iran.
AU - Amiri S
AD - Department of Pharmacology, School of Medicine, Iran University of Medical
Sciences, Tehran, Iran.
AU - Nesari A
AD - Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences,
Ahvaz, Iran.
AU - Hosseinzadeh A
AD - Air Pollution Research Center, Iran University of Medical Sciences, Tehran,
Iran.
AU - Mansouri E
AD - Cellular and Molecular Research Center, Department of Anatomical Sciences,
Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
AU - Mehrzadi S
AD - Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran.
Electronic address: mehrzadi.s@iums.ac.ir.
SO - Life Sci. 2018, Apr 01; 198:38-45. [Life sciences]
AB - OBJECTIVE: Arsenic is a well-known environmental contaminant, causing
toxicity in different organs. The aim of this study was to investigate the
possible neuroprotective effect of ellagic acid (EA) on arsenic-induced
neurotoxicity in rats.
AB - DESIGN: Animals were divided into five groups. The first group received
normal saline (2&#8239;mL/kg) for 21&#8239;days as control group. Group 2
was orally treated with sodium arsenite (SA, 10&#8239;mg/kg) for
21&#8239;days. Groups 3 and 4 were orally treated with SA (10&#8239;mg/kg)
for 7&#8239;days prior to EA (10 and 30&#8239;mg/kg respectively)
treatment and continued up to 21&#8239;days simultaneously with SA
administration. Group 5 was orally treated with EA (30&#8239;mg/kg) for
14&#8239;days. Passive avoidance test and rotarod test were done to
evaluate the behavioral changes following SA and/or EA treatment.
Different biochemical, histological and molecular biomarkers were assessed
in the brain tissue.
AB - RESULTS: Our data showed that SA significantly elevated brain tissue
arsenic levels and malondialdehyde, nitric oxide, protein carbonylation,
tumor necrosis factor-alpha, and interlukein-1&beta; production. A
decrease in the total antioxidant capacity, reduced glutathione content
and glutathione peroxidase activity occurred in the brain of rats exposed
to SA. SA-treated rats showed a significant impairment in
long-term-memory, motor coordination and equilibrium. These results were
supported by histopathological observations of the brain. Results revealed
that administration of EA (30&#8239;mg/kg) reversed all neural markers
alternation and ameliorated behavioral and histopathological changes
induced by SA.
AB - CONCLUSION: EA can effectively protect brain tissue against SA-induced
neurotoxicity via its antioxidant and anti-inflammatory effects.
KW - Ellagic acid
KW - Neuroprotection
KW - Oxidative stress
KW - Rat
KW - Sodium arsenite
RN - 19YRN3ZS9P
RN - 31C4KY9ESH
RN - 7XO134LHLN
RN - EC 1.11.1.9
LA - eng
IS - 1879-0631 (Electronic)
PT - Journal Article
TA - Life Sci
YR - 2018
DATE- 20180409
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Life sciences
EDAT- 20180215
STAT- MEDLINE
DOCNO- medline/29455002

118 - TOXLINE
TI - Speciation, mobilization, and bioaccessibility of arsenic in geogenic soil
profile from Hong Kong.
AU - Cui JL
AD - Department of Civil and Environmental Engineering, The Hong Kong Polytechnic
University, Hung Hom, Kowloon, Hong Kong.
AU - Zhao YP
AD - Department of Civil and Environmental Engineering, The Hong Kong Polytechnic
University, Hung Hom, Kowloon, Hong Kong.
AU - Li JS
AD - Department of Civil and Environmental Engineering, The Hong Kong Polytechnic
University, Hung Hom, Kowloon, Hong Kong.
AU - Beiyuan JZ
AD - Department of Civil and Environmental Engineering, The Hong Kong Polytechnic
University, Hung Hom, Kowloon, Hong Kong.
AU - Tsang DCW
AD - Department of Civil and Environmental Engineering, The Hong Kong Polytechnic
University, Hung Hom, Kowloon, Hong Kong.
AU - Poon CS
AD - Department of Civil and Environmental Engineering, The Hong Kong Polytechnic
University, Hung Hom, Kowloon, Hong Kong.
AU - Chan TS
AD - National Synchrotron Radiation Research Center, 101 Hsin-Ann Road, Hsinchu
Science Park, Hsinchu 30076, Taiwan.
AU - Wang WX
AD - Division of Life Science, The Hong Kong University of Science and Technology
(HKUST), Clearwater Bay, Kowloon, Hong Kong.
AU - Li XD
AD - Department of Civil and Environmental Engineering, The Hong Kong Polytechnic
University, Hung Hom, Kowloon, Hong Kong. Electronic address: cexdli@polyu.edu.hk.
SO - Environ Pollut. 2018, Jan; 232:375-384. [Environmental pollution (Barking,
Essex : 1987)]
AB - The behaviour of arsenic (As) from geogenic soil exposed to aerobic
conditions is critical to predict the impact of As on the environment,
which processes remain unresolved. The current study examined the depth
profile of As in geologically derived subsoil cores from Hong Kong and
investigated the mobilization, plant availability, and bioaccessibility of
As in As-contaminated soil at different depths (0-45.8 m). Results
indicated significant heterogeneity, with high levels of As in three
layers of soil reaching up to 505 mg/kg at a depth of 5 m,
404 mg/kg at a depth of 15 m, and 1510 mg/kg at a depth of
27-32 m. Arsenic in porewater samples was < 11.5 &mu;g/L in
the study site. X-ray absorption spectroscopy (XAS) indicated that main As
species in soil was arsenate (As(V)), as adsorbed fraction to Fe oxides
(41-69% on goethite and 0-8% on ferrihydrite) or the mineral form
scorodite (30-57%). Sequential extraction procedure demonstrated that
0.5 &plusmn; 0.4% of As was exchangeable. Aerobic incubation
experiments exhibited that a very small amount (0.14-0.48 mg/kg) of
As was desorbed from the soil because of the stable As(V) complex
structure on abundant Fe oxides (mainly goethite), where indigenous
microbes partly (59 &plusmn; 18%) contributed to the release of
As comparing with the sterilized control. Furthermore, no As toxicity in
the soil was observed with the growth of ryegrass. The bioaccessibility of
As was < 27% in the surface soil using simplified bioaccessibility
extraction test. Our systematic evaluation indicated that As in the
geogenic soil profile from Hong Kong is relatively stable exposing to
aerobic environment. Nevertheless, children and workers should avoid
incidental contact with excavated soil, because high concentration of As
was present in the digestive solution ( < 0.1-268 &mu;g/L).
KW - Aerobic incubation
KW - Arsenic biogeochemistry
KW - Bioaccessibility
KW - Fe oxide
KW - Mobility
RN - 1310-14-1
RN - 87PZU03K0K
RN - N712M78A8G
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180122
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Environmental pollution (Barking, Essex : 1987)
EDAT- 20170928
STAT- MEDLINE
DOCNO- medline/28966030

119 - TOXLINE
TI - miR-145 via targeting ERCC2 is involved in arsenite-induced DNA damage in
human hepatic cells.
AU - Wei S
AD - The Key Laboratory of Environmental Pollution Monitoring and Disease Control,
Ministry of Education, Department of Toxicology, School of Public Health, Guizhou
Medical University, Guiyang 550025, Guizhou, People's Republic of China.
AU - Xue J
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing 211166, Jiangsu, People's
Republic of China.
AU - Sun B
AD - The Key Laboratory of Environmental Pollution Monitoring and Disease Control,
Ministry of Education, Department of Toxicology, School of Public Health, Guizhou
Medical University, Guiyang 550025, Guizhou, People's Republic of China.
AU - Zou Z
AD - The Key Laboratory of Environmental Pollution Monitoring and Disease Control,
Ministry of Education, Department of Toxicology, School of Public Health, Guizhou
Medical University, Guiyang 550025, Guizhou, People's Republic of China.
AU - Chen C
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing 211166, Jiangsu, People's
Republic of China.
AU - Liu Q
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing 211166, Jiangsu, People's
Republic of China. Electronic address: drqzliu@hotmail.com.
AU - Zhang A
AD - The Key Laboratory of Environmental Pollution Monitoring and Disease Control,
Ministry of Education, Department of Toxicology, School of Public Health, Guizhou
Medical University, Guiyang 550025, Guizhou, People's Republic of China. Electronic
address: aihuagzykd@163.com.
SO - Toxicol Lett. 2018, Apr 26. [Toxicology letters]
AB - Arsenic, an established human carcinogen, causes genetic toxicity.
However, the molecular mechanisms involved remain unknown. MicroRNAs
(miRNAs) are regulators that participate in fundamental cellular
processes. In the present investigation, we selected, as research
subjects, patients with arsenic poisoning caused by burning of coal in
Guizhou Province, China. For these patients, the plasma levels of miR-145
were up-regulated. In L-02 cells, arsenite, an active form of arsenic,
induced up-regulation of miR-145 and down-regulation of ERCC1 and ERCC2,
and caused DNA damage. For L-02 cells, transfection with an miR-145
inhibitor prevented arsenite-induced DNA damage and decreased ERCC2
levels. Luciferase reporter assays showed that miR-145 regulated ERCC2
expression by targeting the 3'-UTR of ERCC2, but not that for ERCC1. The
present results demonstrate that arsenite induces the over-expression of
miR-145 and inhibits DNA repair via targeting ERCC2, thus promoting DNA
damage. The information provides a new mechanism for arsenic-induced liver
injury.
KW - DNA repair
KW - ERCC2
KW - arsenicosis
KW - liver damage
KW - miR-145
KW - microRNAs
LA - eng
IS - 1879-3169 (Electronic)
PT - Journal Article
TA - Toxicol Lett
YR - 2018
DATE- 20180429
CI - Copyright &copy; 2018. Published by Elsevier B.V.
CITO- NLM
CS - Netherlands
FJT - Toxicology letters
EDAT- 20180426
STAT- Publisher
DOCNO- medline/29705342

120 - TOXLINE
TI - Developmental Neurotoxicity of Arsenic: Involvement of Oxidative Stress
and Mitochondrial Functions.
AU - Chandravanshi LP
AD - Developmental Toxicology Division, CSIR-Indian Institute of Toxicology
Research, Post Box No. 80, MG Marg, Lucknow, 226 001, India.
chandravanshi04@gmail.com.
AU - Gupta R
AD - Developmental Toxicology Division, CSIR-Indian Institute of Toxicology
Research, Post Box No. 80, MG Marg, Lucknow, 226 001, India.
AU - Shukla RK
AD - Department of Biochemistry, All India Institute of Medical Sciences, Bhopal,
India.
SO - Biol Trace Elem Res. 2018, Mar 03. [Biological trace element research]
AB - Over the last decade, there has been an increased concern about the health
risks from exposure to arsenic at low doses, because of their neurotoxic
effects on the developing brain. The exact mechanism underlying
arsenic-induced neurotoxicity during sensitive periods of brain
development remains unclear, although enhanced oxidative stresses, leading
to mitochondrial dysfunctions might be involved. Here, we highlight the
generation of reactive oxygen species (ROS) and oxidative stress which
leads to mitochondrial dysfunctions and apoptosis in arsenic-induced
developmental neurotoxicity. Here, the administration of sodium arsenite
at doses of 2 or 4 mg/kg body weight in female rats from gestational
to lactational (GD6-PD21) resulted to increased ROS, led to oxidative
stress, and increased the apoptosis in the frontal cortex, hippocampus,
and corpus striatum of developing rats on PD22, compared to controls.
Enhanced levels of ROS were associated with decreased mitochondrial
membrane potential and the activity of mitochondrial complexes, and
hampered antioxidant levels. Further, neuronal apoptosis, as measured by
changes in the expression of pro-apoptotic (Bax, Caspase-3),
anti-apoptotic (Bcl2), and stress marker proteins (p-p38, pJNK) in
arsenic-exposed rats, was discussed. The severities of changes were found
to more persist in the corpus striatum than in other brain regions of
arsenic-exposed rats even after the withdrawal of exposure on PD45 as
compared to controls. Therefore, our results indicate that perinatal
arsenic exposure leads to abrupt changes in ROS, oxidative stress, and
mitochondrial functions and that apoptotic factor in different brain
regions of rats might contribute to this arsenic-induced developmental
neurotoxicity.
KW - Apoptosis
KW - Arsenic
KW - Developmental neurotoxicity
KW - Mitochondria
KW - Oxidative stress
LA - eng
IS - 1559-0720 (Electronic)
PT - Journal Article
TA - Biol Trace Elem Res
YR - 2018
DATE- 20180304
CITO- NLM
CS - United States
FJT - Biological trace element research
EDAT- 20180303
STAT- Publisher
DOCNO- medline/29502250

121 - TOXLINE
TI - Low arsenic concentrations impair memory in rat offpring exposed during
pregnancy and lactation: Role of &alpha;7 nicotinic receptor, glutamate
and oxidative stress.
AU - M�naco NM
AD - Laboratorio de Toxicolog�a, Instituto de Investigaciones Biol�gicas y
Biom�dicas del Sur (INBIOSUR), Departamento de Biolog�a, Bioqu�mica y Farmacia,
Universidad Nacional del Sur, Consejo Nacional de Investigaciones Cient�ficas y
T�cnicas (CONICET), Depto. de Biolog�a, Bioqu�mica y Farmacia, San Juan 670, 8000
Bah�a Blanca, Argentina.
AU - Bartos M
AD - Laboratorio de Toxicolog�a, Instituto de Investigaciones Biol�gicas y
Biom�dicas del Sur (INBIOSUR), Departamento de Biolog�a, Bioqu�mica y Farmacia,
Universidad Nacional del Sur, Consejo Nacional de Investigaciones Cient�ficas y
T�cnicas (CONICET), Depto. de Biolog�a, Bioqu�mica y Farmacia, San Juan 670, 8000
Bah�a Blanca, Argentina.
AU - Dominguez S
AD - Laboratorio de Toxicolog�a, Instituto de Investigaciones Biol�gicas y
Biom�dicas del Sur (INBIOSUR), Departamento de Biolog�a, Bioqu�mica y Farmacia,
Universidad Nacional del Sur, Consejo Nacional de Investigaciones Cient�ficas y
T�cnicas (CONICET), Depto. de Biolog�a, Bioqu�mica y Farmacia, San Juan 670, 8000
Bah�a Blanca, Argentina.
AU - Gallegos C
AD - Laboratorio de Toxicolog�a, Instituto de Investigaciones Biol�gicas y
Biom�dicas del Sur (INBIOSUR), Departamento de Biolog�a, Bioqu�mica y Farmacia,
Universidad Nacional del Sur, Consejo Nacional de Investigaciones Cient�ficas y
T�cnicas (CONICET), Depto. de Biolog�a, Bioqu�mica y Farmacia, San Juan 670, 8000
Bah�a Blanca, Argentina.
AU - Bras C
AD - Laboratorio de Toxicolog�a, Instituto de Investigaciones Biol�gicas y
Biom�dicas del Sur (INBIOSUR), Departamento de Biolog�a, Bioqu�mica y Farmacia,
Universidad Nacional del Sur, Consejo Nacional de Investigaciones Cient�ficas y
T�cnicas (CONICET), Depto. de Biolog�a, Bioqu�mica y Farmacia, San Juan 670, 8000
Bah�a Blanca, Argentina.
AU - Esandi MDC
AD - Instituto de Investigaciones Bioqu�micas de Bah�a Blanca (INIBIBB),
Departamento de Biolog�a, Bioqu�mica y Farmacia, Universidad Nacional del Sur,
Consejo Nacional de Investigaciones Cient�ficas y T�cnicas (CONICET), Depto. de
Biolog�a, Bioqu�mica y Farmacia, Camino La Carrindanga km7, Bah�a Blanca,
Argentina.
AU - Bouzat C
AD - Instituto de Investigaciones Bioqu�micas de Bah�a Blanca (INIBIBB),
Departamento de Biolog�a, Bioqu�mica y Farmacia, Universidad Nacional del Sur,
Consejo Nacional de Investigaciones Cient�ficas y T�cnicas (CONICET), Depto. de
Biolog�a, Bioqu�mica y Farmacia, Camino La Carrindanga km7, Bah�a Blanca,
Argentina.
AU - Giannuzzi L
AD - Centro de Investigaci�n y Desarrollo en Criotecnolog�a de Alimentos (CIDCA),
CCT-La Plata, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, 1900
La Plata, Argentina.
AU - Minetti A
AD - Laboratorio de Toxicolog�a, Instituto de Investigaciones Biol�gicas y
Biom�dicas del Sur (INBIOSUR), Departamento de Biolog�a, Bioqu�mica y Farmacia,
Universidad Nacional del Sur, Consejo Nacional de Investigaciones Cient�ficas y
T�cnicas (CONICET), Depto. de Biolog�a, Bioqu�mica y Farmacia, San Juan 670, 8000
Bah�a Blanca, Argentina.
AU - Gumilar F
AD - Laboratorio de Toxicolog�a, Instituto de Investigaciones Biol�gicas y
Biom�dicas del Sur (INBIOSUR), Departamento de Biolog�a, Bioqu�mica y Farmacia,
Universidad Nacional del Sur, Consejo Nacional de Investigaciones Cient�ficas y
T�cnicas (CONICET), Depto. de Biolog�a, Bioqu�mica y Farmacia, San Juan 670, 8000
Bah�a Blanca, Argentina. Electronic address: fgumilar@criba.edu.ar.
SO - Neurotoxicology. 2018, Apr 17; 67:37-45. [Neurotoxicology]
AB - Inorganic arsenic (iAs) is an important natural pollutant. Millions of
individuals worldwide drink water with high levels of iAs. Arsenic
exposure has been associated to cognitive deficits. However, the
underlying mechanisms remain unknown. In the present work we investigated
in female adult offspring the effect of the exposure to low arsenite
sodium levels through drinking water during pregnancy and lactation on
short- and long-term memory. We also considered a possible underlying
neurotoxic mechanism. Pregnant rats were exposed during pregnancy and
lactation to environmentally relevant iAs concentrations (0.05 and
0.10&#8239;mg/L). In 90-day-old female offspring, short-term memory (STM)
and long-term memory (LTM) were evaluated using a step-down inhibitory
avoidance task. In addition, we evaluated the &alpha;7 nicotinic receptor
(&alpha;7-nAChR) expression, the transaminases and the oxidative stress
levels in hippocampus. The results showed that the exposure to
0.10&#8239;mg/L iAs in this critical period produced a significant
impairment in the LTM retention. This behavioral alteration might be
associated with several events that occur in the hippocampus: decrease in
&alpha;7-nAChR expression, an increase of glutamate levels that may
produce excitotoxicity, and a decrease in the antioxidant enzyme catalase
(CAT) activity.
KW - Arsenic
KW - Female rats
KW - Glutamate
KW - Oxidative stress
KW - α7-nicotinic receptor
LA - eng
IS - 1872-9711 (Electronic)
PT - Journal Article
TA - Neurotoxicology
YR - 2018
DATE- 20180616
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Neurotoxicology
EDAT- 20180417
STAT- Publisher
DOCNO- medline/29678590

122 - TOXLINE
TI - Mussels and clams from the italian fish market. is there a human
exposition risk to metals and arsenic?
AU - Chiesa LM
AD - Department of Health, Animal Science and Food Safety, University of Milan,
Via Celoria, 10, 20133 Milan, Italy.
AU - Ceriani F
AD - Department of Health, Animal Science and Food Safety, University of Milan,
Via Celoria, 10, 20133 Milan, Italy.
AU - Caligara M
AD - Department of Biomedical Sciences for Health, University of Milan, Via L.
Mangiagalli, 37, 20133 Milan, Italy.
AU - Di Candia D
AD - Department of Biomedical, Surgical and Dental Sciences, University of Milan,
Via L. Mangiagalli, 37, 20133 Milan, Italy.
AU - Malandra R
AD - ATS Milano-Citt� metropolitana, Veterinary Unit, Via Celoria 10, 20133 Milan,
Italy.
AU - Panseri S
AD - Department of Health, Animal Science and Food Safety, University of Milan,
Via Celoria, 10, 20133 Milan, Italy. Electronic address: sara.panseri@unimi.it.
AU - Arioli F
AD - Department of Health, Animal Science and Food Safety, University of Milan,
Via Celoria, 10, 20133 Milan, Italy.
SO - Chemosphere. 2018, Mar; 194:644-649. [Chemosphere]
AB - Seafood is associated with many beneficial effects on human health.
However, the overall level of contaminants in biota has increased over the
last two centuries and seafood is one of the source of oral exposition to
contaminants. Therefore, this work aimed to evaluate cadmium, lead,
mercury, arsenic, chromium and nickel presence in mussels and clams, from
the Italian market, and the associated risk. The samples were from five
different FAO areas. Analyses were carried out using inductively-coupled
plasms-mass spectrometry. The sample concentrations were below the maximum
levels stated by Commission Regulation (EC) 1881/2006, except one mussel
sample, which was non-compliant for cadmium
(2.13 &plusmn; 0.20 mg kg-1). For arsenic, nickel and
chromium, maximum levels are not stated by the European Union. In this
study, arsenic ranged from 1.29 to 13.35 mg kg-1 and nickel
ranged from < LOQ-3.98 mg kg-1, except one sample, whose
nickel concentration was 21.70 mg kg-1. Chromium was found only
in 15 samples, with a maximum concentration of
2.81 &plusmn; 0.27 mg kg-1, in one clam sample. Our
results indicate that the average Italian consumption of molluscs, does
not pose a risk for consumers, except nickel, which can cause allergic
dermatitis in nickel-sensitive individuals. However a particular concern
is caused by the exposition to As of the 95th percentile consumers: the
Hazard Index for skin lesions, was > 1, and BMDL10 for lung bladder and
skin cancer in all mussel samples was overcome, in the 100% and 25% of
mussel and clam samples, respectively.
KW - Arsenic
KW - Clams
KW - Health risk
KW - ICP-MS
KW - Metals
KW - Mussels
RN - N712M78A8G
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180402
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171222
STAT- MEDLINE
DOCNO- medline/29241139

123 - TOXLINE
TI - Effects of elevated sulfate concentration on the mobility of arsenic in
the sediment-water interface.
AU - Li S
AD - School of Ecology and Environmental Science &amp; Yunnan Key Laboratory for
Plateau Mountain Ecology and Restoration of Degraded Environments, Yunnan
University, Kunming 650091, China; Institute of Environment Sciences, Department of
Biology Science, University of Quebec at Montreal, Montreal, Canada C3H 3P8.
AU - Yang C
AD - School of Ecology and Environmental Science &amp; Yunnan Key Laboratory for
Plateau Mountain Ecology and Restoration of Degraded Environments, Yunnan
University, Kunming 650091, China. Electronic address: YANGCL227@163.com.
AU - Peng C
AD - Institute of Environment Sciences, Department of Biology Science, University
of Quebec at Montreal, Montreal, Canada C3H 3P8.
AU - Li H
AD - Institute of Environment Sciences, Department of Biology Science, University
of Quebec at Montreal, Montreal, Canada C3H 3P8; Faculty of Land Resource
Engineering, Kunming University of Science and Technology, Kunming 650093, China.
AU - Liu B
AD - School of Ecology and Environmental Science &amp; Yunnan Key Laboratory for
Plateau Mountain Ecology and Restoration of Degraded Environments, Yunnan
University, Kunming 650091, China.
AU - Chen C
AD - Institute of International rivers and eco-security, Yunnan University,
Kunming 650091, China.
AU - Chen B
AD - Institute of International rivers and eco-security, Yunnan University,
Kunming 650091, China.
AU - Bai J
AD - Institute of International rivers and eco-security, Yunnan University,
Kunming 650091, China.
AU - Lin C
AD - Institute of International rivers and eco-security, Yunnan University,
Kunming 650091, China.
SO - Ecotoxicol Environ Saf. 2018, Jun 15; 154:311-320. [Ecotoxicology and
environmental safety]
AB - The adsorption/desorption of arsenic (As) at the sediment-water interface
in lakes is the key to understanding whether As can enter the ecosystem
and participate in material circulation. In this study, the concentrations
of As(III), total arsenic [As(T)], sulfide, iron (Fe), and dissolved
organic carbon (DOC) in overlying water were observed after the initial
sulfate (SO42-) concentrations were increased by four gradients in the
presence and absence of microbial systems. The results indicate that
increased SO42- concentrations in overlying water triggered As desorption
from sediments. Approximately 10% of the desorbed As was desorbed directly
as arsenite or arsenate by competitive adsorption sites on the iron salt
surface; 21% was due to the reduction of iron (hydr)oxides; and 69% was
due to microbial activity, as compared with a system with no microbial
activity. The intensity of microbial activity was controlled by the SO42-
and DOC concentrations in the overlying water. In anaerobic systems, which
had SO42- and DOC concentrations higher than 47 and 7&#8239;mg/L,
respectively, microbial activity was promoted by SO42- and DOC; As(III)
was desorbed under these indoor simulation conditions. When either the
SO42- or DOC concentration was lower than its respective threshold of 47
or 7&#8239;mg/L, or when either of these indices was below its
concentration limit, it was difficult for microorganisms to use SO42- and
DOC to enhance their own activities. Therefore, conditions were
insufficient for As desorption. The migration of As in lake sediments was
dominated by microbial activity, which was co-limited by SO42- and DOC.
The concentrations of SO42- and DOC in the overlying water are thus
important for the prevention and control of As pollution in lakes. We
recommend controlling SO42- and DOC concentrations as a method for
controlling As inner-source pollution in lake water.
KW - Arsenic contamination
KW - Lake sediment
KW - Sediment–water interface
KW - Water pollution
RN - E1UOL152H7
LA - eng
IS - 1090-2414 (Electronic)
PT - Journal Article
TA - Ecotoxicol Environ Saf
YR - 2018
DATE- 20180614
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Ecotoxicology and environmental safety
STAT- MEDLINE
DOCNO- medline/29482126

124 - TOXLINE
TI - Effect of subchronic exposure to inorganic arsenic on the structure and
function of the intestinal epithelium.
AU - Chiocchetti GM
AD - Instituto de Agroqu�mica y Tecnolog�a de Alimentos (IATA-CSIC), Calle Agust�n
Escardino 7, 46980, Paterna, Valencia, Spain.
AU - V�lez D
AD - Instituto de Agroqu�mica y Tecnolog�a de Alimentos (IATA-CSIC), Calle Agust�n
Escardino 7, 46980, Paterna, Valencia, Spain.
AU - Devesa V
AD - Instituto de Agroqu�mica y Tecnolog�a de Alimentos (IATA-CSIC), Calle Agust�n
Escardino 7, 46980, Paterna, Valencia, Spain. Electronic address:
vdevesa@iata.csic.es.
SO - Toxicol Lett. 2018, Apr; 286:80-88. [Toxicology letters]
AB - Inorganic arsenic (As), the most toxic form of As found in water and food,
is considered a human carcinogen. Numerous studies show its systemic
toxicity, describing pathologies associated with chronic exposure. The
main pathway of exposure to inorganic As is oral, but many of the events
that occur during its passage through the gastrointestinal tract are
unknown. This study evaluates the effect of subchronic exposure to
inorganic As [As(III): 0.025-0.1&#8239;mg/L; As(V): 0.25-1&#8239;mg/L, up
to 21&#8239;days] on the intestinal epithelium, using Caco-2 cells as in
vitro model. Inorganic As produces a pro-inflammatory response throughout
the exposure time, with an increase in IL-8 release (up to 488%). It also
causes changes in the program of cell proliferation and differentiation,
which leads to impairment of the cell repair process. In addition,
subchronic exposure affects the epithelial structure, causing loss of
microvilli, fundamental structures in the processes of intestinal
absorption and digestion. Moreover, the exposure affects the epithelial
barrier function, evidenced by an increase of Lucifer Yellow transport
(103-199%). Therefore, it can be concluded that subchronic exposure to
inorganic As can alter intestinal homeostasis, affecting the mucosal
layer, which performs the most important functions of the intestinal wall.
KW - Caco-2 cells
KW - Differentiation
KW - Inflammation
KW - Inorganic arsenic
KW - Intestinal epithelium
KW - Permeability
KW - Proliferation
KW - Subchronic exposure
KW - Wound healing
LA - eng
IS - 1879-3169 (Electronic)
PT - Journal Article
TA - Toxicol Lett
YR - 2018
DATE- 20180213
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Toxicology letters
EDAT- 20180131
STAT- In-Process
DOCNO- medline/29355690

125 - TOXLINE
TI - Association of H3K79 monomethylation (an epigenetic signature) with
arsenic-induced skin lesions.
AU - Bhattacharjee P
AD - Department of Zoology and Department of Environmental Science, University of
Calcutta, Kolkata 700019, India.
AU - Paul S
AD - Molecular Genetics Division, CSIR-Indian Institute of Chemical Biology,
Kolkata 700032, India.
AU - Bhattacharjee S
AD - Health-Management in Occupational Health, Siemens, India.
AU - Giri AK
AD - Molecular Genetics Division, CSIR-Indian Institute of Chemical Biology,
Kolkata 700032, India.
AU - Bhattacharjee P
AD - Department of Environmental Science, University of Calcutta, Kolkata 700019,
India. Electronic address: 777.pritha@gmail.com.
SO - Mutat Res. 2018, Jan; 807:1-9. [Mutation research]
AB - Arsenic, a non mutagenic carcinogen, poses a profound health risk upon
prolonged exposure. The objective of the study was to analyze the
post-translational modifications of the major histone H3 and the
associated molecular crosstalk to identify the epigenetic signature of
arsenic susceptibility. Herein, we identified significant upregulation of
H3K79me1, in individuals with arsenic-induced skin lesion (WSL), and
H3K79me1 was found to be regulated by the upstream methyltransferase
DOT1L. Moreover, the downstream target molecule 53BP1, a tumor suppressor
protein that has a docking preference for H3K79me1 at a site of a
double-strand break (DSB), was downregulated, indicating greater DNA
damage in the WSL group. Western blot data confirmed higher levels of
&gamma;H2AX, a known marker of DSBs, in group WSL. In vitro dose-response
analysis also confirmed the association of the H3K79me1 signature with
arsenic toxicity. Taken together, our findings revealed that H3K79me1 and
DOT1L could be a novel epigenetic signature of the arsenic-exposed WSL
group.
KW - Arsenic-induced skin lesion
KW - DNA damage
KW - DOT1L
KW - Epigenetic signature
KW - H3K79me1
LA - eng
IS - 1873-135X (Electronic)
PT - Journal Article
TA - Mutat Res
YR - 2018
DATE- 20180206
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Mutation research
EDAT- 20171114
STAT- In-Data-Review
DOCNO- medline/29161537

126 - TOXLINE
TI - Proteomics and genetic analyses reveal the effects of arsenite oxidation
on metabolic pathways and the roles of AioR in Agrobacterium tumefaciens
GW4.
AU - Shi K
AD - State Key Laboratory of Agricultural Microbiology, College of Life Science
and Technology, Huazhong Agricultural University, Wuhan, 430070, PR China.
AU - Wang Q
AD - State Key Laboratory of Agricultural Microbiology, College of Life Science
and Technology, Huazhong Agricultural University, Wuhan, 430070, PR China.
AU - Fan X
AD - State Key Laboratory of Agricultural Microbiology, College of Life Science
and Technology, Huazhong Agricultural University, Wuhan, 430070, PR China.
AU - Wang G
AD - State Key Laboratory of Agricultural Microbiology, College of Life Science
and Technology, Huazhong Agricultural University, Wuhan, 430070, PR China.
Electronic address: gejiao@mail.hzau.edu.cn.
SO - Environ Pollut. 2018, Apr; 235:700-709. [Environmental pollution (Barking,
Essex : 1987)]
AB - A heterotrophic arsenite [As(III)]-oxidizing bacterium Agrobacterium
tumefaciens GW4 isolated from As(III)-rich groundwater sediment showed
high As(III) resistance and could oxidize As(III) to As(V). The As(III)
oxidation could generate energy and enhance growth, and AioR was the
regulator for As(III) oxidase. To determine the related metabolic pathways
mediated by As(III) oxidation and whether AioR regulated other cellular
responses to As(III), isobaric tags for relative and absolute quantitation
(iTRAQ) was performed in four treatments, GW4 (+AsIII)/GW4 (-AsIII),
GW4-&Delta;aioR (+AsIII)/GW4-&Delta;aioR (-AsIII), GW4-&Delta;aioR
(-AsIII)/GW4 (-AsIII) and GW4-&Delta;aioR (+AsIII)/GW4 (+AsIII). A total
of 41, 71, 82 and 168 differentially expressed proteins were identified,
respectively. Using electrophoretic mobility shift assay (EMSA) and
qRT-PCR, 12 genes/operons were found to interact with AioR. These results
indicate that As(III) oxidation alters several cellular processes related
to arsenite, such as As resistance (ars operon), phosphate (Pi) metabolism
(pst/pho system), TCA cycle, cell wall/membrane, amino acid metabolism and
motility/chemotaxis. In the wild type with As(III), TCA cycle flow is
perturbed, and As(III) oxidation and fermentation are the main energy
resources. However, when strain GW4-&Delta;aioR lost the ability of
As(III) oxidation, the TCA cycle is the main way to generate energy. A
regulatory cellular network controlled by AioR is constructed and shows
that AioR is the main regulator for As(III) oxidation, besides, several
other functions related to As(III) are regulated by AioR in parallel.
KW - Arsenite oxidation regulator
KW - Arsenite resistance
KW - Comparative proteomics
KW - Energy
KW - Phosphate
RN - N5509X556J
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180604
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Environmental pollution (Barking, Essex : 1987)
EDAT- 20180112
STAT- MEDLINE
DOCNO- medline/29339339

127 - TOXLINE
TI - Antimony and arsenic partitioning during Fe2+-induced transformation of
jarosite under acidic conditions.
AU - Karimian N
AD - Southern Cross GeoScience, Southern Cross University, Lismore, NSW 2480,
Australia. Electronic address: niloofar.karimian@scu.edu.au.
AU - Johnston SG
AD - Southern Cross GeoScience, Southern Cross University, Lismore, NSW 2480,
Australia.
AU - Burton ED
AD - Southern Cross GeoScience, Southern Cross University, Lismore, NSW 2480,
Australia.
SO - Chemosphere. 2018, Mar; 195:515-523. [Chemosphere]
AB - Jarosite [KFe3(SO4)2(OH)6] is considered a potent scavenger for arsenic
(As) and antimony (Sb) under oxidizing conditions. Fluctuations in water
levels in re-flooded acid sulfate soils (ASS) can lead to high Fe2+(aq)
concentrations (&sim;10-20&#8239;mM) in the soil solution under acidic to
circumneutral pH conditions. This may create favorable conditions for the
Fe2+-induced transformation of jarosite. In this study, synthetic arsenate
[As(V)]/antimonate [Sb(V)]-bearing jarosite was subjected to Fe2+(aq)
(20&#8239;mM) at pH 4.0 and 5.5 for 24&#8239;h to simulate the pH and
Fe2+(aq) conditions of re-flooded freshwater ASS/acid mine drainage
(AMD)-affected environments at early and mid-stages of remediation,
respectively. The addition of Fe2+ at pH 5.5 resulted in the formation of
a metastable green rust sulfate (GR- SO4) phase within &sim;60&#8239;min,
which was replaced by goethite within 24&#8239;h. In contrast, at pH 4.0,
jarosite underwent no significant mineralogical transformation. Although
the addition of Fe2+(aq) induced the dissolution/transformation of
jarosite at pH 5.5 and increased the mobility of Sb during the initial
stages of the experiment (Sb(aq) = &sim;0.05&#8239;&mu;mol&#8239;L-1),
formation of metastable green rust (GR-SO4) and subsequent transformation
to goethite effectively sequestered dissolved Sb. Aqueous concentrations
of As remained negligible in both pH treatments, with As being mostly
repartitioned to the labile (&sim;10%) and poorly crystalline
Fe(III)-associated phases (&sim;10-30%). The results imply that, under
moderately acidic conditions (i.e. pH 5.5), reaction of Fe2+(aq) with
jarosite can drive the dissolution of jarosite and increase Sb mobility
prior to the formation of GR-SO4 and goethite. In addition, repartitioning
of As to the labile fractions at pH 5.5 may enhance the risk of its
mobilisation during future mineral transformation processes in Fe2+-rich
systems.
KW - Antimony
KW - Arsenic
KW - Fe(2+)
KW - Green rust
KW - Jarosite
KW - pH
RN - 1310-14-1
RN - 9IT35J3UV3
RN - N712M78A8G
RN - N7CIZ75ZPN
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180606
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171227
STAT- MEDLINE
DOCNO- medline/29277031

128 - TOXLINE
TI - Inorganic arsenic causes apoptosis cell death and immunotoxicity on
European sea bass (Dicentrarchus labrax).
AU - Cordero H
AD - Fish Innate Immune System Group, Department of Cell Biology and Histology,
Faculty of Biology, Regional Campus of International Excellence "Campus Mare
Nostrum", University of Murcia, 30100 Murcia, Spain.
AU - Morcillo P
AD - Albert Einstein College of Medicine, Jack and Pearl Resnick Campus, 1300
Morris Park Avenue, Bronx, 10461, NY, USA.
AU - Mart�nez S
AD - Department of Agricultural Chemistry, Geology and Pedology, Faculty of
Chemistry, Campus Regional de Excelencia Internacional "Campus Mare Nostrum",
University of Murcia, 30100 Murcia, Spain.
AU - Meseguer J
AD - Fish Innate Immune System Group, Department of Cell Biology and Histology,
Faculty of Biology, Regional Campus of International Excellence "Campus Mare
Nostrum", University of Murcia, 30100 Murcia, Spain.
AU - P�rez-Sirvent C
AD - Department of Agricultural Chemistry, Geology and Pedology, Faculty of
Chemistry, Campus Regional de Excelencia Internacional "Campus Mare Nostrum",
University of Murcia, 30100 Murcia, Spain.
AU - Chaves-Pozo E
AD - Centro Oceanogr�fico de Murcia, Instituto Espa�ol de Oceanograf�a (IEO),
Carretera de la Azoh�a s/n., 30860 Puerto de Mazarr�n, Murcia, Spain.
AU - Mart�nez-Sanchez MJ
AD - Department of Agricultural Chemistry, Geology and Pedology, Faculty of
Chemistry, Campus Regional de Excelencia Internacional "Campus Mare Nostrum",
University of Murcia, 30100 Murcia, Spain.
AU - Cuesta A
AD - Fish Innate Immune System Group, Department of Cell Biology and Histology,
Faculty of Biology, Regional Campus of International Excellence "Campus Mare
Nostrum", University of Murcia, 30100 Murcia, Spain.
AU - �ngeles Esteban M
AD - Fish Innate Immune System Group, Department of Cell Biology and Histology,
Faculty of Biology, Regional Campus of International Excellence "Campus Mare
Nostrum", University of Murcia, 30100 Murcia, Spain. Electronic address:
aesteban@um.es.
SO - Mar Pollut Bull. 2018, Mar; 128:324-332. [Marine pollution bulletin]
AB - Inorganic arsenic (As) is one of the most toxic pollutants in the water.
We have studied their effects on the marine teleost European sea bass
(Dicentrarchus labrax) at 2 and 10&#8239;days of 5&#8239;&mu;M of As2O3
(sub-lethal doses) waterborne exposure. Arsenic accumulates in liver and
gill tissues. The expression profile of five genes (bax, blc2, casp3,
casp8 and casp9) involved in apoptosis cell death confirmed apoptotic
effects in liver, slight changes in gill and no effects in skin according
with the histopathology findings. Total IgM level and peroxidase
activities were increased at 2 and 10&#8239;days, respectively. The
bactericidal activity was decreased at 2&#8239;days after As exposure. A
general decrease of cellular immune activities with significant
differences in the case of respiratory burst activity was observed after 2
and 10&#8239;days of exposure. This work describes for the first time the
effects of As exposure on European sea bass.
KW - Apoptosis
KW - Arsenic
KW - European sea bass (Dicentrarchus labrax)
KW - Immunotoxicology
LA - eng
IS - 1879-3363 (Electronic)
PT - Journal Article
TA - Mar Pollut Bull
YR - 2018
DATE- 20180324
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Marine pollution bulletin
EDAT- 20180206
STAT- In-Process
DOCNO- medline/29571380

129 - TOXLINE
TI - Urinary Arsenic in Human Samples from Areas Characterized by Natural or
Anthropogenic Pollution in Italy.
AU - Minichilli F
AD - National Research Council-Institute of Clinical Physiology, 56100 Pisa,
Italy. fabrizio.minichilli@ifc.cnr.it.
AU - Bianchi F
AD - National Research Council-Institute of Clinical Physiology, 56100 Pisa,
Italy. fabriepi@ifc.cnr.it.
AU - Ronchi AM
AD - Laboratory of Experimental and Clinical Toxicology, Maugeri Clinical
Scientific Institutes, 27100 Pavia, Italy. anna.ronchi@fsm.it.
AU - Gorini F
AD - National Research Council-Institute of Clinical Physiology, 56100 Pisa,
Italy. francesca.gorini@gmail.com.
AU - Bustaffa E
AD - National Research Council-Institute of Clinical Physiology, 56100 Pisa,
Italy. elisa.bustaffa@ifc.cnr.it.
SO - Int J Environ Res Public Health. 2018, Feb 09. [International journal of
environmental research and public health]
AB - Arsenic is ubiquitous and has a potentially adverse impact on human
health. We compared the distribution of concentrations of urinary
inorganic arsenic plus methylated forms (uc(iAs+MMA+DMA)) in four Italian
areas with other international studies, and we assessed the relationship
between uc(iAs+MMA+DMA) and various exposure factors. We conducted a human
biomonitoring study on 271 subjects (132 men) aged 20-44, randomly sampled
and stratified by area, gender, and age. Data on environmental and
occupational exposure and dietary habits were collected through a
questionnaire. Arsenic was speciated using chromatographic separation and
inductively coupled mass spectrometry. Associations between
uc(iAs+MMA+DMA) and exposure factors were evaluated using the geometric
mean ratio (GMR) with a 90% confidence interval by stepwise multiple
regression analysis. The 95th percentile value of uc(iAs+MMA+DMA) for the
whole sample (86.28 &micro;g/L) was higher than other national studies
worldwide. A statistical significant correlation was found between
uc(iAs+MMA+DMA) and occupational exposure (GMR: 2.68 [1.79-4.00]), GSTT
gene (GMR: 0.68 [0.52-0.80]), consumption of tap water (GMR: 1.35
[1.02-1.77]), seafood (GMR: 1.44 [1.11-1.88]), whole milk (GMR: 1.34
[1.04-1.73]), and fruit/vegetables (GMR: 1.37 [1.03-1.82]). This study
demonstrated the utility of uc(iAs+MMA+DMA) as a biomarker to assess
environmental exposure. In a public health context, this information could
be used to support remedial action, to prevent individuals from being
further exposed to environmental arsenic sources.
COI - The authors declare no conflict of interest.
KW - arsenic
KW - biomarker
KW - biomonitoring
KW - epidemiology
KW - urinary species
LA - eng
IS - 1660-4601 (Electronic)
PT - Journal Article
TA - Int J Environ Res Public Health
YR - 2018
DATE- 20180209
CITO- NLM
CS - Switzerland
FJT - International journal of environmental research and public health
EDAT- 20180209
STAT- In-Data-Review
DOCNO- medline/29425136

130 - TOXLINE
TI - Dimethylarsinic acid modulates the aryl hydrocarbon receptor-regulated
genes in C57BL/6 mice: in vivo study.
AU - Elshenawy OH
AD - a Faculty of Pharmacy and Pharmaceutical Sciences , University of Alberta ,
Edmonton , AB , Canada.
AU - Abdelhamid G
AD - b Department of Pharmacology and Toxicology , Faculty of Pharmacy, Helwan
University , Greater Cairo , Egypt , and.
AU - Althurwi HN
AD - c Department of Pharmacology , College of Pharmacy, Prince Sattam Bin
Abdulaziz University , Al Kharj , Kingdom of Saudi Arabia.
AU - El-Kadi AOS
AD - a Faculty of Pharmacy and Pharmaceutical Sciences , University of Alberta ,
Edmonton , AB , Canada.
SO - Xenobiotica. 2018, Feb; 48(2):124-134. [Xenobiotica; the fate of foreign
compounds in biological systems]
AB - 1.&emsp;Dimethylarsinic acid (DMA(V)) is the major metabolite of inorganic
arsenic in human body. Thus we investigated the effect of DMA(V) on the
alteration of phase I (typified by Cyp1a) and phase II (typified by Nqo1)
AhR-regulated genes in vivo. C57BL/6 mice received DMA(V)
(13.3&thinsp;mg/kg, i.p.) with or without TCDD (15&thinsp;&mu;g/kg, i.p.),
thereafter the liver, lung, and kidney were harvested at 6 and 24&thinsp;h
post-treatment. 2.&emsp;Results demonstrated that DMA(V) has no
significant effect on Cyp1a mRNA and protein expression or catalytic
activity in the liver. On the other hand, DMA(V) significantly potentiated
the TCDD-mediated induction of Cyp1a mRNA and protein expression, with a
subsequent potentiation of catalytic activity in the lung. Moreover,
DMA(V) significantly inhibited the TCDD-mediated induction of Cyp1a mRNA
and protein expression with subsequent inhibition of catalytic activity in
the kidney. 3.&emsp;Regarding to phase II AhR-regulated genes, DMA(V) has
no significant effect on Nqo1 mRNA and protein expression, or activity
neither in the liver, lung, or kidney. 4.&emsp;In conclusion, the present
work demonstrates for the first time that DMA(V) modulates AhR-regulated
genes in a tissue- and enzyme-specific manner. This modulation may play a
crucial role in arsenic-induced toxicity and carcinogenicity.
KW - AhR
KW - Cyp1a
KW - DMA(V)
KW - Nqo1
KW - arsenic
KW - cacodylic acid
KW - carcinogen-activating enzymes
KW - dimethylarsinic acid
RN - AJ2HL7EU8K
RN - EC 1.6.5.2
LA - eng
IS - 1366-5928 (Electronic)
PT - Journal Article
TA - Xenobiotica
YR - 2018
DATE- 20180102
CITO- NLM
CS - England
CSET- IM
FJT - Xenobiotica; the fate of foreign compounds in biological systems
EDAT- 20170221
STAT- MEDLINE
DOCNO- medline/28134025

131 - TOXLINE
TI - The secretome of adipose-derived mesenchymal stem cells protects SH-SY5Y
cells from arsenic-induced toxicity, independent of a neuron-like
differentiation mechanism.
AU - Curtis TM
AD - Department of Biological Sciences, State University of New York at Cortland,
Cortland, NY, United States. Electronic address: Theresa.curtis@cortland.edu.
AU - Hannett JM
AD - Department of Biological Sciences, State University of New York at Cortland,
Cortland, NY, United States.
AU - Harman RM
AD - Baker Institute for Animal Health, College of Veterinary Medicine, Cornell
University, Ithaca, NY, United States.
AU - Puoplo NA
AD - Department of Biological Sciences, State University of New York at Cortland,
Cortland, NY, United States.
AU - Van de Walle GR
AD - Baker Institute for Animal Health, College of Veterinary Medicine, Cornell
University, Ithaca, NY, United States.
SO - Neurotoxicology. 2018, Apr 13; 67:54-64. [Neurotoxicology]
AB - Arsenic exposure through contaminated food, water, and air causes
irreversible neural damage and affects millions of people worldwide.
Several studies have demonstrated that the secreted factors (secretome)
from mesenchymal stromal/stem cells (MSCs) can promote neural recovery
after several forms of injury including stroke and neurodegenerative
diseases. The present study was conducted to determine if the secretome
from adipose-derived MSCs (ADSCs) prevents arsenic damage to SH-SY5Y
cells. To this end, human neuroblastoma cells (SH-SY5Y) were pre-treated
with the secretome from ADSCs and then challenged with different
concentrations of arsenic. After various doses and exposure times, the
extent of neuronal injury was assessed using MTT reduction and LDH release
assays as well as LIVE/DEAD staining. These data demonstrate that the ADSC
secretome protects SH-SY5Y cells from arsenic-induced toxicity. Previous
reports have shown that the secretome of MSCs can induce neuroblast
differentiation and mature neurons are less susceptible to
chemical-induced toxicity. In the current study, proliferation assays,
neurite length assessment, and quantitative RT-PCR of differentiation
markers indicated that the ADSC secretome does not induce SH-SY5Y
differentiation into a mature neuron-like phenotype. In contrast, our
results demonstrated that soluble factor(s) in the ADSC secretome enhance
SH-SY5Y cell substrate-dependent adhesion. The present study is the first
to illustrate that the secretome from ADSCs protects SH-SY5Y cells from
arsenic-induced toxicity. Additionally, we showed that protection against
arsenic toxicity is not dependent on SH-SY5Y cell differentiation into a
mature neuron-like phenotype, but involves soluble factor(s) in the
secretome that appear to enhance cell survival by an adhesion-dependent
mechanism.
KW - Arsenic
KW - Cell adhesion
KW - Cell differentiation
KW - Mesenchymal stem cells
KW - Neuroprotection
KW - SH-SY5Y cells
KW - Secretome
LA - eng
IS - 1872-9711 (Electronic)
PT - Journal Article
TA - Neurotoxicology
YR - 2018
DATE- 20180616
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Neurotoxicology
EDAT- 20180413
STAT- Publisher
DOCNO- medline/29660375

132 - TOXLINE
TI - Vacuolar Phosphate Transporter 1 (VPT1) Affects Arsenate Tolerance by
Regulating Phosphate Homeostasis in Arabidopsis.
AU - Luan M
AD - State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University-
Nanjing Forestry University Joint Institute for Plant Molecular Biology, School of
Life Sciences, Nanjing University, Nanjing 210093, PR China.
AU - Liu J
AD - College of Animal Science &amp; Technology, Northwest A&amp;F University,
Yangling, Shanxi, 712100, China.
AU - Liu Y
AD - State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University-
Nanjing Forestry University Joint Institute for Plant Molecular Biology, School of
Life Sciences, Nanjing University, Nanjing 210093, PR China.
AU - Han X
AD - State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University-
Nanjing Forestry University Joint Institute for Plant Molecular Biology, School of
Life Sciences, Nanjing University, Nanjing 210093, PR China.
AU - Sun G
AD - State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University-
Nanjing Forestry University Joint Institute for Plant Molecular Biology, School of
Life Sciences, Nanjing University, Nanjing 210093, PR China.
AU - Lan W
AD - State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University-
Nanjing Forestry University Joint Institute for Plant Molecular Biology, School of
Life Sciences, Nanjing University, Nanjing 210093, PR China.
AU - Luan S
AD - Department of Plant and Microbial Biology, University of California,
Berkeley, CA 94720, USA.
SO - Plant Cell Physiol. 2018, Feb 06. [Plant & cell physiology]
AB - Arsenate [As(V)] is toxic to nearly all organisms. Soil-borne As(V) enters
plant cells mainly through the plasma membrane-localized phosphate (Pi)
transporters PHT1 family proteins due to its chemical similarity to Pi. We
report here that VPT1, a major vacuolar phosphate transporter contributes
to vacuolar Pi sequestration, is associated with As(V) tolerance in
Arabidopsis. vpt1 mutants displayed enhanced tolerance to As(V) toxicity,
whereas plants overexpressing VPT1 were more sensitive to As(V) as
compared to the wild type plants. Measurements of arsenic content
indicated that vpt1 mutants accumulated less arsenic and, in the contrast,
upregulating VPT1 expression contributed to higher levels of arsenic
accumulation in plants. To examine further how VPT1 may modulate arsenic
contents in plants, we surveyed the expression patterns of all the PHT1
family members that play roles in As(V) uptake and found that many of PHT1
genes were down regulated in the vpt1 mutant as compared to WT under Pi
sufficient condition, but not when Pi levels were low in medium.
Interestingly, As(V) sensitivity assays indicated that As(V) resistance in
vpt1 mutants were prominent only under Pi-sufficient but not under
Pi-deficient condition. These results suggest that under Pi-sufficient
condition, loss of VPT1 leads to elevated levels of Pi in the cytosol,
which in turn suppressed the expression of PHT1-type transporters and
reduced accumulation of arsenic.
KW - As(V) tolerance
KW - PHT1 genes
KW - Phosphate balance
KW - Vacuolar Phosphate Transporter1
LA - eng
IS - 1471-9053 (Electronic)
PT - Journal Article
TA - Plant Cell Physiol
YR - 2018
DATE- 20180208
CI - &copy; The Author 2018. Published by Oxford University Press on behalf of
Japanese Society of Plant Physiologists. All rights reserved. For
Permissions, please e-mail: journals.permissions@oup.com.
CITO- NLM
CS - Japan
FJT - Plant &amp; cell physiology
EDAT- 20180206
STAT- Publisher
DOCNO- medline/29420798

133 - TOXLINE
TI - The Arsenic Contamination of Drinking and Groundwaters in Bangladesh:
Featuring Biogeochemical Aspects and Implications on Public Health.
AU - Raessler M
AD - Max-Planck-Institut f�r Biogeochemie, Hans-Knoell-Strasse 10, PF 100164,
07745, Jena, Germany. raessler@bgc-jena.mpg.de.
SO - Arch Environ Contam Toxicol. 2018, Jul; 75(1):1-7. [Archives of
environmental contamination and toxicology]
AB - Arsenic is a widespread contaminant of drinking and groundwaters in the
world. Even if these contaminations have a geogenic origin, they often are
exacerbated by anthropogenic activities. This is particularly true for the
Bengal delta. Millions of people in Bangladesh are consuming drinking
water with arsenic concentrations &ge; 50 &micro;g/L. Their
drinking water supply is based on groundwaters extracted by pumping wells,
which were part of a well-drilling program by the United Nations. The
intention was to provide the people with groundwater instead of surface
water due to its critical hygienic conditions. Unfortunately, many wells
extract the groundwater at depths where arsenic concentrations are
highest. Arsenic is being dissolved from the aquifer by biogeochemical
processes that are fueled by the presence of high amounts of organics in
the Bengal delta sediments. This problem was not encountered at the time
due to a lack of chemical analyses of the waters.
RN - N712M78A8G
LA - eng
IS - 1432-0703 (Electronic)
PT - Journal Article
PT - Review
TA - Arch Environ Contam Toxicol
YR - 2018
DATE- 20180618
CITO- NLM
CS - United States
CSET- IM
FJT - Archives of environmental contamination and toxicology
EDAT- 20180308
STAT- MEDLINE
CM - Cites: Food Chem. 2017 Nov 1;234:76-80 (medline /28551270)
CM - Cites: Environ Health. 2014 Dec 04;13:101 (medline /25471535)
CM - Cites: Sci Total Environ. 2000 Aug 30;258(3):171-81 (medline /11007288)
CM - Cites: Environ Int. 2009 May;35(4):743-59 (medline /19232730)
CM - Cites: Sci Total Environ. 2017 Dec 1;601-602:122-131 (medline /28550725)
CM - Cites: Int J Epidemiol. 1998 Oct;27(5):871-7 (medline /9839746)
CM - Cites: Water Res. 2010 Nov;44(19):5556-74 (medline /20875661)
CM - Cites: Bull World Health Organ. 2000;78(9):1093-103 (medline /11019458)
CM - Cites: Ecotoxicol Environ Saf. 2015 Feb;112:247-70 (medline /25463877)
CM - Cites: PLoS One. 2015 Jul 22;10(7):e0131608 (medline /26200355)
CM - Cites: Environ Res. 2016 Nov;151:671-688 (medline /27619212)
CM - Cites: Environ Health Perspect. 2008 Jul;116(7):963-9 (medline /18629322)
CM - Cites: Chemosphere. 2016 Sep;158:37-49 (medline /27239969)
CM - Cites: Environ Sci Technol. 2009 Mar 1;43(5):1612-7 (medline /19350943)
CM - Cites: Nature. 2008 Jul 24;454(7203):505-8 (medline /18650922)
CM - Cites: Arch Environ Contam Toxicol. 2013 Jan;64(1):151-9 (medline
/23052359)
CM - Cites: Science. 2002 Nov 22;298(5598):1602-6 (medline /12446905)
CM - Cites: Science. 2003 May 9;300(5621):939-44 (medline /12738852)
CM - Cites: Trends Microbiol. 2005 Feb;13(2):45-9 (medline /15680760)
CM - Cites: Sci Total Environ. 2007 Jul 1;379(2-3):180-9 (medline /17067657)
CM - Cites: Environ Sci Technol. 2016 Apr 5;50(7):3469-76 (medline /27010474)
CM - Cites: Sci Total Environ. 2015 Sep 15;527-528:540-51 (medline /26004539)
CM - Cites: Environ Sci Technol. 2014 May 6;48(9):4699-706 (medline /24712677)
DOCNO- medline/29520432

134 - TOXLINE
TI - Arsenic exposure during embryonic development alters the expression of the
long noncoding RNA growth arrest specific-5 (Gas5) in a sex-dependent
manner.
AU - Caldwell KK
AD - Department of Neurosciences, University of New Mexico Health Sciences Center,
Albuquerque, NM 87131, United States.
AU - Hafez A
AD - Department of Neurosciences, University of New Mexico Health Sciences Center,
Albuquerque, NM 87131, United States.
AU - Solomon E
AD - Department of Neurosciences, University of New Mexico Health Sciences Center,
Albuquerque, NM 87131, United States.
AU - Cunningham M
AD - Department of Neurosciences, University of New Mexico Health Sciences Center,
Albuquerque, NM 87131, United States.
AU - Allan AM
AD - Department of Neurosciences, University of New Mexico Health Sciences Center,
Albuquerque, NM 87131, United States. Electronic address: aallan@salud.unm.edu.
SO - Neurotoxicol Teratol. 2018 Mar - Apr; 66:102-112. [Neurotoxicology and
teratology]
AB - Our previous studies suggest that prenatal arsenic exposure (50ppb)
modifies epigenetic control of the programming of the glucocorticoid
receptor (GR) signaling system in the developing mouse brain. These
deficits may lead to long-lasting consequences, including deficits in
learning and memory, increased depressive-like behaviors, and an altered
set-point of GR feedback throughout life. To understand the
arsenic-induced changes within the GR system, we assessed the impact of in
utero arsenic exposure on the levels of the GR and growth
arrest-specific-5 (Gas5), a noncoding RNA, across a key gestational period
for GR programming (gestational days, GD 14-18) in mice. Gas5 contains a
glucocorticoid response element (GRE)-like sequence that binds the GR,
thereby decreasing GR-GRE-dependent gene transcription and potentially
altering GR programming. Prenatal arsenic exposure resulted in
sex-dependent and age-dependent shifts in the levels of GR and Gas5
expression in fetal telencephalon. Nuclear GR levels were reduced in
males, but unchanged in females, at all gestational time points tested.
Total cellular Gas5 levels were lower in arsenic-exposed males with no
changes seen in arsenic-exposed females at GD16 and 18. An increase in
total cellular Gas-5 along with increased nuclear levels in GD14
arsenic-exposed females, suggests a differential regulation of cellular
compartmentalization of Gas5. RIP assays revealed reduced Gas5 associated
with the GR on GD14 in the nuclear fraction prepared from arsenic-exposed
males and females. This decrease in levels of GR-Gas5 binding continued
only in the females at GD18. Thus, nuclear GR signaling potential is
decreased in prenatal arsenic-exposed males, while it is increased or
maintained at levels approaching normal in prenatal arsenic-exposed
females. These findings suggest that females, but not males, exposed to
arsenic are able to regulate the levels of nuclear free GR by altering
Gas5 levels, thereby keeping GR nuclear signaling closer to control
(unexposed) levels.
KW - Arsenic
KW - Brain
KW - Development
KW - Gas5
KW - Glucocorticoid
KW - Sex differences
KW - lncRNA
LA - eng
IS - 1872-9738 (Electronic)
PT - Journal Article
TA - Neurotoxicol Teratol
YR - 2018
DATE- 20180318
CI - Copyright &copy; 2017 Elsevier Inc. All rights reserved.
CITO- NLM
CS - United States
FJT - Neurotoxicology and teratology
EDAT- 20171111
STAT- In-Data-Review
CM - Cites: Alcohol Clin Exp Res. 2006 Dec;30(12):2055-64 (medline /17117971)
CM - Cites: Mol Cell Biol. 1992 Aug;12(8):3514-21 (medline /1630459)
CM - Cites: Nat Rev Genet. 2004 Jul;5(7):522-31 (medline /15211354)
CM - Cites: Environ Health Perspect. 2012 Aug;120(8):1208-14 (medline
/22504586)
CM - Cites: Curr Mol Med. 2015;15(1):94-9 (medline /25601472)
CM - Cites: Nucleic Acids Res. 2015 Apr 20;43(7):3712-25 (medline /25779046)
CM - Cites: PLoS One. 2013 Sep 03;8(9):e73720 (medline /24019935)
CM - Cites: Environ Res. 2001 Oct;87(2):92-8 (medline /11683592)
CM - Cites: Front Physiol. 2015 Aug 19;6:230 (medline /26347657)
CM - Cites: Biochem J. 1998 Feb 15;330 ( Pt 1):573-9 (medline /9461558)
CM - Cites: Epigenetics. 2017 Aug;12 (8):607-615 (medline /28548590)
CM - Cites: BMC Cancer. 2012 Aug 29;12 :378 (medline /22931209)
CM - Cites: J Appl Toxicol. 2014 May;34(5):498-505 (medline /23765520)
CM - Cites: Early Hum Dev. 2004 Jan;76(1):47-54 (medline /14729162)
CM - Cites: Am J Public Health. 2004 Nov;94(11):1936-7 (medline /15514231)
CM - Cites: Endocrinology. 2002 Oct;143(10):3866-74 (medline /12239098)
CM - Cites: Sci Signal. 2010 Feb 02;3(107):ra8 (medline /20124551)
CM - Cites: J Biol Chem. 2015 Nov 20;290(47):28286-98 (medline /26446789)
CM - Cites: Oncogene. 2009 Jan 15;28(2):195-208 (medline /18836484)
CM - Cites: J Endocrinol. 2004 Apr;181(1):105-16 (medline /15072571)
CM - Cites: Oncol Res Treat. 2015;38(7-8):362-6 (medline /26278580)
CM - Cites: Mol Cell Biol. 1998 Dec;18(12):6897-909 (medline /9819378)
CM - Cites: Environ Health Perspect. 2011 Feb;119(2):258-64 (medline /20940111)
CM - Cites: Neurotoxicol Teratol. 2016 Jan-Feb;53:75-80 (medline /26689609)
CM - Cites: Neuroscience. 2017 Feb 7;342:4-20 (medline /26232714)
CM - Cites: Neurotoxicology. 2008 Jul;29(4):647-55 (medline /18573533)
CM - Cites: Toxicol Rep. 2015 Oct;2:1376-1390 (medline /26855884)
CM - Cites: Toxicol Sci. 2007 Sep;99(1):244-53 (medline /17569693)
CM - Cites: Environ Res. 2011 Jul;111(5):670-6 (medline /21439564)
CM - Cites: Biomed Res Int. 2013;2013:358015 (medline /24319682)
CM - Cites: J Dev Orig Health Dis. 2017 Apr;8(2):244-255 (medline /28103963)
CM - Cites: Environ Health. 2014 Mar 12;13(1):15 (medline /24621105)
CM - Cites: Clin Cancer Drugs. 2015;2(2):138-147 (medline /27054085)
CM - Cites: Brain Res Dev Brain Res. 1995 Jan 14;84(1):55-61 (medline /7720217)
CM - Cites: J Pharmacol Exp Ther. 2010 Oct;335(1):114-23 (medline /20605902)
CM - Cites: Mol Med. 1996 Nov;2(6):735-44 (medline /8972488)
CM - Cites: Mol Reprod Dev. 1997 Nov;48(3):310-6 (medline /9322241)
CM - Cites: Biochim Biophys Acta. 2013 Oct;1832(10):1613-23 (medline /23676682)
CM - Cites: Neurosci Biobehav Rev. 2017 May 18;:null (medline /28528960)
CM - Cites: Sci China Life Sci. 2016 Mar;59(3):227-35 (medline /26825947)
CM - Cites: Hippocampus. 2010 Sep;20(9):1027-36 (medline /19739230)
CM - Cites: Endocrinology. 2013 Dec;154(12):4560-9 (medline /24064364)
CM - Cites: Neurotoxicology. 2012 Oct;33(5):1338-45 (medline /22960421)
CM - Cites: Neurotoxicol Teratol. 2017 Jan - Feb;59:1-15 (medline /27751817)
CM - Cites: J Neuroendocrinol. 2016 Aug;28(8): (medline /26708929)
CM - Cites: J Cell Sci. 2008 Apr 1;121(Pt 7):939-46 (medline /18354083)
CM - Cites: Am J Hum Biol. 2010 May-Jun;22(3):330-5 (medline /19844898)
CM - Cites: J R Soc Interface. 2012 Dec 12;10(79):20120835 (medline /23235262)
CM - Cites: Am J Respir Crit Care Med. 2003 Dec 1;168(11):1317-23 (medline
/14500261)
CM - Cites: Biochim Biophys Acta. 2014 Mar;1840(3):1063-71 (medline /24184936)
CM - Cites: Sci Rep. 2015 May 11;5:10159 (medline /25959498)
CM - Cites: Int J Hyg Environ Health. 2014 Jul;217(6):678-86 (medline
/24698386)
CM - Cites: Pharmacol Biochem Behav. 2009 Dec;94(2):271-7 (medline /19751756)
CM - Cites: Physiol Behav. 2000 Nov 1-15;71(3-4):353-62 (medline /11150568)
CM - Cites: Environ Health. 2016 Mar 12;15:44 (medline /26968381)
CM - Cites: J Neuroendocrinol. 2014 Oct;26(10):707-23 (medline /25039443)
CM - Cites: Genes Dev. 2007 Aug 15;21(16):1993-8 (medline /17675447)
CM - Cites: Annu Rev Nutr. 2009;29:381-99 (medline /19575603)
CM - Cites: Genome Biol. 2015 Jan 29;16:20 (medline /25630241)
CM - Cites: Nat Neurosci. 2004 Aug;7(8):847-54 (medline /15220929)
CM - Cites: Curr Environ Health Rep. 2014 Mar 21;1:132-147 (medline /24860722)
CM - Cites: J Physiol. 2014 Jul 15;592(14 ):3127-41 (medline /24801305)
CM - Cites: Cell. 1988 Sep 9;54(6):787-93 (medline /3409319)
CM - Cites: Methods Mol Biol. 2004;261:15-32 (medline /15064447)
CM - Cites: Neuroscience. 2016 Apr 21;320:43-56 (medline /26844389)
CM - Cites: Arch Dis Child Fetal Neonatal Ed. 2000 Nov;83(3):F182-5 (medline
/11040165)
CM - Cites: Nucleic Acids Res. 2006 Mar 31;34(6):1765-71 (medline /16582102)
CM - Cites: EMBO J. 2014 May 2;33(9):937-8 (medline /24719208)
CM - Cites: Neurotoxicol Teratol. 2015 Jan-Feb;47:66-79 (medline /25459689)
CM - Cites: Birth Defects Res. 2017 Jul 17;109 (12 ):888-897 (medline
/28714605)
CM - Cites: Toxicol Appl Pharmacol. 2015 Oct 1;288(1):40-51 (medline /26193056)
CM - Cites: Trends Biochem Sci. 2016 Sep;41(9):761-772 (medline /27499234)
CM - Cites: Trends Cell Biol. 2017 Sep;27(9):685-696 (medline /28528987)
CM - Cites: Science. 2007 Jun 8;316(5830):1484-8 (medline /17510325)
CM - Cites: Environ Toxicol Pharmacol. 2012 Sep;34(2):381-387 (medline
/22728250)
CM - Cites: Ann N Y Acad Sci. 2004 Jun;1024:182-212 (medline /15265782)
CM - Cites: Endocrinology. 2012 Oct;153(10):4749-56 (medline /22962254)
CM - Cites: Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):14182-7 (medline
/8943081)
CM - Cites: Environ Res. 2017 Jul;156:74-79 (medline /28334644)
CM - Cites: Chem Soc Rev. 2008 Aug;37(8):1629-51 (medline /18648687)
CM - Cites: Am J Physiol Renal Physiol. 2015 May 15;308(10):F1065-73 (medline
/25715988)
CM - Cites: Int J Epidemiol. 2011 Dec;40(6):1593-604 (medline /22158669)
CM - Cites: J Endocrinol. 2017 Jan;232(1):37-48 (medline /27754933)
CM - Cites: Neurotoxicology. 2014 Sep;44:98-109 (medline /24952232)
CM - Cites: Crit Care Med. 2012 Oct;40(10):2745-53 (medline /22846781)
CM - Cites: J Endocrinol. 2013 Apr 15;217(2):161-73 (medline /23428582)
CM - Cites: Cell Death Differ. 2013 Nov;20(11):1558-68 (medline /23933812)
CM - Cites: Brain Res. 1992 Nov 13;595(2):195-200 (medline /1467966)
CM - Cites: Nat Commun. 2014 Nov 07;5:5395 (medline /25377354)
CM - Cites: PLoS One. 2013;8(1):e55684 (medline /23383264)
CM - Cites: PLoS One. 2015 Mar 24;10(3):e0120992 (medline /25803364)
CM - Cites: Anal Biochem. 2003 Sep 15;320(2):193-8 (medline /12927824)
CM - Cites: PLoS One. 2016 Jul 11;11(7):e0158807 (medline /27398996)
CM - Cites: Endocrinology. 2012 Nov;153(11):5500-11 (medline /22919064)
CM - Cites: Gend Med. 2007 Mar;4(1):19-30 (medline /17584623)
CM - Cites: Sci Rep. 2016 Nov 23;6:37227 (medline /27876813)
CM - Cites: Exp Clin Endocrinol. 1991;98(2):123-9 (medline /1663870)
CM - Cites: J Environ Health. 2011 Sep;74(2):16-22 (medline /21949980)
DOCNO- medline/29132937

135 - TOXLINE
TI - Arsenite and methylarsonite inhibit mitochondrial metabolism and
glucose-stimulated insulin secretion in INS-1 832/13 &beta; cells.
AU - Dover EN
AD - Curriculum in Toxicology, School of Medicine, University of North Carolina,
Chapel Hill, NC, USA.
AU - Beck R
AD - Department of Genetics, School of Medicine, University of North Carolina at
Chapel Hill, Chapel Hill, NC, USA.
AU - Huang MC
AD - Curriculum in Toxicology, School of Medicine, University of North Carolina,
Chapel Hill, NC, USA.
AU - Douillet C
AD - Department of Nutrition, CB# 74612, Gillings School of Global Public Health,
University of North Carolina, Chapel Hill, NC, 27599-7461, USA.
AU - Wang Z
AD - School of Environmental Science and Engineering, Shandong University, No. 27
Shanda South Road, Jinan, 250100, China.
AU - Klett EL
AD - Department of Medicine, School of Medicine, University of North Carolina,
Chapel Hill, NC, USA.
AU - St�blo M
AD - Department of Nutrition, CB# 74612, Gillings School of Global Public Health,
University of North Carolina, Chapel Hill, NC, 27599-7461, USA. styblo@med.unc.edu.
SO - Arch Toxicol. 2018, Feb; 92(2):693-704. [Archives of toxicology]
AB - Growing evidence suggests that exposure to environmental contaminants
contributes to the current diabetes epidemic. Inorganic arsenic (iAs), a
drinking water and food contaminant, is one of the most widespread
environmental diabetogens according to epidemiological studies. Several
schemes have been proposed to explain the diabetogenic effects of iAs
exposure; however, the exact mechanism remains unknown. We have shown that
in vitro exposure to low concentrations of arsenite (iAsIII) or its
trivalent methylated metabolites, methylarsonite (MAsIII) and
dimethylarsinite (DMAsIII), inhibits glucose-stimulated insulin secretion
(GSIS) from isolated pancreatic islets, with little effect on insulin
transcription or total insulin content. The goal of this study was to
determine if exposure to trivalent arsenicals impairs mitochondrial
metabolism, which plays a key role in the regulation of GSIS in &beta;
cells. We used a Seahorse extracellular flux analyzer to measure oxygen
consumption rate (OCR), a proxy for mitochondrial metabolism, in cultured
INS-1 832/13 &beta; cells exposed to iAsIII, MAsIII, or DMAsIII and
stimulated with either glucose or pyruvate, a final product of glycolysis
and a substrate for the Krebs cycle. We found that 24-h exposure to 2
&mu;M iAsIII or 0.375-0.5 &mu;M MAsIII inhibited OCR in both glucose- and
pyruvate-stimulated &beta; cells in a manner that closely paralleled GSIS
inhibition. In contrast, 24-h exposure to DMAsIII (up to 2 &micro;M)
had no effects on either OCR or GSIS. These results suggest that iAsIII
and MAsIII may impair GSIS in &beta; cells by inhibiting mitochondrial
metabolism, and that at least one target of these arsenicals is pyruvate
decarboxylation or downstream reactions.
KW - Arsenic
KW - Diabetes
KW - Insulin secretion
KW - Mitochondrial respiration
KW - β cells
LA - eng
IS - 1432-0738 (Electronic)
PT - Journal Article
TA - Arch Toxicol
YR - 2018
DATE- 20180220
CITO- NLM
CS - Germany
FJT - Archives of toxicology
EDAT- 20170927
STAT- In-Data-Review
DOCNO- medline/28956099

136 - TOXLINE
TI - Effective rhizoinoculation and biofilm formation by arsenic immobilizing
halophilic plant growth promoting bacteria (PGPB) isolated from mangrove
rhizosphere: A step towards arsenic rhizoremediation.
AU - Mallick I
AD - Department of Biochemistry, Bose Institute, P1/12, C.I.T Road, Scheme VIIM,
Kolkata 700054, West Bengal, India.
AU - Bhattacharyya C
AD - Department of Biochemistry, Bose Institute, P1/12, C.I.T Road, Scheme VIIM,
Kolkata 700054, West Bengal, India.
AU - Mukherji S
AD - Department of Biochemistry, Bose Institute, P1/12, C.I.T Road, Scheme VIIM,
Kolkata 700054, West Bengal, India.
AU - Dey D
AD - Department of Biochemistry, Bose Institute, P1/12, C.I.T Road, Scheme VIIM,
Kolkata 700054, West Bengal, India.
AU - Sarkar SC
AD - West Bengal Pollution Control Board, Kolkata, West Bengal, India.
AU - Mukhopadhyay UK
AD - West Bengal Pollution Control Board, Kolkata, West Bengal, India.
AU - Ghosh A
AD - Department of Biochemistry, Bose Institute, P1/12, C.I.T Road, Scheme VIIM,
Kolkata 700054, West Bengal, India. Electronic address:
abhrajyoti.ghosh@jcbose.ac.in.
SO - Sci Total Environ. 2018, Jan 01; 610-611:1239-1250. [The Science of the
total environment]
AB - Arsenic (As) uptake by plants is largely influenced by the presence of
microbial consortia and their interactions with As. In the coastal region
of Bengal deltaic plain of Eastern India, the As-contaminated groundwater
is frequently used for irrigation purposes resulting in an elevated level
of soil As in agricultural lands. The health hazards associated with As
necessitates development of cost-effective remediation strategies to
reclaim contaminated agricultural lands. Among the available technologies
developed in recent times, bioremediation using bacteria has been found to
be the most propitious. In this study, two As-resistant halophilic
bacterial strains Kocuria flava AB402 and Bacillus vietnamensis AB403 were
isolated, identified and characterized from mangrove rhizosphere of
Sundarban. The isolates, AB402 and AB403, could tolerate 35mM and 20mM of
arsenite, respectively. The effect of As on the exopolysaccharide (EPS)
synthesis, biofilm formation, and root association was evaluated for both
the bacterial strains. Arsenic adsorption on the cell surfaces and
intracellular accumulation in both the bacterial strains were promising
under culture conditions. Moreover, both the strains when used as
inoculum, not only promoted the growth of rice seedlings but also
decreased As uptake and accumulation in plants.
KW - Accumulation
KW - Adsorption
KW - Arsenic resistance
KW - Biofilm
KW - Halophiles
KW - Plant growth promoting rhizobacteria
RN - N712M78A8G
LA - eng
IS - 1879-1026 (Electronic)
PT - Journal Article
TA - Sci Total Environ
YR - 2018
DATE- 20180504
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - The Science of the total environment
EDAT- 20170830
STAT- MEDLINE
DOCNO- medline/28851144

137 - TOXLINE
TI - Ellagic acid attenuates arsenic induced neuro-inflammation and
mitochondrial dysfunction associated apoptosis.
AU - Firdaus F
AD - Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University,
Aligarh, Uttar Pradesh, India.
AU - Zafeer MF
AD - Interdisciplinary Brain Research Centre, Faculty of Medicine, Aligarh Muslim
University, Aligarh, Uttar Pradesh, India.
AU - Anis E
AD - Interdisciplinary Brain Research Centre, Faculty of Medicine, Aligarh Muslim
University, Aligarh, Uttar Pradesh, India.
AU - Ahmad M
AD - Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim
University, Aligarh, Uttar Pradesh, India.
AU - Afzal M
AD - Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University,
Aligarh, Uttar Pradesh, India.
SO - Toxicol Rep. 2018; 5:411-417. [Toxicology reports]
AB - Arsenic, being a global pollutant needs a potential remedy which could
fight against its associated toxicities. Ellagic acid (EA) is a known
agent for its anti-inflammatory, antioxidant and antiapoptotic effects,
and it is commonly found in fruits. The present study is designed to
determine protective efficacy of EA against arsenic induced toxicity with
special mention to inflammation and mitochondrial dysfunction in
hippocampi of wistar rats. Rats were pre-treated with EA (20 and
40&#8239;mg/kg b.wt; p.o. for 11&#8239;days) along with arsenic
(10&#8239;mg/kg; p.o. for 8&#8239;days). Total reactive oxygen species
level and mitochondrial membrane potential were analyzed using flow
cytometry. Protein and mRNA expression of apoptotic and inflammatory
markers were also evaluated in rat hippocampus. Our results show that
arsenic exposure increased total ROS generation and DNA fragmentation,
decreased mitochondrial membrane potential alongwith an increase in
expression of pro-apoptotic and inflammatory markers. suggesting that EA
complementation downregulated total ROS generation dose dependently.
Apoptotic markers, BAX and Bcl2 as well as inflammatory markers,
IL-1&beta;, TNF&alpha;, INF&gamma; got altered significantly on its
administration. Moreover, it also attenuated effects on mitochondrial
membrane potential. Based on our findings, EA might substantiate to be a
budding therapeutic candidate against arsenic induced neurotoxicity.
KW - Arsenic
KW - Ellagic acid
KW - Inflammation
KW - Mitochondrial membrane potential
KW - Neurotoxicity
KW - ROS generation
LA - eng
IS - 2214-7500 (Electronic)
PT - Journal Article
TA - Toxicol Rep
YR - 2018
DATE- 20180603
CITO- NLM
CS - Ireland
FJT - Toxicology reports
EDAT- 20180309
STAT- PubMed-not-MEDLINE
CM - Cites: Toxicol Lett. 2003 Nov 1;145(1):1-18 (medline /12962969)
CM - Cites: Int J Oncol. 2000 May;16(5):871-86 (medline /10762622)
CM - Cites: J Biol Chem. 2010 Dec 17;285(51):39922-34 (medline /20889981)
CM - Cites: Environ Toxicol Pharmacol. 2012 May;33(3):394-402 (medline
/22387601)
CM - Cites: Brain Res. 2017 May 1;1662:23-30 (medline /28238669)
CM - Cites: Free Radic Biol Med. 1996;21(6):783-90 (medline /8902524)
CM - Cites: Trends Cell Biol. 2000 Sep;10(9):369-77 (medline /10932094)
CM - Cites: Cell. 2010 Mar 19;140(6):918-34 (medline /20303880)
CM - Cites: Trends Cell Biol. 2001 Dec;11(12):526-34 (medline /11719060)
CM - Cites: Toxicol Lett. 2009 Jan 30;184(2):121-5 (medline /19041379)
CM - Cites: Mol Biol Cell. 2002 Mar;13(3):978-88 (medline /11907276)
CM - Cites: J Chromatogr B Analyt Technol Biomed Life Sci. 2003 Oct
25;796(1):189-94 (medline /14552830)
CM - Cites: Digestion. 2001;64(4):214-21 (medline /11842277)
CM - Cites: J Nutr. 2001 Nov;131(11):2837-42 (medline /11694605)
CM - Cites: Immunology. 2010 Feb;129(2):154-69 (medline /20561356)
CM - Cites: J Agric Food Chem. 2002 Apr 10;50(8):2432-8 (medline /11929309)
CM - Cites: Environ Res. 2006 Jul;101(3):349-55 (medline /16458287)
CM - Cites: Environ Health Perspect. 2007 Sep;115(9):1371-5 (medline /17805430)
CM - Cites: J Toxicol Clin Toxicol. 2001;39(7):675-82 (medline /11778665)
CM - Cites: Neurol Sci. 2012 Jun;33(3):567-74 (medline /21922312)
CM - Cites: Psychopharmacology (Berl). 2017 Jun;234(12 ):1841-1852 (medline
/28303372)
CM - Cites: Science. 2004 Jul 30;305(5684):626-9 (medline /15286356)
CM - Cites: Toxicol Appl Pharmacol. 2009 Oct 15;240(2):236-44 (medline
/19460394)
CM - Cites: Toxicol Lett. 2005 Jan 15;155(1):27-34 (medline /15585356)
CM - Cites: J Signal Transduct. 2012;2012:329635 (medline /22175013)
CM - Cites: Mutat Res. 2003 Dec 10;533(1-2):173-82 (medline /14643419)
CM - Cites: BMC Biol. 2015 Oct 29;13:89 (medline /26515107)
CM - Cites: Exp Cell Res. 1988 Mar;175(1):184-91 (medline /3345800)
CM - Cites: Free Radic Biol Med. 2011 Jul 15;51(2):257-81 (medline /21554949)
CM - Cites: Food Chem Toxicol. 2010 Jan;48(1):326-35 (medline /19852998)
CM - Cites: J Agric Food Chem. 2002 Mar 27;50(7):2200-6 (medline /11902978)
CM - Cites: Cytotechnology. 2016 Oct;68(5):1763-70 (medline /26660314)
CM - Cites: Biomed Pharmacother. 2010 Apr;64(4):264-70 (medline /20347566)
CM - Cites: Neurotoxicol Teratol. 2009 Sep-Oct;31(5):318-22 (medline /19410645)
CM - Cites: J Cell Sci. 2008 Jan 1;121(Pt 1):75-85 (medline /18073239)
CM - Cites: Int J Environ Res Public Health. 2011 Jul;8(7):2980-3018 (medline
/21845170)
CM - Cites: Brain Res Bull. 2001 May 15;55(2):301-8 (medline /11470331)
CM - Cites: Cancer Lett. 1995 May 4;91(1):139-44 (medline /7750089)
CM - Cites: Environ Health Perspect. 1998 Aug;106(8):487-91 (medline /9681976)
CM - Cites: Int Immunopharmacol. 2014 Oct;22(2):341-5 (medline /25038320)
CM - Cites: Biochem Pharmacol. 1996 Feb 23;51(4):395-402 (medline /8619883)
CM - Cites: J Agric Food Chem. 2002 Jun 5;50(12):3495-500 (medline /12033817)
CM - Cites: Life Sci. 2002 Jan 25;70(10):1139-50 (medline /11848298)
CM - Cites: Mediators Inflamm. 2017;2017:5048616 (medline /28154473)
CM - Cites: Environ Mol Mutagen. 1995;26(3):248-54 (medline /7588651)
CM - Cites: Toxicol Lett. 1997 Aug 22;92(3):201-8 (medline /9334831)
CM - Cites: Toxicology. 2005 May 15;210(1):25-36 (medline /15804455)
CM - Cites: Circ Res. 2000 Mar 17;86(5):514-9 (medline /10720412)
CM - Cites: Mol Cell Oncol. 2014 Oct 31;1(2):e955995 (medline /27308326)
CM - Cites: J Biochem Mol Toxicol. 2008 Feb;22(1):15-26 (medline /18273903)
CM - Cites: Chem Res Toxicol. 2006 Jan;19(1):1-15 (medline /16411650)
DOCNO- medline/29854611

138 - TOXLINE
TI - Inhibition of miR-219 Alleviates Arsenic-Induced Learning and Memory
Impairments and Synaptic Damage Through Up-regulating CaMKII in the
Hippocampus.
AU - Wang D
AD - Department of Occupational and Environmental Health, Dalian Medical
University, Dalian, 116044, People's Republic of China.
AU - Wang X
AD - Digestive Endoscopic Department of the second Hospital of Jilin University,
Changchun, 130000, People's Republic of China.
AU - Liu X
AD - 3Department of Food Nutrition and Safety, Dalian Medical University, Dalian,
Liaoning, 116044, People's Republic of China.
AU - Jiang L
AD - Liaoning Anti-Degenerative Diseases Natural Products Engineering Research
Center, Dalian Medical University, Dalian, 116044, People's Republic of China.
AU - Yang G
AD - 3Department of Food Nutrition and Safety, Dalian Medical University, Dalian,
Liaoning, 116044, People's Republic of China.
AU - Shi X
AD - Department of Occupational and Environmental Health, Dalian Medical
University, Dalian, 116044, People's Republic of China.
AU - Zhang C
AD - 3Department of Food Nutrition and Safety, Dalian Medical University, Dalian,
Liaoning, 116044, People's Republic of China. congzhang1203@hotmail.com.
AU - Piao F
AD - Department of Occupational and Environmental Health, Dalian Medical
University, Dalian, 116044, People's Republic of China.
SO - Neurochem Res. 2018, Apr; 43(4):948-958. [Neurochemical research]
AB - Epidemiological investigations and experimental studies indicate that
chronic arsenic exposure can reduce learning and memory function. However,
the underlying mechanism of this effect remains largely unknown. Emerging
evidence suggests that microRNA (miRNA) play an important role in toxicant
exposure and a regulatory role in cognitive function. In this study, we
observed that subchronic arsenic exposure induced impairment of learning
and memory and significantly up-regulated miRNA-219 (miR-219) expression
in the mouse hippocampus. Furthermore, the expression of CaMKII, an
experimentally validated target of miR-219, was decreased in the mice
exposed to arsenic. Suppression of miR-219 by adeno-associated viral
(AAV)-delivered anti-miR-219 prevented the arsenic-induced impairment of
learning and memory and relieved the pathological changes in the synaptic
structure of the hippocampus. Furthermore, we observed that the NMDA
receptor subunit 2 (NR2) and the memory-related proteins c-Fos and c-Jun
were up-regulated by inhibition of miR-219 in the mouse hippocampus. Taken
together, the results of this study indicate that inhibition of miR-219
regulates arsenic-induced damage in the structure of the hippocampus and
impairment of learning and memory, possibly by targeting CaMKII.
Suppression of miR-219 may be a potential strategy to ameliorate
arsenic-induced neurotoxicity.
KW - Arsenic
KW - CaMKII
KW - Hippocampus
KW - Learning and memory
KW - miR-219
LA - eng
IS - 1573-6903 (Electronic)
PT - Journal Article
TA - Neurochem Res
YR - 2018
DATE- 20180410
CITO- NLM
CS - United States
FJT - Neurochemical research
EDAT- 20180224
STAT- In-Process
CM - Cites: Neurotoxicology. 2012 Oct;33(5):1033-9 (medline /22561869)
CM - Cites: J Exp Zool A Ecol Genet Physiol. 2009 Dec 1;311(10):763-75 (medline
/19658087)
CM - Cites: Proc Natl Acad Sci U S A. 2008 Jul 1;105(26):9093-8 (medline
/18577589)
CM - Cites: Trends Cell Biol. 2013 Jan;23(1):30-6 (medline /23026030)
CM - Cites: Neurotoxicology. 2006 Mar;27(2):210-6 (medline /16310252)
CM - Cites: J Biol Chem. 2014 Apr 4;289(14):10201-10 (medline /24554719)
CM - Cites: J Neurosci. 2011 Jun 22;31(25):9170-8 (medline /21697368)
CM - Cites: Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3507-12 (medline
/19196972)
CM - Cites: Toxicol Lett. 2009 Jan 30;184(2):121-5 (medline /19041379)
CM - Cites: Adv Exp Med Biol. 2015;888:107-21 (medline /26663181)
CM - Cites: J Neurosci. 2014 Jul 16;34(29):9476-83 (medline /25031391)
CM - Cites: Environ Toxicol. 2015 May-Jun;30(6):712-23 (medline /24420840)
CM - Cites: Neuron. 2012 Aug 9;75(3):363-79 (medline /22884321)
CM - Cites: J Neurosci. 1996 Sep 1;16(17):5425-36 (medline /8757255)
CM - Cites: Psychopharmacology (Berl). 2004 May;173(3-4):337-45 (medline
/14985918)
CM - Cites: Genome Biol. 2004;5(3):R13 (medline /15003116)
CM - Cites: Oncotarget. 2017 Apr 25;8(17 ):28203-28214 (medline /28423675)
CM - Cites: Annu Rev Neurosci. 2008;31:47-67 (medline /18284372)
CM - Cites: Nat Rev Genet. 2008 Feb;9(2):102-14 (medline /18197166)
CM - Cites: Eur J Nutr. 2017 Mar;56(2):865-877 (medline /26695409)
CM - Cites: Neurotoxicology. 2010 Sep;31(5):575-81 (medline /20553758)
CM - Cites: Neurobiol Learn Mem. 2011 Jul;96(1):89-94 (medline /21524708)
CM - Cites: Taiwan Yi Xue Hui Za Zhi. 1962 Jul 28;61:611-8 (medline /14040660)
CM - Cites: Toxicol Lett. 2014 Aug 4;228(3):260-9 (medline /24831965)
CM - Cites: Toxicol Lett. 2012 May 20;211(1):39-44 (medline /22421273)
CM - Cites: Neuron. 2007 Jun 7;54(5):813-29 (medline /17553428)
CM - Cites: Proc Natl Acad Sci U S A. 2010 Apr 27;107(17):7945-50 (medline
/20351272)
CM - Cites: Trends Neurosci. 2012 May;35(5):325-34 (medline /22436491)
CM -Cites: Genes Dev. 2007 Apr 1;21(7):744-9 (medline /17403776)
CM -Cites: Neuron. 2008 May 22;58(4):571-83 (medline /18498738)
CM -Cites: Eur J Neurosci. 2010 Feb;31(4):636-45 (medline /20384810)
CM -Cites: J Comp Neurol. 2010 Oct 15;518(20):4243-60 (medline /20878786)
CM -Cites: Comp Biochem Physiol C Toxicol Pharmacol. 2012 May;155(4):566-72
(medline /22265774)
CM - Cites: J Neurosci. 2013 Oct 23;33(43):17008-22 (medline /24155305)
CM - Cites: Mol Med Rep. 2014 May;9(5):1715-22 (medline /24626427)
CM - Cites: Toxicol Lett. 2014 Aug 17;229(1):158-66 (medline /24960059)
CM - Cites: J Inorg Biochem. 2009 Nov;103(11):1591-5 (medline /19540598)
CM - Cites: J Neurosci. 2012 Apr 18;32(16):5678-5687 (medline /22514329)
CM - Cites: Nat Rev Neurosci. 2002 Mar;3(3):175-90 (medline /11994750)
CM - Cites: Environ Health Perspect. 2000 May;108(5):393-7 (medline /10811564)
CM - Cites: Stroke. 2008 Dec;39(12):3397-404 (medline /18772448)
CM - Cites: Toxicology. 2013 Jan 7;303:43-53 (medline /23146754)
CM - Cites: Am J Epidemiol. 1998 Jul 15;148(2):198-203 (medline /9676702)
CM - Cites: Neuroscience. 2008 Jan 2;151(1):43-55 (medline /18082335)
CM - Cites: Neuroreport. 2007 Feb 12;18(3):297-300 (medline /17314675)
CM - Cites: Environ Sci Technol. 2013 Jul 2;47(13):7466-74 (medline /23745839)
CM - Cites: Neurosci Lett. 1980 Apr;17(1-2):27-31 (medline /6302580)
CM - Cites: Cell. 2009 Jan 23;136(2):215-33 (medline /19167326)
CM - Cites: Science. 2002 Oct 25;298(5594):776-80 (medline /12399578)
CM - Cites: Biomed Res Int. 2015 ;2015 :302653 (medline /26649298)
CM - Cites: Neurotoxicology. 2012 Oct;33(5):1230-8 (medline /22824511)
CM - Cites: Curr Opin Genet Dev. 2011 Aug;21(4):491-7 (medline /21561760)
CM - Cites: Environ Health Perspect. 2004 Sep;112(13):1329-33 (medline
/15345348)
CM - Cites: BMC Genomics. 2014;15 Suppl 11:S1 (medline /25559034)
DOCNO- medline/29478199

139 - TOXLINE
TI - Arsenic removal by Japanese oak wood biochar in aqueous solutions and well
water: Investigating arsenic fate using integrated spectroscopic and
microscopic techniques.
AU - Niazi NK
AD - Institute of Soil and Environmental Sciences, University of Agriculture
Faisalabad, Faisalabad 38040, Pakistan; MARUM and Department of Geosciences,
University of Bremen, Bremen D-28359, Germany. Electronic address:
nabeel.niazi@uaf.edu.pk.
AU - Bibi I
AD - Institute of Soil and Environmental Sciences, University of Agriculture
Faisalabad, Faisalabad 38040, Pakistan; MARUM and Department of Geosciences,
University of Bremen, Bremen D-28359, Germany.
AU - Shahid M
AD - Department of Environmental Sciences, COMSATS Institute of Information
Technology, Vehari, Pakistan.
AU - Ok YS
AD - Korea Biochar Research Center, O-Jeong Eco-Resilience Institute (OJERI) &amp;
Division of Environmental Science and Ecological Engineering, Korea University,
Seoul, 02841, Republic of Korea.
AU - Shaheen SM
AD - University of Kafrelsheikh, Faculty of Agriculture, Department of Soil and
Water Sciences, 33 516 Kafr El-Sheikh, Egypt; University of Wuppertal, School of
Architecture and Civil Engineering, Institute of Foundation Engineering, Water- and
Waste-Management, Laboratory of Soil- and Groundwater-Management,
Pauluskirchstra&szlig;e 7, 42285 Wuppertal, Germany.
AU - Rinklebe J
AD - University of Wuppertal, School of Architecture and Civil Engineering,
Institute of Foundation Engineering, Water- and Waste-Management, Laboratory of
Soil- and Groundwater-Management, Pauluskirchstra&szlig;e 7, 42285 Wuppertal,
Germany; Department of Environment and Energy, Sejong University, 98 Gunja-Dong,
Guangjin-Gu, Seoul, Republic of Korea. Electronic address: rinklebe@uni-
wuppertal.de.
AU - Wang H
AD - Key Laboratory of Soil Contamination Bioremediation of Zhejiang Province,
Zhejiang A &amp; F University, Lin'an, Hangzhou 311300, China; School of
Environment and Chemical Engineering, Foshan University, Foshan 528000, China.
AU - Murtaza B
AD - Department of Environmental Sciences, COMSATS Institute of Information
Technology, Vehari, Pakistan.
AU - Islam E
AD - Environmental Biotechnology Division, National Institute for Biotechnology
and Genetic Engineering (NIBGE), Faisalabad 38000, Pakistan.
AU - Farrakh Nawaz M
AD - Department of Forestry and Range Management, University of Agriculture
Faisalabad, Faisalabad 38040, Pakistan.
AU - L�ttge A
AD - MARUM and Department of Geosciences, University of Bremen, Bremen D-28359,
Germany.
SO - Sci Total Environ. 2018, Apr 15; 621:1642-1651. [The Science of the total
environment]
AB - In this study, we examined the sorption of arsenite (As(III)) and arsenate
(As(V)) to Japanese oak wood-derived biochar (OW-BC) in aqueous solutions,
and determined its efficiency to remove As from As-contaminated well
water. Results revealed that, among the four sorption isotherm models,
Langmuir model showed the best fit to describe As(III) and As(V) sorption
on OW-BC, with slightly greater sorption affinity for As(V) compared to
As(III) (QL=3.89 and 3.16mgg-1; R2=0.91 and 0.85, respectively). Sorption
edge experiments indicated that the maximum As removal was 81% and 84% for
As(III)- and As(V)-OW-BC systems at pH7 and 6, respectively, which
decreased above these pH values (76-69% and 80-58%). Surface functional
groups, notably OH, COOH, CO, CH3, were involved in As sequestration by
OW-BC, suggesting the surface complexation/precipitation and/or
electrostatic interaction of As on OW-BC surface. Arsenic K-edge X-ray
absorption near edge structure (XANES) spectroscopy indicated that 36% of
the added As(III) was partially oxidized to As(V) in the As(III) sorption
experiment, and in As(V) sorption experiment, 48% of As(V) was, albeit
incompletely, reduced to As(III) on OW-BC surface. Application of OW-BC to
As-contaminated well water (As: 27-144&mu;gL-1; n=10) displayed that 92 to
100% of As was depleted despite in the presence of co-occurring competing
anions (e.g., SO42-, CO32-, PO43-). This study shows that OW-BC has a
great potential to remove As from solution and drinking (well) water.
Overall, the combination of macroscopic sorption data and integrated
spectroscopic and microscopic techniques highlight that the fate of As on
biochar involves complex redox transformation and association with surface
functional moieties in aquatic systems, thereby providing crucial
information required for implication of biochar in environmental
remediation programs.
KW - Arsenic contamination
KW - Drinking water, FTIR, remediation
KW - SEM-EDX
KW - Sorbent
KW - Toxicity, XANES
LA - eng
IS - 1879-1026 (Electronic)
PT - Journal Article
TA - Sci Total Environ
YR - 2018
DATE- 20180309
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - The Science of the total environment
EDAT- 20171018
STAT- PubMed-not-MEDLINE
DOCNO- medline/29054629

140 - TOXLINE
TI - Assessment of the effect of cooking on speciation and
bioaccessibility/cellular uptake of arsenic in rice, using in vitro
digestion and Caco-2 and PSI cells as model.
AU - Lee SG
AD - Department of Biotechnology, College of Life Sciences and Biotechnology,
Korea University, Seoul 02841, South Korea.
AU - Kim J
AD - Department of Biotechnology, College of Life Sciences and Biotechnology,
Korea University, Seoul 02841, South Korea.
AU - Park H
AD - Graduate School of Advanced Green Energy and Environment, Handong Global
University, Pohang, Gyeongbuk 37554, South Korea.
AU - Holzapfel W
AD - Graduate School of Advanced Green Energy and Environment, Handong Global
University, Pohang, Gyeongbuk 37554, South Korea.
AU - Lee KW
AD - Department of Biotechnology, College of Life Sciences and Biotechnology,
Korea University, Seoul 02841, South Korea. Electronic address:
kwangwon@korea.ac.kr.
SO - Food Chem Toxicol. 2018, Jan; 111:597-604. [Food and chemical toxicology :
an international journal published for the British Industrial Biological
Research Association]
AB - In vitro digestion/Caco-2 or pig small intestinal epithelium cell line
(PSI) uptake models were used to study the bioaccessibility and cellular
uptake of arsenic (As) in cooked white rice and brown rice. The
arsenite(AsIII), was the predominant species in cooked rice and in its
bioaccessible fractions. The percentage of total As bioaccessibility in
white rice (75%) was slightly higher (p=0.061) than that in brown
rice(66%). However, there was no difference in the inorganic As (iAs)
bioaccessibility between white rice (95%) and brown rice (96%). In Caco-2
cell monolayer, total As retention was 7-31%, transport was 4-25%, and
uptake (sum of retention and transport) was 16-38%. In PSI cell model, the
retention, transport, and uptake of tAs were 10-28%, 14-31%, and 29-50%,
respectively. In both cells, the cellular uptake of tAs in brown rice was
1.4-1.5 folds lower (p < 0.05) than that of white rice. These results
indicate that the cellular uptake of As can be affected by nutritional
compositions. These in vitro screening methods can serve as preliminary
screens to predict the relative impact in rice matrix having different As
species and processing conditions, although more research efforts should
be applied to validating the existing in vitro methods.
KW - Bioaccessibility
KW - Cellular uptake
KW - Cooked rice
KW - In vitro digestion/Caco-2 cell model
KW - Inorganic arsenic
RN - N712M78A8G
LA - eng
IS - 1873-6351 (Electronic)
PT - Journal Article
TA - Food Chem Toxicol
YR - 2018
DATE- 20180507
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Food and chemical toxicology : an international journal published for the
British Industrial Biological Research Association
EDAT- 20171206
STAT- MEDLINE
DOCNO- medline/29222053

141 - TOXLINE
TI - Ferroptosis is newly characterized form of neuronal cell death in response
to arsenite exposure.
AU - Tang Q
AD - Department of Occupational and Environmental Health, School of Public Health
and Management, Research Center for Medicine and Social Development, Innovation
Center for Social Risk Governance in Health, Chongqing Medical University,
Chongqing, People's Republic of China.
AU - Bai L
AD - Department of Occupational and Environmental Health, School of Public Health
and Management, Research Center for Medicine and Social Development, Innovation
Center for Social Risk Governance in Health, Chongqing Medical University,
Chongqing, People's Republic of China.
AU - Zou Z
AD - Institute of Life Sciences, Chongqing Medical University, Chongqing, People's
Republic of China.
AU - Meng P
AD - Department of Occupational and Environmental Health, School of Public Health
and Management, Research Center for Medicine and Social Development, Innovation
Center for Social Risk Governance in Health, Chongqing Medical University,
Chongqing, People's Republic of China.
AU - Xia Y
AD - Department of Occupational and Environmental Health, School of Public Health
and Management, Research Center for Medicine and Social Development, Innovation
Center for Social Risk Governance in Health, Chongqing Medical University,
Chongqing, People's Republic of China.
AU - Cheng S
AD - Department of Occupational and Environmental Health, School of Public Health
and Management, Research Center for Medicine and Social Development, Innovation
Center for Social Risk Governance in Health, Chongqing Medical University,
Chongqing, People's Republic of China.
AU - Mu S
AD - Post-doctoral Research Stations of Nursing Science, School of Nursing,
Chongqing Medical University, Chongqing, People's Republic of China.
AU - Zhou J
AD - Post-doctoral Research Stations of Nursing Science, School of Nursing,
Chongqing Medical University, Chongqing, People's Republic of China.
AU - Wang X
AD - Department of Neurology, The First Affiliated Hospital of Chongqing Medical
University, Chongqing Key Laboratory of Neurology, Chongqing, People's Republic of
China.
AU - Qin X
AD - Department of Pharmacy, The First Affiliated Hospital of Chongqing Medical
University, Chongqing, People's Republic of China.
AU - Cao X
AD - Department of Occupational and Environmental Health, School of Public Health
and Management, Research Center for Medicine and Social Development, Innovation
Center for Social Risk Governance in Health, Chongqing Medical University,
Chongqing, People's Republic of China.
AU - Jiang X
AD - Center of Experimental Teaching for Public Health, Experimental Teaching and
Management Center, Chongqing Medical University, Chongqing, People's Republic of
China; Laboratory of Tissue and Cell Biology, Experimental Teaching and Management
Center, Chongqing Medical University, Chongqing, People's Republic of China.
Electronic address: jiangxuejun312@163.com.
AU - Chen C
AD - Department of Occupational and Environmental Health, School of Public Health
and Management, Research Center for Medicine and Social Development, Innovation
Center for Social Risk Governance in Health, Chongqing Medical University,
Chongqing, People's Republic of China; Post-doctoral Research Stations of Nursing
Science, School of Nursing, Chongqing Medical University, Chongqing, People's
Republic of China. Electronic address: chengzhichen@cqmu.edu.cn.
SO - Neurotoxicology. 2018, Apr 17; 67:27-36. [Neurotoxicology]
AB - Ferroptosis is a novel iron-dependent form of cell death implicated in
brain pathology. However, whether arsenite is an inducer of ferroptosis in
the neuron remains completely unknown. In this study, the seven-week-old
healthy C57BL/6&#8239;J male mice were treated with environmental related
doses (0.5, 5 and 50&#8239;mg/L) of arsenite for 6 months via drinking
water, and the ferroptosis-related indicators were further determined. Our
results demonstrated for the first time that, arsenite exposure
significantly reduced the number of neuron and caused the pathological
changes of mitochondria in the cerebral cortex of mice. We further
revealed that arsenite induced ferroptotic cell death in neuron by
accumulation of reactive oxygen species and lipid peroxidation products,
disruption of Fe2+ homeostasis, depletion of glutathione and adenosine
triphosphate, inhibition of cysteine/glutamate antiporter, activation of
mitogen-activated protein kinases and mitochondrial voltage-dependent
anion channels pathways, up-regulation of endoplasmic reticulum stress,
all of which were involved in the process of ferroptosis. These findings
were also verified in the cultured PC-12 cells by using ferropotosis
inhibitor, desferoxamine. Taken together, our results not only reveal a
novel mechanism that chronic arsenite exposure may trigger the new form of
cell death, ferroptosis, but also shed a new light on a potential clue for
the intervention and prevention against arsenite-related neurodegenerative
diseases.
KW - Arsenite
KW - Cell death
KW - Ferroptosis
KW - Mitochondrial dysfunction
KW - ROS
LA - eng
IS - 1872-9711 (Electronic)
PT - Journal Article
TA - Neurotoxicology
YR - 2018
DATE- 20180616
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Neurotoxicology
EDAT- 20180417
STAT- Publisher
DOCNO- medline/29678591

142 - TOXLINE
TI - Thymoquinone alleviates arsenic induced hippocampal toxicity and
mitochondrial dysfunction by modulating mPTP in Wistar rats.
AU - Firdaus F
AD - Interdisciplinary Brain Research Centre, Faculty of Medicine, Aligarh Muslim
University, Aligarh, Uttar Pradesh, India; Department of Zoology, Faculty of Life
Sciences, Aligarh Muslim University, Aligarh, Uttar Pradesh, India.
AU - Zafeer MF
AD - Interdisciplinary Brain Research Centre, Faculty of Medicine, Aligarh Muslim
University, Aligarh, Uttar Pradesh, India.
AU - Waseem M
AD - School of Life Sciences, B.S. Abdur Rahman Crescent Institute of Science and
Technology, Chennai, India.
AU - Ullah R
AD - Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University,
Aligarh, Uttar Pradesh, India.
AU - Ahmad M
AD - Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim
University, Aligarh, Uttar Pradesh, India.
AU - Afzal M
AD - Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University,
Aligarh, Uttar Pradesh, India. Electronic address: afzalgenetics@gmail.com.
SO - Biomed Pharmacother. 2018, Jun; 102:1152-1160. [Biomedicine &
pharmacotherapy = Biomedecine & pharmacotherapie]
AB - Arsenic is a pervasive environmental pollutant that is found in ground
waters globally and is related to numerous morbidities in the high-risk
population areas in countries including Bangladesh, India, and the USA.
Arsenic exposure has been ubiquitously reported for exacerbating free
radical generation, mitochondrial dysfunction, and apoptosis by
interfering with the mPTP functioning. Over the past decades,
nutraceuticals with antioxidant properties have shown promising efficacy
in arsenic poisoning. In the present study, we have examined, the
protective efficacy of thymoquinone (TQ), an active component of seed oil
of Nigella sativa with antioxidant and anti-inflammatory activity on
arsenic-induced toxicity in hippocampi of Wistar rats. In our results,
arsenic conditioning (10&#8239;mg/kg b.wt.; p.o.) for 8 days has caused a
significant increase in intracellular ROS generation, mitochondrial
dysfunction and apoptotic events. On the contrary pretreatment with TQ
(2.5 and 5&#8239;mg/kg b.wt.; p.o.) inhibited arsenic-induced
mitochondrial dysfunction such as lowering of mitochondrial membrane
potential (&Delta;&psi;m). Our results indicated that the neuroprotective
efficacy of TQ in arsenic-induced stress is mediated through or in part by
inhibition of mPTP opening. Demonstration of neuroprotective action of TQ
provides insight into the pathogenesis of arsenic-related
neuropathological morbidities.
KW - Hippocampus
KW - Membrane potential
KW - Mitochondria
KW - Thymoquinone
KW - mPTP
LA - eng
IS - 1950-6007 (Electronic)
PT - Journal Article
TA - Biomed Pharmacother
YR - 2018
DATE- 20180504
CI - Copyright &copy; 2018 Elsevier Masson SAS. All rights reserved.
CITO- NLM
CS - France
FJT - Biomedicine &amp; pharmacotherapy = Biomedecine &amp; pharmacotherapie
EDAT- 20180405
STAT- In-Process
DOCNO- medline/29710533

143 - TOXLINE
TI - Arsenic levels in cutaneous appendicular organs are correlated with
digitally evaluated hyperpigmented skin of the forehead but not the sole
in Bangladesh residents.
AU - Yajima I
AD - Voluntary Body for International Health Care in Universities, 65 Tsurumai-
cho, Showa-ku, Nagoya, Aichi 466-8550, Japan.
AU - Ahsan N
AD - Department of Genetic Engineering and Biotechnology, University of Dhaka,
Dhaka 1000, Bangladesh.
AU - Akhand AA
AD - Department of Genetic Engineering and Biotechnology, University of Dhaka,
Dhaka 1000, Bangladesh.
AU - Al Hossain MA
AD - Department of Occupational and Environmental Health, Nagoya University
Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550,
Japan.
AU - Yoshinaga M
AD - Department of Occupational and Environmental Health, Nagoya University
Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550,
Japan.
AU - Ohgami N
AD - Voluntary Body for International Health Care in Universities, 65 Tsurumai-
cho, Showa-ku, Nagoya, Aichi 466-8550, Japan.
AU - Iida M
AD - Voluntary Body for International Health Care in Universities, 65 Tsurumai-
cho, Showa-ku, Nagoya, Aichi 466-8550, Japan.
AU - Oshino R
AD - Voluntary Body for International Health Care in Universities, 65 Tsurumai-
cho, Showa-ku, Nagoya, Aichi 466-8550, Japan.
AU - Naito M
AD - Department of Preventive Medicine, Nagoya University Graduate School of
Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550, Japan.
AU - Wakai K
AD - Department of Preventive Medicine, Nagoya University Graduate School of
Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550, Japan.
AU - Kato M
AD - Voluntary Body for International Health Care in Universities, 65 Tsurumai-
cho, Showa-ku, Nagoya, Aichi 466-8550, Japan.
SO - J Expo Sci Environ Epidemiol. 2018, Jan; 28(1):64-68. [Journal of exposure
science & environmental epidemiology]
AB - There has been no report showing the effect of arsenic level on digitized
skin pigmentation level, a typical diagnostic marker for arsenicosis.
Correlations among history of drinking well water, arsenic levels in hair
and toenails, and digitalized skin pigmentation levels (L*-value) in
sunlight-exposed (forehead) and unexposed (sole) skin areas digitally
evaluated by using a reflectance spectrophotometer were examined in 150
residents of Bangladesh. Univariate analysis showed that arsenic levels in
hair and toenails of subjects with a history of drinking well water were
10.6-fold and 7.1-fold higher, respectively, than those in subjects
without a history of drinking well water. The mean L*-value of foreheads,
but not that of soles, in subjects with a history of drinking well water
was 1.15-fold lower (more pigmented) than that in subjects without a
history of drinking well water. Significant correlations were found
between duration of drinking well water and arsenic concentrations in hair
(r=0.63; P < 0.01) and toenails (r=0.60; P < 0.01). Multivariate
analysis showed that the arsenic levels in hair and toenails and the
duration of drinking well water were strongly correlated with the
digitized pigmented level of the forehead but not that of the sole. An
increase in the duration of drinking well water may increase
hyperpigmentation in the forehead, but not that in the sole, through an
increased arsenic level in the human body as shown in cutaneous
appendicular organs (hair and toenails).
RN - N712M78A8G
LA - eng
IS - 1559-064X (Electronic)
PT - Comparative Study
PT - Journal Article
TA - J Expo Sci Environ Epidemiol
YR - 2018
DATE- 20180507
CITO- NLM
CS - United States
CSET- IM
FJT - Journal of exposure science &amp; environmental epidemiology
EDAT- 20161214
STAT- MEDLINE
CM - Cites: FASEB J. 2007 Apr;21(4):976-94 (medline /17242160)
CM - Cites: IARC Monogr Eval Carcinog Risks Hum. 2004;84:1-477 (medline
/15645577)
CM - Cites: Cancer Epidemiol Biomarkers Prev. 1998 Mar;7(3):203-6 (medline
/9521433)
CM - Cites: Environ Health Perspect. 1977 Aug;19:109-19 (medline /908285)
CM - Cites: Cancer Epidemiol Biomarkers Prev. 2011 Aug;20(8):1622-8 (medline
/21680533)
CM - Cites: J Korean Med Sci. 2005 Feb;20(1):105-8 (medline /15716613)
CM - Cites: Int J Epidemiol. 1998 Oct;27(5):871-7 (medline /9839746)
CM - Cites: J Health Popul Nutr. 2010 Feb;28(1):14-22 (medline /20214082)
CM - Cites: Arch Toxicol. 2012 Jun;86(6):961-73 (medline /22526373)
CM - Cites: J Invest Dermatol. 2015 Apr;135(4):1147-1156 (medline /25493652)
CM - Cites: PLoS One. 2013 Jun 21;8(6):e66681 (medline /23805262)
CM - Cites: Indian J Community Med. 2010 Apr;35(2):331-8 (medline /20922118)
CM - Cites: Arch Toxicol. 2013 Mar;87(3):439-47 (medline /23100159)
CM - Cites: J Cell Biol. 2004 Apr 26;165(2):275-85 (medline /15117970)
CM - Cites: Pigment Cell Res. 2003 Dec;16(6):629-38 (medline /14629720)
CM - Cites: Toxicol Appl Pharmacol. 2004 Aug 1;198(3):243-52 (medline
/15276403)
CM - Cites: J Environ Sci Health A Tox Hazard Subst Environ Eng. 2003
Jan;38(1):141-63 (medline /12635824)
CM - Cites: Hum Toxicol. 1983 Jan;2(1):121-33 (medline /6840787)
CM - Cites: Phys Med Biol. 1988 Jun;33(6):711-22 (medline /3406055)
CM - Cites: Mol Cell Biochem. 2005 Nov;279(1-2):105-12 (medline /16283519)
CM - Cites: J Indian Med Assoc. 1998 Jan;96(1):4-7, 18 (medline /9601181)
CM - Cites: J Expo Sci Environ Epidemiol. 2016 Sep;26(5):488-93 (medline
/26464097)
DOCNO- medline/27966667

144 - TOXLINE
TI - Revisiting the biogeochemistry of arsenic in the Baltic Sea: Impact of
anthropogenic activity.
AU - Li L
AD - Key Laboratory of Marine Chemistry Theory and Technology, Ministry of
Education, Ocean University of China, 238 Songling Road, Qingdao 266100, PR China;
Laboratory for Marine Ecology and Environmental Science, Qingdao National
Laboratory for Marine Science and Technology, Qingdao 266071, PR China.
AU - Pohl C
AD - Leibniz-Institute for Baltic Sea Research, Seestra&szlig;e 15, D-18119
Warnem�nde, Germany.
AU - Ren JL
AD - Key Laboratory of Marine Chemistry Theory and Technology, Ministry of
Education, Ocean University of China, 238 Songling Road, Qingdao 266100, PR China;
Laboratory for Marine Ecology and Environmental Science, Qingdao National
Laboratory for Marine Science and Technology, Qingdao 266071, PR China. Electronic
address: renjingl@ouc.edu.cn.
AU - Schulz-Bull D
AD - Leibniz-Institute for Baltic Sea Research, Seestra&szlig;e 15, D-18119
Warnem�nde, Germany.
AU - Cao XH
AD - Key Laboratory of Marine Chemistry Theory and Technology, Ministry of
Education, Ocean University of China, 238 Songling Road, Qingdao 266100, PR China.
AU - Nausch G
AD - Leibniz-Institute for Baltic Sea Research, Seestra&szlig;e 15, D-18119
Warnem�nde, Germany.
AU - Zhang J
AD - State Key Laboratory of Estuarine and Coastal Research, East China Normal
University, 3663 Zhongshan Road North, Shanghai 200062, PR China.
SO - Sci Total Environ. 2018, Feb 01; 613-614:557-568. [The Science of the
total environment]
AB - With the increase in anthropogenic environmental disruption, the behavior
of arsenic in the Baltic Sea has received more scientific attention
because of its complex forms and toxicity, and was re-visited to determine
if there have been measurable changes recently. A cruise was conducted in
10-19 May 2011 to investigate the species and distribution of total
dissolved inorganic arsenic (TDIAs: [TDIAs]=[As(V)]+[As(III)]) revealing
links between the hydrographic dynamics and biological/chemical reactions
in the Baltic Sea. In addition, long-term (2002-2010) time-series
investigations of particulate arsenic in the Gotland Basin were also
conducted in February every year for monitoring purposes. The behavior of
TDIAs was non-conservative due to the removal and regeneration processes
occurring in the Baltic Sea. Biological scavenging plays a dominant role
as sink for TDIAs, with removal amount of 3.1&plusmn;1.6nmol/L above the
pycnocline of the Baltic Sea. Significant regeneration of TDIAs was
observed below the pycnocline of the Baltic Sea, which was closely related
to hypoxia. The decomposition of organic arsenic and release from the
sediment by desorption of As-bearing Fe and Mn oxides were thought to be
two major sources for TDIAs regeneration. The median concentration of
TDIAs (8.4nmol/L) was much lower than in most marginal seas and oceans,
including the near-bottom water around a chemical weapon dumpsite
(13.9nmol/L). The hypoxia in the deep water contributed to the increase in
As(III) concentrations based on the relationship between As(III)/TDIAs
ratio and apparent oxygen utilization. If the difference of As(III)
profiles (1981 and 2011) actually represents a long-term increase in
As(III) concentrations and a shoaling of the As(III) chemocline, these
factors could enhance the toxic effects and extend the residence time of
arsenic and, hence, potentially have negative impacts on fisheries and
ecosystem health in the Baltic Sea.
KW - Arsenic
KW - Baltic Sea
KW - Chemical weapon dump
KW - Hypoxia
KW - Inorganic species
LA - eng
IS - 1879-1026 (Electronic)
PT - Journal Article
TA - Sci Total Environ
YR - 2018
DATE- 20180319
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - The Science of the total environment
EDAT- 20170926
STAT- PubMed-not-MEDLINE
DOCNO- medline/28926810

145 - TOXLINE
TI - Determination of Arsenic Species in Ophiocordyceps sinensis from Major
Habitats in China by HPLC-ICP-MS and the Edible Hazard Assessment.
AU - Guo LX
AD - Dongguan Key Laboratory of Environmental Medicine, School of Public Health,
Guangdong Medical University, Dongguan 523808, China. glx525@gdmu.edu.cn.
AU - Zhang GW
AD - Shenzhen Academy of Metrology and Quality Inspection, Shenzhen 518000, China.
zhguiw98@163.com.
AU - Wang JT
AD - Dongguan Key Laboratory of Environmental Medicine, School of Public Health,
Guangdong Medical University, Dongguan 523808, China. Vivian_jtw@163.com.
AU - Zhong YP
AD - Dongguan Key Laboratory of Environmental Medicine, School of Public Health,
Guangdong Medical University, Dongguan 523808, China. ZYP13415680421@live.com.
AU - Huang ZG
AD - Dongguan Key Laboratory of Environmental Medicine, School of Public Health,
Guangdong Medical University, Dongguan 523808, China. hzg@gdmu.edu.cn.
SO - Molecules. 2018, Apr 26. [Molecules (Basel, Switzerland)]
AB - This study sought to determine the concentration and distribution of
arsenic (As) species in Ophiocordyceps sinensis (O. sinensis), and to
assess its edible hazard for long term consumption. The total arsenic
concentrations, measured through inductively coupled plasma mass
spectrometry (ICP-MS), ranged from 4.00 mg/kg to 5.25 mg/kg. As determined
by HPLC-ICP-MS, the most concerning arsenic species&amp;mdash;AsB, MMAV,
DMAV, AsV, and As&#1064;&amp;mdash;were either not detected (MMAV and
DMAV) or were detected as minor As species (AsB: 1.4&#8315;2.9%; AsV:
1.3&#8315;3.2%, and As&#1064;: 4.1&#8315;6.0%). The major components were
a cluster of unknown organic As (uAs) compounds with As&#1064;, which
accounted for 91.7&#8315;94.0% of the As content. Based on the
H&#8322;O&#8322; test and the chromatography behavior, it can be inferred
that, the uAs might not be toxic organic As. Estimated daily intake (EDI),
hazard quotient (HQ), and cancer risk (CR) caused by the total As content;
the sum of inorganic As (iAs) and uAs, namely i+uAs; and iAs exposure from
long term O. sinensis consumption were calculated and evaluated through
equations from the US Environmental Protection Agency and the
uncertainties were analyzed by Monte-Carlo Simulation (MCS). EDItotal As
and EDIi+uAs are approximately ten times more than EDIiAs; HQtotalAs and
HQi+uAs > 1 while HQiAs < 1; and CRtotal As and CRi+uAs > 1
&amp;times; 10&amp;minus;4 while CRiAs < 1 &amp;times; 10&amp;minus;4.
Thus, if the uAs is non-toxic, there is no particular risk to local
consumers and the carcinogenic risk is acceptable for consumption of O.
sinensis because the concentration of toxic iAs is very low.
KW - HPLC-ICP-MS
KW - Ophiocordyceps sinensis
KW - arsenic speciation
KW - risk assessment
LA - eng
IS - 1420-3049 (Electronic)
PT - Journal Article
TA - Molecules
YR - 2018
DATE- 20180427
CITO- NLM
CS - Switzerland
FJT - Molecules (Basel, Switzerland)
EDAT- 20180426
STAT- In-Process
DOCNO- medline/29701658

146 - TOXLINE
TI - Phosphate starvation response controls genes required to synthesize the
phosphate analog arsenate.
AU - Wang Q
AD - Departments of Land Resources &amp; Environmental Sciences, Montana State
University, Bozeman, MT 59717, USA.
AU - Kang YS
AD - Departments of Land Resources &amp; Environmental Sciences, Montana State
University, Bozeman, MT 59717, USA.
AU - Alowaifeer A
AD - Departments of Land Resources &amp; Environmental Sciences, Montana State
University, Bozeman, MT 59717, USA.
AU - Shi K
AD - State Key Laboratory of Agricultural Microbiology, College of Life Science
and Technology, Huazhong Agricultural University, Wuhan, 430070, People's Republic
of China.
AU - Fan X
AD - State Key Laboratory of Agricultural Microbiology, College of Life Science
and Technology, Huazhong Agricultural University, Wuhan, 430070, People's Republic
of China.
AU - Wang L
AD - State Key Laboratory of Agricultural Microbiology, College of Life Science
and Technology, Huazhong Agricultural University, Wuhan, 430070, People's Republic
of China.
AU - Jetter J
AD - Departments of Land Resources &amp; Environmental Sciences, Montana State
University, Bozeman, MT 59717, USA.
AU - Bothner B
AD - Chemistry and Biochemistry, Montana State University, Bozeman, MT 59717, USA.
AU - Wang G
AD - State Key Laboratory of Agricultural Microbiology, College of Life Science
and Technology, Huazhong Agricultural University, Wuhan, 430070, People's Republic
of China.
AU - McDermott TR
AD - Departments of Land Resources &amp; Environmental Sciences, Montana State
University, Bozeman, MT 59717, USA.
SO - Environ Microbiol. 2018, May; 20(5):1782-1793. [Environmental
microbiology]
AB - Environmental arsenic poisoning affects roughly 200 million people
worldwide. The toxicity and mobility of arsenic in the environment is
significantly influenced by microbial redox reactions, with arsenite
(AsIII ) being more toxic than arsenate (AsV ). Microbial oxidation of
AsIII to AsV is known to be regulated by the AioXSR signal transduction
system and viewed to function for detoxification or energy generation.
Here, we show that AsIII oxidation is ultimately regulated by the
phosphate starvation response (PSR), requiring the sensor kinase PhoR for
expression of the AsIII oxidase structural genes aioBA. The PhoRB and
AioSR signal transduction systems are capable of transphosphorylation
cross-talk, closely integrating AsIII oxidation with the PSR. Further,
under PSR conditions, AsV significantly extends bacterial growth and
accumulates in the lipid fraction to the apparent exclusion of phosphorus.
This could spare phosphorus for nucleic acid synthesis or triphosphate
metabolism wherein unstable arsenic esters are not tolerated, thereby
enhancing cell survival potential. We conclude that AsIII oxidation is
logically part of the bacterial PSR, enabling the synthesis of the
phosphate analog AsV to replace phosphorus in specific biomolecules or to
synthesize other molecules capable of a similar function, although not for
total replacement of cellular phosphate.
LA - eng
IS - 1462-2920 (Electronic)
PT - Journal Article
TA - Environ Microbiol
YR - 2018
DATE- 20180426
CI - &copy; 2018 Society for Applied Microbiology and John Wiley &amp; Sons
Ltd.
CITO- NLM
CS - England
FJT - Environmental microbiology
EDAT- 20180410
STAT- In-Data-Review
DOCNO- medline/29575522

147 - TOXLINE
TI - Ellagic acid: A promising protective remedy against testicular toxicity
induced by arsenic.
AU - Mehrzadi S
AD - Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran.
AU - Bahrami N
AD - Department of Midwifery, Faculty of Nursing and Midwifery, Dezful University
of Medical Sciences, Dezful, Iran.
AU - Mehrabani M
AD - Physiology Research Center, Institute of Basic and Clinical Physiology
Sciences, Kerman University of Medical Sciences, Kerman, Iran.
AU - Motevalian M
AD - Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran.
AU - Mansouri E
AD - Cellular and Molecular Research Center, Department of Anatomical Sciences,
Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
AU - Goudarzi M
AD - Medicinal Plant Research Center, Ahvaz Jundishapur University of Medical
Sciences, Ahvaz, Iran. Electronic address: Mehrzadi.s@iums.ac.ir.
SO - Biomed Pharmacother. 2018, Jul; 103:1464-1472. [Biomedicine &
pharmacotherapy = Biomedecine & pharmacotherapie]
AB - Chronic exposure to arsenic, an inducer of oxidative stress, is one of the
major causes of male infertility. Therefore, the present study
investigated the protective role of Ellagic acid (EA), as a natural
antioxidant, against testicular toxicity evoked by arsenic. Thirty-five
male Wistar rats were divided into 5 treatment groups. Group 1 served as
control, group 2 were orally exposed to sodium arsenite (SA,
10&#8239;mg/kg; 21 days), groups 3 and 4 were initially exposed to SA for
7 days and then were treated with both EA (10 and 30&#8239;mg/kg) and SA
up to 21 days, and group 5 was treated with EA for 14 days. After this
period, biochemical and histopathological parameters were evaluated in
serum samples and testicular tissue. SA markedly reduced levels of serum
testosterone, total antioxidant capacity, reduced glutathione as well as
the activity of antioxidant enzymes. Furthermore, SA enhanced levels of
malondialdehyde, tumor necrosis factor-&alpha;, interleukin-1&beta; and
nitric oxide in testes. Treatment with EA was found to reduce testicular
arsenic accumulation and oxidative stress parameters. In addition, EA
improved the serum testosterone level, testicular antioxidant markers and
histological parameters after exposure to SA. EA may emerge as a promising
therapeutic option to protect testes from arsenic-induced toxicity through
reducing oxidative stress and inflammatory responses.
KW - Arsenic
KW - Ellagic acid
KW - Male infertility
KW - Oxidative stress
KW - Rat
KW - Testes
LA - eng
IS - 1950-6007 (Electronic)
PT - Journal Article
TA - Biomed Pharmacother
YR - 2018
DATE- 20180605
CI - Copyright &copy; 2018 Elsevier Masson SAS. All rights reserved.
CITO- NLM
CS - France
FJT - Biomedicine &amp; pharmacotherapy = Biomedecine &amp; pharmacotherapie
EDAT- 20180507
STAT- In-Process
DOCNO- medline/29864931

148 - TOXLINE
TI - Rapid evaluation of arsenic contamination in paddy soils using field
portable X-ray fluorescence spectrometry.
AU - Liang JH
AD - Key Laboratory of Karst Ecosystem and Treatment of Rocky Desertification,
Institute of Karst Geology, Chinese Academy of Geological Sciences, Guilin 541004,
China; State Key Laboratory of Urban and Regional Ecology, Research Center for Eco-
Environmental Sciences, Chinese Academy of Sciences, Beijing, 100085, China.
AU - Liu PP
AD - State Key Joint Laboratory of Environment Simulation and Pollution Control,
School of Environment, Tsinghua University, Beijing 100084, China; State Key
Laboratory of Urban and Regional Ecology, Research Center for Eco-Environmental
Sciences, Chinese Academy of Sciences, Beijing, 100085, China.
AU - Chen Z
AD - State Key Laboratory of Urban and Regional Ecology, Research Center for Eco-
Environmental Sciences, Chinese Academy of Sciences, Beijing, 100085, China;
Department of Environmental Science, Xi'an Jiaotong-Liverpool University, Suzhou
215123, China. Electronic address: zheng.chen@xjtlu.edu.cn.
AU - Sun GX
AD - State Key Laboratory of Urban and Regional Ecology, Research Center for Eco-
Environmental Sciences, Chinese Academy of Sciences, Beijing, 100085, China.
AU - Li H
AD - College of Urban Construction and Environmental Engineering, Chongqing
University, Chongqing 400045, China.
SO - J Environ Sci (China). 2018, Feb; 64:345-351. [Journal of environmental
sciences (China)]
AB - Arsenic (As) in paddy fields is deteriorating food security and human
health through rice ingestion. Rice is the dominant food source of arsenic
exposure to half of the world's population. Therefore, an in situ
effective method for As risk evaluation in paddy soil is strongly needed
to avoid As exposure through rice ingestion. Herein, we developed a rapid
analytical methodology for determination of As in plant tissues using
field portable X-ray fluorescence spectrometry (FP-XRF). This method was
applied to rice roots in order to evaluate the As contamination in paddy
soils. The results showed that rice roots with iron plaques were superior
to rhizosphere soils for generating FP-XRF signals, especially for field
sites with As concentrations lower than the soil detection limit of FP-XRF
(30.0mg/kg). Moreover, the strong linear relationships of As
concentrations between the rice roots and corresponding leaves and grains
proved that the rice root, rather than the soil, is a better predictor of
As concentrations in rice grains. The research provides an efficient As
monitoring method for As contaminated paddy fields by using wetland plant
roots with iron plaques and XRF-based analytical techniques.
KW - Arsenic
KW - Iron plaque
KW - Rhizosphere soils
KW - Rice roots
KW - Risk evaluation
KW - XRF
RN - N712M78A8G
LA - eng
IS - 1001-0742 (Print)
PT - Journal Article
TA - J Environ Sci (China)
YR - 2018
DATE- 20180301
CI - Copyright &copy; 2017. Published by Elsevier B.V.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Journal of environmental sciences (China)
EDAT- 20171124
STAT- MEDLINE
DOCNO- medline/29478657

149 - TOXLINE
TI - Toxicity assessment of arsenate and arsenite on growth, chlorophyll a
fluorescence and antioxidant machinery in Nostoc muscorum.
AU - Patel A
AD - Ranjan Plant physiology and Biochemistry Laboratory, Department of Botany,
University of Allahabad, Allahabad 211002, India.
AU - Tiwari S
AD - Ranjan Plant physiology and Biochemistry Laboratory, Department of Botany,
University of Allahabad, Allahabad 211002, India.
AU - Prasad SM
AD - Ranjan Plant physiology and Biochemistry Laboratory, Department of Botany,
University of Allahabad, Allahabad 211002, India. Electronic address:
profsmprasad@gmail.com.
SO - Ecotoxicol Environ Saf. 2018, Aug 15; 157:369-379. [Ecotoxicology and
environmental safety]
AB - The present study deals with impact of varied doses of arsenite (AsIII;
50, 100 and 150&#8239;&micro;M) and arsenate (AsV; 50, 100 and
150&#8239;mM) on growth, photosynthetic pigments, photochemistry of
photosystem II, oxidative biomarkers, (O2&bull;&macr;, H2O2 and MDA
equivalents contents) and activity of antioxidant enzymes in diazotrophic
cyanobacterium Nostoc muscorum after 48 and 96&#8239;h of the treatments.
The reduction in growth, pigment contents (Chl a, Phy and Car) and PS II
photochemistry was found to increase with enhanced accumulation of test
metal in cells, and the damaging effect on photosynthetic pigments showed
the order (Phy > chl a > Car). The negative effect on PS II
photochemistry was due to significant decrease in the value of JIP
kinetics &#981;P0, FV/F0, &#981;E0,&Psi;0 and PIABS except F0/FV and
significant rise in values of energy flux parameters such as ABS/RC,
TR0/RC, ET0/RC and DI0/RC. Both the species of arsenic caused significant
rise in oxidative biomarkers as evident by in vitro and in vivo analysis
of (O2&bull;&macr;, H2O2 and MDA equivalents contents) despite of
appreciable rise in the activity antioxidative enzymes such as SOD, POD,
CAT and GST. The study concludes that in among both forms of arsenic,
arsenite effect was more dominant on growth, photosynthetic pigments;
oxidative stress biomarkers as evident by weak induction of anti-oxidative
defense system to overcome the stress as compared to arsenate.
KW - Antioxidant defense system
KW - Arsenic accumulation
KW - Growth
KW - Isoenzyme profiling
KW - Oxidative biomarkers
KW - PS II photochemistry
LA - eng
IS - 1090-2414 (Electronic)
PT - Journal Article
TA - Ecotoxicol Environ Saf
YR - 2018
DATE- 20180424
CI - Published by Elsevier Inc.
CITO- NLM
CS - Netherlands
FJT - Ecotoxicology and environmental safety
EDAT- 20180406
STAT- In-Process
DOCNO- medline/29631092

150 - TOXLINE
TI - Geographical variations of cadmium and arsenic concentrations and arsenic
speciation in Chinese rice.
AU - Chen H
AD - State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of
Resources and Environmental Sciences, Nanjing Agricultural University, Nanjing,
210095, China.
AU - Tang Z
AD - State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of
Resources and Environmental Sciences, Nanjing Agricultural University, Nanjing,
210095, China.
AU - Wang P
AD - State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of
Resources and Environmental Sciences, Nanjing Agricultural University, Nanjing,
210095, China.
AU - Zhao FJ
AD - State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of
Resources and Environmental Sciences, Nanjing Agricultural University, Nanjing,
210095, China. Electronic address: Fangjie.Zhao@njau.edu.cn.
SO - Environ Pollut. 2018, Jul; 238:482-490. [Environmental pollution (Barking,
Essex : 1987)]
AB - Rapid industrialization in China in recent decades has resulted in soil
contamination in some areas, raising the concern about food safety.
Consumption of rice represents a major exposure route for the toxic
elements cadmium (Cd) and arsenic (As). We collected 160 polished rice
from local markets in 20 provinces in China and determined total Cd and As
concentrations and As speciation. Total Cd concentration ranged from below
the detection limit to 0.77&#8239;mg&#8239;kg-1, with 10% of the samples
exceeding the Chinese limit (0.2&#8239;mg&#8239;kg-1). Rice Cd
concentration showed a distinct geographical pattern, increasing from low
levels in the north to high levels in the south of China. Median daily Cd
intake from rice varied from 0.01&#8239;&mu;g&#8239;kg-1 body weight in
the north to 0.61&#8239;&mu;g&#8239;kg-1 body weight in the south of
China, representing between 1% and 73% of the tolerable daily intake (TDI)
recommended by FAO/WHO. The highest median Cd intake from rice was in
Hunan province with 2 times TDI. Total As concentration ranged from 0.011
to 0.186&#8239;mg&#8239;kg-1, with inorganic As (iAs) and dimethylarsinic
acid (DMAs) on average accounting for 69% and 31%, respectively. All
samples were below the Chinese limit for iAs in rice
(0.2&#8239;mg&#8239;kg-1). There was no clear geographical pattern in rice
total As concentration, but rice produced in northeastern China contained
higher percentages of DMAs and lower percentages of iAs. This study
highlights a high risk of Cd exposure from rice consumption for the
population of southern China and suggested strategies for reducing Cd
accumulation in rice crop.
KW - Arsenic
KW - Arsenic speciation
KW - Cadmium
KW - Dietary intake
KW - Rice
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180515
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Environmental pollution (Barking, Essex : 1987)
EDAT- 20180330
STAT- In-Process
DOCNO- medline/29602104

151 - TOXLINE
TI - Arsenate biotransformation by Microcystis aeruginosa under different
nitrogen and phosphorus levels.
AU - Che F
AD - Key Laboratory of Urban Environment and Health, Institute of Urban
Environment, Chinese Academy of Sciences, Xiamen 361021, China. Electronic address:
cheff411@sina.com.
AU - Du M
AD - Key Laboratory of Urban Environment and Health, Institute of Urban
Environment, Chinese Academy of Sciences, Xiamen 361021, China.
AU - Yan C
AD - Key Laboratory of Urban Environment and Health, Institute of Urban
Environment, Chinese Academy of Sciences, Xiamen 361021, China. Electronic address:
czyan@iue.ac.cn.
SO - J Environ Sci (China). 2018, Apr; 66:41-49. [Journal of environmental
sciences (China)]
AB - The arsenate (As(V)) biotransformation by Microcystis aeruginosa in a
medium with different concentrations of nitrogen (N) and phosphorus (P)
has been studied under laboratory conditions. When 15&mu;g/L As(V) was
added, N and P in the medium showed effective regulation on arsenic (As)
metabolism in M. aeruginosa, resulting in significant differences in the
algal growth among different N and P treatments. Under 0.2mg/L P
treatment, increases in N concentration (4-20mg/L) significantly
stimulated the cell growth and therefore indirectly enhanced the
production of dimethylarsinic acid (DMA), the main As metabolite,
accounting for 71%-79% of the total As in the medium. Meanwhile, 10-20mg/L
N treatments accelerated the ability of As metabolization by M.
aeruginosa, leading to higher contents of DMA per cell. However, As(V)
uptake by M. aeruginosa was significantly impeded by 0.5-1.0mg/L P
treatment, resulting in smaller rates of As transformation in M.
aeruginosa as well as lower contents of As metabolites in the medium. Our
data demonstrated that As(V) transformation by M. aeruginosa was
significantly accelerated by increasing N levels, while it was inhibited
by increasing P levels. Overall, both P and N play key roles in As(V)
biotransformation processes.
KW - Arsenate
KW - Biotransformation
KW - M. aeruginosa
KW - Nitrogen
KW - Phosphorus
RN - 27YLU75U4W
RN - N762921K75
LA - eng
IS - 1001-0742 (Print)
PT - Journal Article
TA - J Environ Sci (China)
YR - 2018
DATE- 20180419
CI - Copyright &copy; 2017. Published by Elsevier B.V.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Journal of environmental sciences (China)
EDAT- 20170607
STAT- MEDLINE
DOCNO- medline/29628107

152 - TOXLINE
TI - Cellular shear stiffness reflects progression of arsenic-induced
transformation during G1.
AU - Mu�oz A
AD - Centre for Symmetry and Deformation, Department of Mathematical Sciences,
University of Copenhagen, Copenhagen &Oslash;, Denmark.
AU - Eldridge WJ
AD - Department of Biomedical Engineering, Duke University, Durham, NC, USA.
AU - Jakobsen NM
AD - Department of Applied Mathematics and Computer Science, Technical University
of Denmark, Lyngby, Denmark.
AU - S�rensen H
AD - Laboratory for Applied Statistics, Department of Mathematical Sciences,
University of Copenhagen, Copenhagen &Oslash;, Denmark.
AU - Wax A
AD - Department of Biomedical Engineering, Duke University, Durham, NC, USA.
AU - Costa M
AD - Department of Environmental Medicine, New York University School of Medicine,
Tuxedo, NY, USA.
SO - Carcinogenesis. 2018, Feb 09; 39(2):109-117. [Carcinogenesis]
AB - Cancer cells consistently exhibit decreased stiffness; however, the onset
and progression of this change have not been characterized. To study the
development of cell stiffness changes, we evaluated the shear stiffness of
populations of cells during transformation to a carcinogenic state.
Bronchial epithelial cells were exposed to sodium arsenite to initiate
early stages of transformation. Exposed cells were cultured in soft agar
to further transformation and select for clonal populations exhibiting
anchorage-independent growth. Shear stiffness of various cell populations
in G1 was assessed using a novel non-invasive assay that applies shear
stress with fluid flow and evaluates nanoscale deformation using
quantitative phase imaging (QPI). Arsenic-treated cells exhibited reduced
stiffness relative to control cells, while arsenic clonal lines, selected
by growth in soft agar, were found to have reduced stiffness relative to
control clonal lines, which were cultured in soft agar but did not receive
arsenic treatment. The relative standard deviation (RSD) of the stiffness
of Arsenic clones was reduced compared with control clones, as well as to
the arsenic-exposed cell population. Cell stiffness at the population
level exhibits potential to be a novel and sensitive framework for
identifying the development of cancerous cells.
LA - eng
IS - 1460-2180 (Electronic)
PT - Journal Article
TA - Carcinogenesis
YR - 2018
DATE- 20180330
CI - &copy; The Author(s) 2017. Published by Oxford University Press. All
rights reserved. For Permissions, please email:
journals.permissions@oup.com.
CITO- NLM
CS - England
FJT - Carcinogenesis
STAT- In-Data-Review
CM - Cites: Science. 2005 Nov 18;310(5751):1139-43 (medline /16293750)
CM - Cites: Opt Lett. 2016 Jan 15;41(2):352-5 (medline /26766712)
CM - Cites: Environ Health Perspect. 2010 Jan;118(1):108-15 (medline /20056578)
CM - Cites: Biochem Biophys Res Commun. 2008 Oct 3;374(4):609-13 (medline
/18656442)
CM - Cites: J Biomed Opt. 2010 Jan-Feb;15(1):010505 (medline /20210420)
CM - Cites: J Natl Cancer Inst. 2010 May 5;102(9):638-49 (medline /20339138)
CM - Cites: Environ Health Perspect. 2011 Jan;119(1):11-9 (medline /20682481)
CM - Cites: J Expo Sci Environ Epidemiol. 2006 Mar;16(2):191-205 (medline
/16160703)
CM - Cites: Exp Cell Res. 1971 Sep;68(1):163-8 (medline /5165443)
CM - Cites: Environ Health Perspect. 2008 Feb;116(2):158-64 (medline /18288312)
CM - Cites: Nat Rev Cancer. 2009 Feb;9(2):108-22 (medline /19165226)
CM - Cites: Phys Rev E Stat Nonlin Soft Matter Phys. 2015 Oct;92(4):040702
(medline /26565151)
CM - Cites: Cell. 2011 Mar 4;144(5):646-74 (medline /21376230)
CM - Cites: Br J Cancer. 2012 Jul 10;107(2):224-9 (medline /22691969)
CM - Cites: Free Radic Biol Med. 2011 Jul 15;51(2):257-81 (medline /21554949)
CM - Cites: Toxicol Sci. 2007 Jul;98(1):75-86 (medline /17283378)
CM - Cites: Curr Opin Cell Biol. 2010 Oct;22(5):697-706 (medline /20822891)
CM - Cites: Biomed Opt Express. 2012 May 1;3(5):958-65 (medline /22567588)
CM - Cites: FASEB J. 2006 May;20(7):811-27 (medline /16675838)
CM - Cites: Cancer Res. 2011 Aug 1;71(15):5075-80 (medline /21642375)
CM - Cites: Cancer Res. 2009 Mar 1;69(5):1728-32 (medline /19223529)
CM - Cites: Cancer Res. 1978 Oct;38(10):3174-81 (medline /210930)
CM - Cites: Annu Rev Public Health. 2012 Apr;33:137-56 (medline /22224878)
CM - Cites: J Biomed Opt. 2011 Mar;16(3):030506 (medline /21456860)
CM - Cites: Environ Health Perspect. 2013 Jul;121(7):832-8 (medline /23665672)
CM - Cites: Metallomics. 2013 Oct;5(10):1357-67 (medline /23963610)
CM - Cites: PLoS One. 2011 Mar 18;6(3):e17982 (medline /21437242)
CM - Cites: Biophys J. 2005 May;88(5):3689-98 (medline /15722433)
CM - Cites: Environ Geochem Health. 2009 Apr;31 Suppl 1:189-200 (medline
/19190988)
CM - Cites: Analyst. 2008 Nov;133(11):1498-500 (medline /18936825)
CM - Cites: Exp Cell Res. 2002 Aug 1;278(1):92-100 (medline /12126961)
CM - Cites: Nat Methods. 2015 Mar;12(3):199-202, 4 p following 202 (medline
/25643151)
CM - Cites: Acta Biomater. 2007 Jul;3(4):413-38 (medline /17540628)
CM - Cites: Cancer Cell. 2005 Sep;8(3):241-54 (medline /16169468)
CM - Cites: Eur Biophys J. 1999;28(4):312-6 (medline /10394623)
CM - Cites: Cancer Res. 2016 Jun 1;76(11):3136-44 (medline /27009166)
CM - Cites: Clin Cancer Res. 2015 Jul 1;21(13):2916-23 (medline /25838394)
CM - Cites: Environ Health Perspect. 2006 Aug;114(8):1193-8 (medline /16882524)
CM - Cites: J Cell Sci. 2003 Apr 1;116(Pt 7):1157-73 (medline /12615960)
CM - Cites: Biochim Biophys Acta. 2012 Jul;1820(7):1111-20 (medline /22366469)
CM - Cites: Biomed Opt Express. 2010 Aug 23;1(2):706-719 (medline /21258502)
CM - Cites: Nat Rev Cancer. 2015 Aug;15(8):473-83 (medline /26156638)
CM - Cites: Trends Mol Med. 2012 Sep;18(9):509-15 (medline /22795735)
CM - Cites: Nanotechnology. 2008 Sep 24;19(38):384003 (medline /21832563)
CM - Cites: Science. 1977 Aug 26;197(4306):893-5 (medline /887927)
CM - Cites: Mt Sinai J Med. 2004 Nov;71(6):361-7 (medline /15592654)
CM - Cites: Nat Rev Mol Cell Biol. 2011 May;12(5):308-19 (medline /21508987)
DOCNO- medline/29069374

153 - TOXLINE
TI - ZFAND1 Recruits p97 and the 26S Proteasome to Promote the Clearance of
Arsenite-Induced Stress Granules.
AU - Turakhiya A
AD - Department of Biochemistry, Biocenter, University of W�rzburg, 97074
W�rzburg, Germany.
AU - Meyer SR
AD - Department of Biochemistry, Biocenter, University of W�rzburg, 97074
W�rzburg, Germany.
AU - Marincola G
AD - Department of Biochemistry, Biocenter, University of W�rzburg, 97074
W�rzburg, Germany.
AU - B�hm S
AD - Department of Biochemistry, Biocenter, University of W�rzburg, 97074
W�rzburg, Germany.
AU - Vanselow JT
AD - Rudolf Virchow Center for Experimental Biomedicine, University of W�rzburg,
97080 W�rzburg, Germany.
AU - Schlosser A
AD - Rudolf Virchow Center for Experimental Biomedicine, University of W�rzburg,
97080 W�rzburg, Germany.
AU - Hofmann K
AD - Institute for Genetics, University of Cologne, 50674 Cologne, Germany.
AU - Buchberger A
AD - Department of Biochemistry, Biocenter, University of W�rzburg, 97074
W�rzburg, Germany. Electronic address: alexander.buchberger@uni-wuerzburg.de.
SO - Mol Cell. 2018, Jun 07; 70(5):906-919.e7. [Molecular cell]
AB - Stress granules (SGs) are cytoplasmic assemblies of mRNPs stalled in
translation initiation. They are induced by various stress conditions,
including exposure to the environmental toxin and carcinogen arsenic.
While perturbed SG turnover is linked to the pathogenesis of
neurodegenerative diseases, the molecular mechanisms underlying SG
formation and turnover are still poorly understood. Here, we show that
ZFAND1 is an evolutionarily conserved regulator of SG clearance. ZFAND1
interacts with two key factors of protein degradation, the 26S proteasome
and the ubiquitin-selective segregase p97, and recruits them to
arsenite-induced SGs. In the absence of ZFAND1, SGs lack the 26S
proteasome and p97, accumulate defective ribosomal products, and persist
after arsenite removal, indicating their transformation into aberrant,
disease-linked SGs. Accordingly, ZFAND1 depletion is epistatic to the
expression of pathogenic mutant p97 with respect to SG clearance,
suggesting that ZFAND1 function is relevant to the multisystem
degenerative disorder IBMPFD/ALS.
KW - Cdc48
KW - DRiPs
KW - UPS
KW - VCP
KW - arsenic
KW - autophagy
KW - proteasome
KW - proteostasis
KW - stress granules
LA - eng
IS - 1097-4164 (Electronic)
PT - Journal Article
TA - Mol Cell
YR - 2018
DATE- 20180608
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - United States
FJT - Molecular cell
EDAT- 20180524
STAT- In-Data-Review
DOCNO- medline/29804830

154 - TOXLINE
TI - Effects of Combined Exposure to Chronic High-Fat Diet and Arsenic on
Thyroid Function and Lipid Profile in Male Mouse.
AU - Ahangarpour A
AD - Health Research Institute, Diabetes Research Center, Department of
Physiology, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
AU - Alboghobeish S
AD - Department of Pharmacology, School of Medicine, Student Research Committee of
Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
alboghobeish.s@ajums.ac.ir.
AU - Oroojan AA
AD - Department of Physiology, Student Research Committee of Ahvaz Jundishapur
University of Medical Science, Ahvaz, Iran.
AU - Zeidooni L
AD - Department of Toxicology, School of Pharmacy, Student Research Committee of
Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
AU - Samimi A
AD - Department of Toxicology, School of Pharmacy, Student Research Committee of
Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
AU - Afshari G
AD - Golestan Hospital Clinical Research Development Unit, Ahvaz Jundishapur
University of Medical Sciences, Ahvaz, Iran.
SO - Biol Trace Elem Res. 2018, Mar; 182(1):37-48. [Biological trace element
research]
AB - The thyroid is one of the major endocrine glands that contribute to body
and fat metabolism. The present study evaluated the effects of combined
exposure to chronic high-fat diet (HFD) and arsenic on thyroid function
and lipid profile. In this experimental study, 72 male Naval Medical
Research Institute mice were divided into six groups and fed HFD or
low-fat diet (LFD) while being exposed to 25 or 50 ppm of arsenic in
drinking water for 20 weeks. After 24 h of the last experimental
day, blood samples were collected for hormonal and biochemical
measurements. The data indicated that exposure to HFD alone increased the
levels of triiodothyronine (T3), thyroid-stimulating hormone (TSH),
leptin, lipid profile, reactive oxygen species (ROS), and malondialdehyde
(MDA) and decreased the levels of high-density lipoprotein, albumin,
adiponectin, and glutathione sulfhydryl reductase (GSH), whereas exposure
to arsenic alone decreased the levels of T3 and GSH and increased the
levels of TSH, leptin, ROS, MDA, and T4/T3 ratio compared to those in the
control LFD group. Furthermore, concomitant administration of HFD and
arsenic decreased the lipid profile and levels of T4, albumin, total
protein, T3, and GSH and increased the levels of TSH, adiponectin, leptin,
ROS, MDA, and T4/T3 ratio compared to those in the control LFD or HFD
group. In conclusion, combined exposure to HFD and arsenic induced
hypothyroidism via reduction of thyroid hormones and enhancement of plasma
TSH and T3 uptake levels concomitant with hypolipidemia, hyperleptinemia,
hyperadiponectinemia, induction of oxidative stress, and reduction of GSH
levels.
KW - Arsenic
KW - High-fat diet
KW - Lipid profile
KW - Oxidant/antioxidant
KW - Thyroid hormone
LA - eng
IS - 1559-0720 (Electronic)
PT - Journal Article
TA - Biol Trace Elem Res
YR - 2018
DATE- 20180211
CITO- NLM
CS - United States
FJT - Biological trace element research
EDAT- 20170608
STAT- In-Process
DOCNO- medline/28593471

155 - TOXLINE
TI - Preconcentration and speciation of arsenic by using a graphene oxide
nanoconstruct functionalized with a hyperbranched polyethyleneimine.
AU - Ahmad H
AD - Centre for Nanoscience and Nanotechnology, Jamia Millia Islamia (A Central
University), New Delhi, 110025, India. hilalahmad418@gmail.com.
AU - Umar K
AD - Centre for Environmental Sustainability and Water Security (IPASA), Research
Institute for Sustainable Environment, Universiti Teknologi Malaysia, 81310, Johor
Bahru, Johor, Malaysia.
AU - Ali SG
AD - Department of Microbiology, Nanotechnology and Antimicrobial Drug Resistance
Research Laboratory, Jawaharlal Nehru Medical College and Hospital, Aligarh Muslim
University, Aligarh, Uttar Pradesh, 202001, India.
AU - Singh P
AD - Centre for Nanoscience and Nanotechnology, Jamia Millia Islamia (A Central
University), New Delhi, 110025, India.
AU - Islam SS
AD - Centre for Nanoscience and Nanotechnology, Jamia Millia Islamia (A Central
University), New Delhi, 110025, India.
AU - Khan HM
AD - Department of Microbiology, Nanotechnology and Antimicrobial Drug Resistance
Research Laboratory, Jawaharlal Nehru Medical College and Hospital, Aligarh Muslim
University, Aligarh, Uttar Pradesh, 202001, India.
SO - Mikrochim Acta. 2018, May 10; 185(6):290. [Mikrochimica acta]
AB - A column sorbent for arsenic was obtained through immobilization of highly
branched polyethylenimine (PEI) on graphene oxide (GO). The composite
material enables speciation of arsenic by tuning the pH of the sample
solution which governs the surface charge of the sorbent, depending on
whether amino groups (-NH2) are present (at high pH) or ammonium groups
(-NH3+; at low pH). The composite can be applied to improved speciation of
arsenic (compared to unmodified GO). There is no need for oxidation or
reduction of arsenic. A column procedure was applied for the sequestered
extraction and speciation of As(III) and As(V) from environmental water
samples before their determination by hydride generation-microwave induced
plasma-atomic emission spectrometry. The method has a preconcentration
factor of 440 for As(III) and of 400 for As(V). The limits of detection
(at 3 S/N) are extremely low, being 1.8 &plusmn;&thinsp;0.2
ngL-1 for As(III) and 1.3 &plusmn;&thinsp;0.08 ngL-1 for As(V). This
is much lower than the arsenic guideline value of 10 &mu;gL-1 as given by
the WHO. Graphical abstract Graphene oxide interconnected with
polyethyleneimine has been employed for the speciation and determination
of arsenic. Quantitation by atomic emission spectroscopy reveals a high
preconcentration factor (440 and 400) and low LODs of
1.8&thinsp;&plusmn;&thinsp;0.2 and 1.3&thinsp;&plusmn;&thinsp;0.08
ngL-1for As(III) and As(V), respectively.
KW - Adsorption
KW - Nanosorbent
KW - Remediation
KW - Removal
KW - Selectivity
KW - Solid phase extraction
KW - Toxicity
KW - Wastewater
LA - eng
IS - 1436-5073 (Electronic)
PT - Journal Article
TA - Mikrochim Acta
YR - 2018
DATE- 20180514
CITO- NLM
CS - Austria
FJT - Mikrochimica acta
EDAT- 20180510
STAT- In-Data-Review
CM - Cites: Science. 2013 Aug 23;341(6148):866-8 (medline /23970694)
CM - Cites: Anal Chim Acta. 2014 Jun 27;834:22-9 (medline /24928241)
CM - Cites: ACS Appl Mater Interfaces. 2014 Aug 13;6(15):13257-65 (medline
/25003835)
CM - Cites: Anal Chem. 2015 Aug 18;87(16):8503-9 (medline /26211572)
CM - Cites: ACS Appl Mater Interfaces. 2013 Apr 24;5(8):3304-11 (medline
/23528072)
CM - Cites: Science. 2002 Jun 21;296(5576):2143-5 (medline /12077387)
CM - Cites: Chem Commun (Camb). 2013 Aug 14;49(63):7064-6 (medline /23817554)
CM - Cites: Anal Chem. 2016 Jan 5;88(1):228-49 (medline /26616153)
CM - Cites: Chem Soc Rev. 2015 Aug 21;44(16):5861-96 (medline /25812036)
DOCNO- medline/29748777

156 - TOXLINE
TI - Experimental manipulation of dietary arsenic levels in great tit
nestlings: Accumulation pattern and effects on growth, survival and plasma
biochemistry.
AU - S�nchez-Virosta P
AD - Department of Biology, University of Turku, Turku FI-20014, Finland; Area of
Toxicology, Department of Socio-Sanitary Sciences, University of Murcia, Campus de
Espinardo, 30100 Murcia, Spain. Electronic address: pasanv@utu.fi.
AU - Esp�n S
AD - Department of Biology, University of Turku, Turku FI-20014, Finland; Area of
Toxicology, Department of Socio-Sanitary Sciences, University of Murcia, Campus de
Espinardo, 30100 Murcia, Spain. Electronic address: sieslu@utu.fi.
AU - Ruiz S
AD - Department of Biology, University of Turku, Turku FI-20014, Finland.
Electronic address: srruiz@utu.fi.
AU - Salminen JP
AD - Laboratory of Organic Chemistry and Chemical Biology, Department of
Chemistry, University of Turku, Turku FI-20014, Finland. Electronic address: j-
p.salminen@utu.fi.
AU - Garc�a-Fern�ndez AJ
AD - Area of Toxicology, Department of Socio-Sanitary Sciences, University of
Murcia, Campus de Espinardo, 30100 Murcia, Spain. Electronic address: ajgf@um.es.
AU - Eeva T
AD - Department of Biology, University of Turku, Turku FI-20014, Finland.
Electronic address: teeva@utu.fi.
SO - Environ Pollut. 2018, Feb; 233:764-773. [Environmental pollution (Barking,
Essex : 1987)]
AB - Arsenic (As) is a ubiquitous metalloid classified as one of the most
hazardous substances, but information about its exposure and effects in
free-living passerines is lacking. The aim of this study is to elucidate
the effect of an As manipulation experiment on survival, growth and
physiology of great tits (Parus major). Wild P. major nestlings
inhabiting an unpolluted area were dosed with water, 0.2 or
1 &mu;g g-1 d-1 of sodium arsenite (Control, Low and High
As groups), whereas those living in a metal-polluted area were dosed with
water (Smelter group). Birds accumulated As in tissues (liver, bone and
feathers) in a dose-dependent way. Nestlings exposed to
1 &mu;g g-1 d-1 of sodium arsenite showed reduced number of
fledglings per successful nest, and those exposed to
0.2 &mu;g g-1 d-1 had reduced wing growth, which could have
post-fledging consequences such as increased predation risk. These results
suggest that the LOAEL for effects on nestling survival and development in
great tits is likely equal to or below 1 &mu;g g-1 d-1.
However, limited effects on the biochemical parameters evaluated were
found. It has been shown that As may produce oxidative stress and tissue
damage, so further research exploring this issue will be carried out in a
future study.
KW - Breeding success
KW - Insectivorous passerines
KW - Parus major
KW - Pollution
KW - Vitamins
RN - N712M78A8G
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180411
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Environmental pollution (Barking, Essex : 1987)
EDAT- 20171108
STAT- MEDLINE
DOCNO- medline/29127934

157 - TOXLINE
TI - 3,4-Dihydroxybenzaldehyde lowers ROS generation and protects human red
blood cells from arsenic(III) induced oxidative damage.
AU - Maheshwari N
AD - Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim
University, Aligarh, Uttar Pradesh, 202002, India.
AU - Khan FH
AD - Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim
University, Aligarh, Uttar Pradesh, 202002, India.
AU - Mahmood R
AD - Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim
University, Aligarh, Uttar Pradesh, 202002, India.
SO - Environ Toxicol. 2018, May 06. [Environmental toxicology]
AB - Arsenic (As) is a potent environmental toxicant and chronic exposure to it
results in various malignancies in humans. Oxidative stress has been
implicated in the etiopathogenesis of As-induced toxicity. This
investigated the protective effect of plant antioxidant
3,4-dihydroxybenzaldehyde (DHB) on sodium meta-arsenite (SA), an As-(III)
compound, induced oxidative damage in human red blood cells (RBC). The RBC
were first incubated with different concentrations of DHB and then treated
with SA at 37&deg;C. Hemolysates were prepared and assayed for various
biochemical parameters. Treatment of RBC with SA alone enhanced the
generation of reactive oxygen species and increased lipid and protein
oxidation. Reduced glutathione levels, total sulfhydryl content and
cellular antioxidant power were significantly decreased in SA alone
treated RBC, compared to the untreated control cells. This was accompanied
by membrane damage, alterations in activities of antioxidant enzymes and
deranged glucose metabolism. Incubation of RBC with DHB, prior to
treatment with SA, significantly and dose-dependently attenuated the
SA-induced changes in all these parameters. Scanning electron microscopy
of RBC confirmed these biochemical results. Treatment of RBC with SA alone
converted the biconcave discoids to echinocytes but the presence of DHB
inhibited this conversion and the RBC retained their normal shape. These
results show that DHB protects human RBC from SA-induced oxidative damage,
most probably due to its antioxidant character.
KW - 3,4-dihydroxybenzaldehyde
KW - antioxidant
KW - arsenic
KW - oxidative stress
KW - red blood cells
KW - sodium meta-arsenite
LA - eng
IS - 1522-7278 (Electronic)
PT - Journal Article
TA - Environ Toxicol
YR - 2018
DATE- 20180507
CI - &copy; 2018 Wiley Periodicals, Inc.
CITO- NLM
CS - United States
FJT - Environmental toxicology
EDAT- 20180506
STAT- Publisher
DOCNO- medline/29732668

158 - TOXLINE
TI - Long-Term Health Effects and Underlying Biological Mechanisms of
Developmental Exposure to Arsenic.
AU - Smeester L
AD - Department of Environmental Sciences and Engineering, Gillings School of
Global Public Health, University of North Carolina, Chapel Hill, NC, USA.
AU - Fry RC
AD - Curriculum in Toxicology, School of Medicine, University of North Carolina,
Chapel Hill, NC, USA. rfry@unc.edu.
SO - Curr Environ Health Rep. 2018, Mar; 5(1):134-144. [Current environmental
health reports]
AB - PURPOSE OF REVIEW: Exposure to inorganic arsenic (iAs) via drinking water
represents a significant global public health threat with chronic exposure
associated with cancer, skin lesions, neurological impairment, and
cardiovascular diseases. Particularly susceptible populations include the
developing fetus and young children. This review summarizes some of the
critical studies of the long-term health effects and underlying biological
mechanisms related to developmental exposure to arsenic. It also
highlights the complex factors, such as the sex of the exposed individual,
that contribute to susceptibility to the later life health effects of iAs.
AB - RECENT FINDINGS: Studies in animal models, as well as human
population-based studies, have established that prenatal and early life
iAs exposures are associated with long-term effects, and many of these
effects display sexually dimorphic responses. As an underlying molecular
basis, recent epidemiologic and toxicologic studies have demonstrated that
changes to the epigenome may play a key mechanistic role underlying many
of the iAs-associated health outcomes. Developmental exposure to iAs
results in early and later life health effects. Mechanisms underlying
these outcomes are likely complex, and include disrupted key biological
pathways with ties to the epigenome. This highlights the importance of
continued research, particularly in animal models, to elucidate the
important underpinnings (e.g., timing of exposure, metabolism, dose) of
these complex health outcomes and to identify the biological mechanisms
underlying sexual dimorphism in iAs-associated diseases. Future research
should investigate preventative strategies for the protection from the
detrimental health endpoints associated with early life exposure to iAs.
Such strategies could include potential interventions focused on dietary
supplementation for example the adoption of a folate-rich diet.
KW - Arsenic exposure
KW - Early life
KW - Epigenetics
KW - In utero
KW - Sexual dimorphism
LA - eng
IS - 2196-5412 (Electronic)
PT - Journal Article
PT - Review
TA - Curr Environ Health Rep
YR - 2018
DATE- 20180402
CITO- NLM
CS - Switzerland
FJT - Current environmental health reports
STAT- In-Data-Review
CM - Cites: Environ Toxicol Pharmacol. 2017 Jun;52:183-187 (medline /28433805)
CM - Cites: Toxicol Sci. 2014 Jun;139(2):328-37 (medline /24675094)
CM - Cites: PLoS Genet. 2007 Nov;3(11):e207 (medline /18039032)
CM - Cites: FASEB J. 2006 Apr;20(6):779-81 (medline /16461332)
CM - Cites: Environ Health Perspect. 2012 May;120(5):623-6 (medline /22336149)
CM - Cites: Epidemiology. 2007 Jan;18(1):44-51 (medline /17149142)
CM - Cites: Cancer Metastasis Rev. 2010 Mar;29(1):61-72 (medline /20094757)
CM - Cites: Epigenetics. 2014 Feb;9(2):212-21 (medline /24169490)
CM - Cites: JAMA Pediatr. 2016 Jun 1;170(6):609-16 (medline /27111102)
CM - Cites: Mol Carcinog. 2007 Aug;46(8):579-84 (medline /17583566)
CM - Cites: Environ Mol Mutagen. 2014 Apr;55(3):196-208 (medline /24327377)
CM - Cites: Environ Health Perspect. 2015 May;123(5):412-21 (medline /25626053)
CM - Cites: Environ Health Perspect. 2013 Sep;121(9):1090-6 (medline /23757599)
CM - Cites: Toxicol Appl Pharmacol. 2003 Jan 1;186(1):7-17 (medline /12583988)
CM - Cites: Toxicol Appl Pharmacol. 2009 Feb 15;235(1):105-13 (medline
/19095001)
CM - Cites: Environ Health Perspect. 2016 Jun;124(6):840-7 (medline /26359651)
CM - Cites: Am J Epidemiol. 2007 Dec 15;166(12):1381-91 (medline /17875584)
CM - Cites: Ann Intern Med. 2013 Nov 19;159(10):649-59 (medline /24061511)
CM - Cites: Hypertension. 1999 Jan;33(1):74-8 (medline /9931084)
CM - Cites: Am J Epidemiol. 2009 Feb 1;169(3):304-12 (medline /19037006)
CM - Cites: Environ Health Perspect. 2016 Aug;124(8):1299-307 (medline
/26955061)
CM - Cites: Environ Health Perspect. 2011 Feb;119(2):258-64 (medline /20940111)
CM - Cites: Neurotoxicol Teratol. 2016 Jan-Feb;53:75-80 (medline /26689609)
CM - Cites: Environ Health Perspect. 2007 Sep;115(9):1371-5 (medline /17805430)
CM - Cites: Toxicol Sci. 2015 Jan;143(1):97-106 (medline /25304211)
CM - Cites: Epigenomics. 2017 Mar;9(3):267-278 (medline /28234023)
CM - Cites: Toxicol Sci. 2011 Jan;119(1):73-83 (medline /20937726)
CM - Cites: Environ Health. 2015 Feb 28;14:19 (medline /25888735)
CM - Cites: Toxicol Sci. 2012 Jan;125(1):20-9 (medline /22011395)
CM - Cites: Environ Health. 2014 Apr 01;13(1):23 (medline /24684736)
CM - Cites: Int J Epidemiol. 2013 Aug;42(4):1077-86 (medline /24062297)
CM - Cites: Toxicol Lett. 2009 Mar 28;185(3):197-202 (medline /19167470)
CM - Cites: Int J Epidemiol. 2010 Oct;39(5):1206-16 (medline /20085967)
CM - Cites: Arch Toxicol. 2014 Aug;88(8):1619-29 (medline /25005685)
CM - Cites: Environ Toxicol Pharmacol. 2015 Mar;39(2):589-96 (medline
/25682005)
CM - Cites: Environ Health Perspect. 2012 Oct;120(10):1418-24 (medline
/23008276)
CM - Cites: Cancer Res. 2008 Oct 15;68(20):8278-85 (medline /18922899)
CM - Cites: Am J Epidemiol. 2003 Dec 15;158(12):1193-201 (medline /14652304)
CM - Cites: Environ Toxicol Pharmacol. 2013 Nov;36(3):1266-75 (medline
/24211595)
CM - Cites: Environ Health Perspect. 2006 Aug;114(8):1293-6 (medline /16882542)
CM - Cites: Toxicol Sci. 2012 Oct;129(2):305-14 (medline /22713597)
CM - Cites: Environ Health Perspect. 2011 May;119(5):719-24 (medline /21147604)
CM - Cites: Toxicol Sci. 2014 Sep;141(1):166-75 (medline /24924402)
CM - Cites: Toxicol Appl Pharmacol. 2007 May 1;220(3):284-91 (medline
/17350061)
CM - Cites: Environ Health Perspect. 2012 Nov;120(11):1527-31 (medline
/22949133)
CM - Cites: Int J Epidemiol. 2013 Feb;42(1):176-85 (medline /23243118)
CM - Cites: Environ Health Perspect. 2000 Jul;108(7):667-73 (medline /10903622)
CM - Cites: Environ Health. 2013 Sep 02;12(1):73 (medline /24004508)
CM - Cites: Arterioscler Thromb Vasc Biol. 1996 Apr;16(4):504-10 (medline
/8624771)
CM - Cites: PLoS One. 2012;7(6):e38713 (medline /22719926)
CM - Cites: Environ Health Perspect. 2015 Feb;123(2):186-92 (medline /25325819)
CM - Cites: Environ Health. 2006 Oct 31;5:31 (medline /17076881)
CM - Cites: Twin Res Hum Genet. 2007 Aug;10 (4):581-6 (medline /17708699)
CM - Cites: Neurotoxicology. 2011 Aug;32(4):450-7 (medline /21453724)
CM -Cites: Environ Int. 2012 Jan;38(1):10-6 (medline /21982028)
CM -Cites: J Natl Cancer Inst. 2016 May 02;108(9):null (medline /27140955)
CM -Cites: PLoS One. 2013;8(1):e55014 (medline /23383038)
CM -Cites: Carcinogenesis. 2004 Jan;25(1):133-41 (medline /14514661)
CM -Cites: Environ Health Perspect. 2008 Apr;116(4):524-31 (medline /18414638)
CM -Cites: Int J Hyg Environ Health. 2014 Jul;217(6):678-86 (medline
/24698386)
CM - Cites: Cancer Epidemiol Biomarkers Prev. 2008 Aug;17(8):1982-7 (medline
/18708388)
CM - Cites: Environ Res. 2013 Oct;126:24-30 (medline /23769261)
CM - Cites: Annu Rev Nutr. 2009;29:381-99 (medline /19575603)
CM - Cites: J Pediatr (Rio J). 2007 Nov-Dec;83(6):494-504 (medline /18074050)
CM - Cites: Oncotarget. 2014 Mar 15;5(5):1290-303 (medline /24675390)
CM - Cites: Cancer Res. 2006 Feb 15;66(4):1883-90; discussion 1895-6 (medline
/16488983)
CM - Cites: Circulation. 1973 Feb;47(2):270-5 (medline /4684927)
CM - Cites: Environ Res. 2017 Jul;156:426-433 (medline /28410520)
CM - Cites: Environ Health Perspect. 2016 Mar;124(3):336-43 (medline /26295903)
CM - Cites: Hum Exp Toxicol. 2008 May;27(5):381-6 (medline /18715884)
CM - Cites: Toxicol Lett. 2002 Jul 7;133(1):17-31 (medline /12076507)
CM - Cites: Epigenetics. 2012 Oct;7(10):1125-32 (medline /22907587)
CM - Cites: Environ Health. 2015 Mar 30;14:12 (medline /25971349)
CM - Cites: BMJ. 2011 May 05;342:d2431 (medline /21546419)
CM - Cites: J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2007
Jan-Mar;25(1):1-22 (medline /17365340)
CM - Cites: J Natl Cancer Inst. 2004 Mar 17;96(6):466-74 (medline /15026472)
CM - Cites: Toxicology. 2007 Jul 1;236(1-2):7-15 (medline /17451858)
CM - Cites: Nat Genet. 2013 Jan;45(1):76-82 (medline /23202124)
CM - Cites: Environ Health Perspect. 2013 Mar;121(3):295-302 (medline
/23458756)
CM - Cites: Int J Epidemiol. 2011 Dec;40(6):1593-604 (medline /22158669)
CM - Cites: Cell Mol Life Sci. 2014 Jan;71(2):271-85 (medline /23892892)
CM - Cites: Epigenetics. 2014 May;9(5):774-82 (medline /24525453)
CM - Cites: Arch Pathol. 1974 Jun;97(6):360-5 (medline /4825098)
CM - Cites: Environ Int. 2017 Apr;101:108-116 (medline /28159392)
CM - Cites: J Appl Toxicol. 2015 Apr;35(4):358-66 (medline /25131850)
CM - Cites: Toxicol Sci. 1998 Aug;44(2):185-90 (medline /9742656)
CM - Cites: Pediatrics. 2006 Oct;118(4):1486-92 (medline /17015539)
CM - Cites: Int Arch Occup Environ Health. 2011 Aug;84(6):591-600 (medline
/20972800)
CM - Cites: Nutrients. 2014 Jun 02;6(6):2165-78 (medline /24892374)
CM - Cites: Biomed Res Int. 2015;2015:175025 (medline /26339590)
CM - Cites: Arch Toxicol. 2012 Jun;86(6):975-82 (medline /22398986)
CM - Cites: Toxicol Appl Pharmacol. 2007 Aug 1;222(3):271-80 (medline
/17306315)
CM - Cites: Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):204-11 (medline
/18226075)
CM - Cites: Front Neurosci. 2016 Mar 31;10:137 (medline /27064386)
DOCNO- medline/29411302

159 - TOXLINE
TI - Adiponectin gene polymorphisms and obesity increase the susceptibility to
arsenic-related renal cell carcinoma.
AU - Hsueh YM
AD - Department of Family Medicine, Shuang Ho Hospital, Taipei Medical University,
Taipei, Taiwan; Department of Public Health, School of Medicine, College of
Medicine, Taipei Medical University, Taipei, Taiwan.
AU - Chen WJ
AD - Department of Biostatistics and Epidemiology, College of Public Health,
University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; School of
Public Health, College of Public Health, Taipei Medical University, Taipei, Taiwan.
AU - Lin YC
AD - Department of Family Medicine, Shuang Ho Hospital, Taipei Medical University,
Taipei, Taiwan; Department of Health Examination, Wan Fang Hospital, Taipei Medical
University, Taipei, Taiwan; Division of Family Medicine, School of Medicine, Taipei
Medical University, Taipei, Taiwan.
AU - Huang CY
AD - Department of Urology, National Taiwan University Hospital, College of
Medicine, National Taiwan University, Taipei, Taiwan; Department of Urology,
National Taiwan University Hospital, Hsin Chu Branch, Hsin Chu, Taiwan.
AU - Shiue HS
AD - Department of Chinese Medicine, Chang Gung Memorial Hospital and Chang Gung
University, College of Medicine, Taoyuan, Taiwan.
AU - Yang SM
AD - School of Public Health, College of Public Health, Taipei Medical University,
Taipei, Taiwan.
AU - Ao PL
AD - School of Public Health, College of Public Health, Taipei Medical University,
Taipei, Taiwan.
AU - Pu YS
AD - Department of Health Examination, Wan Fang Hospital, Taipei Medical
University, Taipei, Taiwan.
AU - Su CT
AD - School of Public Health, College of Public Health, Taipei Medical University,
Taipei, Taiwan; Department of Family Medicine, Taipei Medical University Hospital,
Taipei, Taiwan. Electronic address: ctsu@tmu.edu.tw.
SO - Toxicol Appl Pharmacol. 2018, Jul 01; 350:11-20. [Toxicology and applied
pharmacology]
AB - Our recent study found that high urinary total arsenic levels were
associated with renal cell carcinoma (RCC). Recent studies demonstrated
that low circulating adiponectin was related to RCC. The aim of the
present study was to explore the relationship between adiponectin gene
(ADIPOQ) polymorphisms and RCC and investigate whether individuals with an
ADIPOQ risk genotype, obesity, and high urinary total arsenic levels have
a modified odds ratio (OR) of RCC. A total of 389 RCC patients and 389
age- and sex-matched controls were recruited between November 2006 and
December 2012 in Taiwan. Image-guided biopsy or surgical resection of
renal tumors was performed to pathologically verify RCC. Genomic DNA was
used to examine the genotypes of the ADIPOQ rs182052, ADIPOQ rs2241766,
ADIPOQ rs1501299, and ADIPOQ rs1063539 SNPs by PCR-RFLP. HPLC-HG-AAS was
used to measure the concentrations of urinary arsenic species.
Participants with the ADIPOQ rs182052 G/A+A/A genotype had a significantly
higher OR of RCC compared with those with the ADIPOQ rs182052 G/G
genotype. The OR (95% confidence interval [CI]) was 1.70 (1.23-2.36). The
OR of RCC for the combined effect of high urinary total arsenic levels and
obesity, which was dose-dependent, in individuals with the ADIPOQ rs182052
G/A+A/A genotype was 9.33 (3.85-22.62). The present study found
significant combined effects of obesity and the ADIPOQ rs182052 G/A+A/A
genotype on the arsenic-related risk of RCC in a population with low
arsenic exposure. Arsenic exposure, obesity, and the ADIPOQ rs182052
polymorphism could be predictors of a higher OR of RCC.
KW - ADIPOQ
KW - Arsenic
KW - Obesity
KW - Polymorphism
KW - Renal Cell Carcinoma
LA - eng
IS - 1096-0333 (Electronic)
PT - Journal Article
TA - Toxicol Appl Pharmacol
YR - 2018
DATE- 20180525
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - United States
FJT - Toxicology and applied pharmacology
EDAT- 20180430
STAT- In-Data-Review
DOCNO- medline/29723618

160 - TOXLINE
TI - Enhanced adsorption performance of aspartic acid intercalated Mg-Zn-Fe-LDH
materials for arsenite.
AU - Lu H
AD - State Key Laboratory of Pollution Control and Resource Reuse, Tongji
University, Shanghai 200092, China. zzl@tongji.edu.cn and Post Doctoral Research
Station, College of Civil Engineering, Tongji University, Shanghai 200092, China.
AU - Lu T
AD - State Key Laboratory of Pollution Control and Resource Reuse, Tongji
University, Shanghai 200092, China. zzl@tongji.edu.cn.
AU - Zhang H
AD - State Key Laboratory of Pollution Control and Resource Reuse, Tongji
University, Shanghai 200092, China. zzl@tongji.edu.cn.
AU - Qiu Y
AD - Key Laboratory of Yangtze River Water Environment, Ministry of Education,
Tongji University, Shanghai 200092, China.
AU - Yin D
AD - Key Laboratory of Yangtze River Water Environment, Ministry of Education,
Tongji University, Shanghai 200092, China.
AU - Zhu Z
AD - State Key Laboratory of Pollution Control and Resource Reuse, Tongji
University, Shanghai 200092, China. zzl@tongji.edu.cn and Key Laboratory of Yangtze
River Water Environment, Ministry of Education, Tongji University, Shanghai 200092,
China.
SO - Dalton Trans. 2018, Apr 03; 47(14):4994-5004. [Dalton transactions
(Cambridge, England : 2003)]
AB - A series of hydrophobic and hydrophilic amino acid (aspartic acid,
phenylalanine, glutamic acid, and proline) intercalated LDH materials were
synthesized and characterized. The results of batch experiments showed
that Mg7Zn1Fe4-Asp-LDH and Mg7Zn1Fe4-Phe-LDH showed good adsorption
performances for both arsenate and arsenite in aqueous solutions. The
effects of various experimental conditions have been investigated by the
batch test, which included the effects of initial pH, arsenic
concentration, contact time and coexisting ions. For Mg7Zn1Fe4-Asp-LDH
under the optimal experimental conditions, the maximum adsorption capacity
of As(iii) and As(v) reached 94.81 mg g-1 and 57.42 mg g-1, respectively.
It showed a higher adsorption capacity for As(iii) than that for As(v),
which is of great significance to remove the trivalent arsenic species
with higher toxicity. When the dosage of Mg7Zn1Fe4-Asp-LDH was 0.8 g L-1,
the concentration of As(iii) in the aqueous solution could be reduced from
2 mg L-1 to below 10 &mu;g L-1.When Mg-Zn-Fe-Asp-LDH was applied in
practical water samples with a dosage of 0.2 g L-1, the residual
concentrations of arsenic in three actual water samples were all lower
than 10 &mu;g L-1 after adsorption. The column test showed that 1.0 g of
Mg7Zn1Fe4-Asp-LDH could continuously treat 2.6 L of As(iii) aqueous
solution (2 mg L-1) and reduced the concentration of As(iii) to below 10
&mu;g L-1 or handle 0.4 L of arsenic-contaminated (10 mg L-1,
As(iii)&thinsp;:&thinsp;As(v) = 1&thinsp;:&thinsp;1) water, and the
effluent concentration was below 10 &mu;g L-1. Compared with the
previously reported hydrophobic amino acid intercalated LDHs, aspartic
acid (hydrophilic amino acid) intercalated LDH has a good removal
efficiency for arsenic. The synthesized Mg7Zn1Fe4-Asp-LDH is considered to
be a potentially functional material that can be used to treat arsenic
contamination in water.
LA - eng
IS - 1477-9234 (Electronic)
PT - Journal Article
TA - Dalton Trans
YR - 2018
DATE- 20180404
CITO- NLM
CS - England
FJT - Dalton transactions (Cambridge, England : 2003)
STAT- PubMed-not-MEDLINE
DOCNO- medline/29557460

161 - TOXLINE
TI - Iron Mesh-Based Metal Organic Framework Filter for Efficient Arsenic
Removal.
AU - Wang D
AU - Gilliland SE 3rd
AU - Yi X
AU - Logan K
AU - Heitger DR
AU - Lucas HR
AU - Wang WN
SO - Environ Sci Technol. 2018, Apr 03; 52(7):4275-4284. [Environmental science
& technology]
AB - Efficient oxidation from arsenite [As(III)] to arsenate [As(V)], which is
less toxic and more readily to be adsorbed by adsorbents, is important for
the remediation of arsenic pollution. In this paper, we report a metal
organic framework (MIL-100(Fe)) filter to efficiently remove arsenic from
synthetic groundwater. With commercially available iron mesh as a
substrate, MIL-100(Fe) is implanted through an in situ growth method.
MIL-100(Fe) is able to capture As(III) due to its microporous structure,
superior surface area, and ample active sites for As adsorption. This
approach increases the localized As concentration around the filter, where
Fenton-like reactions are initiated by the Fe2+/Fe3+ sites within the
MIL-100(Fe) framework to oxidize As(III) to As(V). The mechanism was
confirmed by colorimetric detection of H2O2, fluorescence, and electron
paramagnetic resonance detection of &middot;OH. With the aid of oxygen
bubbling and Joule heating, the removal efficiency of As(III) can be
further boosted. The MIL-100(Fe)-based filter also exhibits satisfactory
structural stability and recyclability. Notably, the adsorption capacity
of the filter can be regenerated satisfactorily. Our results demonstrate
the potential of this filter for the efficient remediation of As
contamination in groundwater.
LA - eng
IS - 1520-5851 (Electronic)
PT - Journal Article
TA - Environ Sci Technol
YR - 2018
DATE- 20180403
CITO- NLM
CS - United States
FJT - Environmental science &amp; technology
EDAT- 20180315
STAT- In-Data-Review
DOCNO- medline/29513011

162 - TOXLINE
TI - Efficient oxidation and sorption of arsenite using a novel
titanium(IV)-manganese(IV) binary oxide sorbent.
AU - Zhang W
AD - State Key Laboratory of Urban Water Resource and Environment, School of
Environment, Harbin Institute of Technology, Harbin, Heilongjiang 150090, China.
AU - Liu C
AD - State Key Laboratory of Urban Water Resource and Environment, School of
Environment, Harbin Institute of Technology, Harbin, Heilongjiang 150090, China.
AU - Zheng T
AD - State Key Laboratory of Urban Water Resource and Environment, School of
Environment, Harbin Institute of Technology, Harbin, Heilongjiang 150090, China.
AU - Ma J
AD - State Key Laboratory of Urban Water Resource and Environment, School of
Environment, Harbin Institute of Technology, Harbin, Heilongjiang 150090, China.
Electronic address: majun@hit.edu.cn.
AU - Zhang G
AD - Collaborative Innovation Center of Water Quality Safety and Protection in
Pearl River Delta, Guangzhou University, Guangzhou 510006, China. Electronic
address: gszhang@gzhu.edu.cn.
AU - Ren G
AD - China University of Mining and Technology, Xuzhou, Jiangsu 221116, China.
AU - Wang L
AD - State Key Laboratory of Urban Water Resource and Environment, School of
Environment, Harbin Institute of Technology, Harbin, Heilongjiang 150090, China.
AU - Liu Y
AD - State Key Laboratory of Urban Water Resource and Environment, School of
Environment, Harbin Institute of Technology, Harbin, Heilongjiang 150090, China.
SO - J Hazard Mater. 2018, Jul 05; 353:410-420. [Journal of hazardous
materials]
AB - Owing to the high toxicity and mobility, the removal of arsenite (As(III))
is significantly more difficult than arsenate (As(V)), thus representing a
major challenge in arsenite-contaminated water treatment. For efficient
elimination of As(III), we successfully fabricated a novel Ti-Mn binary
oxide via a simultaneous oxidation and coprecipitation process. The
amorphous oxide was aggregated from nanosized particles with a high
specific surface area of 349.5&#8239;m2/g. It could effectively oxidize
As(III) to As(V) and had a high As(III) sorption capacity of
107.0&#8239;mg/g. As(III) sorption occurred rapidly and equilibrium was
achieved within 24&#8239;h. The kinetic data was well fitted by the
pseudo-second-order equation, indicating a chemical sorption process. The
material was almost independent upon the presence of competitive ions. The
As(III) removal by the sorbent is a combined process coupled oxidation
with sorption, where the MnO2 content is mainly responsible for oxidizing
As(III) to As(V) and the formed As(V) is then adsorbed onto the surface of
amorphous TiO2 content, through replacing the surface hydroxyl group or
the adsorbed As(III) and forming inner-sphere surface complexes.
Furthermore, the arsenic-containing oxide could be effectively regenerated
and reused. The bi-functional sorbent could be used as a potentially
attractive sorbent for As(III) removal in drinking water treatment and
environmental remediation.
KW - Arsenite
KW - Oxidation
KW - Sorption
KW - Ti-Mn binary oxide
KW - Water treatment
LA - eng
IS - 1873-3336 (Electronic)
PT - Journal Article
TA - J Hazard Mater
YR - 2018
DATE- 20180615
CI - Copyright &copy; 2018. Published by Elsevier B.V.
CITO- NLM
CS - Netherlands
FJT - Journal of hazardous materials
EDAT- 20180419
STAT- In-Data-Review
DOCNO- medline/29702456

163 - TOXLINE
TI - CircLRP6 Regulation of ZEB1 via miR-455 Is Involved in the
Epithelial-Mesenchymal Transition During Arsenite-Induced Malignant
Transformation of Human Keratinocytes.
AU - Xue J
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, People's
Republic of China.
AU - Chen C
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, People's
Republic of China.
AU - Luo F
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, People's
Republic of China.
AU - Pan X
AD - The Key Laboratory of Environmental Pollution Monitoring and Disease Control,
Ministry of Education, School of Public Health, Guizhou Medical University,
Guiyang, Guizhou 550025, People's Republic of China.
AU - Xu H
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, People's
Republic of China.
AU - Yang P
AD - The School of Public Health, Institute for Chemical Carcinogenesis, Guangzhou
Medical University, Guangzhou, Guangdong 510182, People's Republic of China.
AU - Sun Q
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, People's
Republic of China.
AU - Liu X
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, People's
Republic of China.
AU - Lu L
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, People's
Republic of China.
AU - Yang Q
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, People's
Republic of China.
AU - Xiao T
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, People's
Republic of China.
AU - Dai X
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, People's
Republic of China.
AU - Luo P
AD - The Key Laboratory of Environmental Pollution Monitoring and Disease Control,
Ministry of Education, School of Public Health, Guizhou Medical University,
Guiyang, Guizhou 550025, People's Republic of China.
AU - Lu J
AD - The School of Public Health, Institute for Chemical Carcinogenesis, Guangzhou
Medical University, Guangzhou, Guangdong 510182, People's Republic of China.
AU - Zhang A
AD - The Key Laboratory of Environmental Pollution Monitoring and Disease Control,
Ministry of Education, School of Public Health, Guizhou Medical University,
Guiyang, Guizhou 550025, People's Republic of China.
AU - Liu Q
AD - The Key Laboratory of Modern Toxicology, Ministry of Education, School of
Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, People's
Republic of China.
SO - Toxicol Sci. 2018, Apr 01; 162(2):450-461. [Toxicological sciences : an
official journal of the Society of Toxicology]
AB - Circular RNAs (circRNAs), a class of noncoding RNAs generated from
pre-mRNAs, participate in the regulation of tumorigenesis. The mechanism
for regulation, however, is unclear. Here, to determine whether circRNAs
are involved in arsenite-induced epithelial-mesenchymal transition (EMT)
and malignant transformation in human keratinocyte (HaCaT) cells, the
up-regulation of circLRP6 was confirmed in arsenite-transformed HaCaT
(T-HaCaT) cells. In HaCaT cells, circLRP6 acted as an microRNA (miR)-455
sponge. For these cells, chronic exposure to arsenite caused an increase
of circLRP6 and the transcription factor ZEB1, which induced the EMT.
miR-455 suppressed the expression of ZEB1. Further, in T-HaCaT cells,
knockdown of circLRP6 with siRNA inhibited ZEB1 expression, but
cotransfection with circLRP6 siRNA and an miR-455 inhibitor reversed this
inhibition. These results suggest that, in HaCaT cells, arsenite increases
circLRP6 levels, which act as a sponge for miR-455 and up-regulate the
miR-455 target, ZEB1, which subsequently induces the EMT, thus promoting
malignant transformation. Thus, for HaCaT cells chronically exposed to
arsenite, circLRP6 via miR-455 regulation of ZEB1 is involved in the EMT
during malignant transformation. The results establish a previously
unknown mechanism for arsenite-induced carcinogenesis.
LA - eng
IS - 1096-0929 (Electronic)
PT - Journal Article
TA - Toxicol Sci
YR - 2018
DATE- 20180328
CITO- NLM
CS - United States
FJT - Toxicological sciences : an official journal of the Society of Toxicology
STAT- In-Data-Review
DOCNO- medline/29216394

164 - TOXLINE
TI - Inorganic arsenic causes fatty liver and interacts with ethanol to cause
alcoholic liver disease in zebrafish.
AU - Bambino K
AD - Department of Environmental Medicine and Public Health, Icahn School of
Medicine at Mount Sinai, New York, New York 10029, USA.
AU - Zhang C
AD - Program in Biology, New York University Abu Dhabi, Saadiyat Island Campus, PO
Box 129188 Abu Dhabi, United Arab Emirates.
AU - Austin C
AD - Department of Environmental Medicine and Public Health, Icahn School of
Medicine at Mount Sinai, New York, New York 10029, USA.
AU - Amarasiriwardena C
AD - Department of Environmental Medicine and Public Health, Icahn School of
Medicine at Mount Sinai, New York, New York 10029, USA.
AU - Arora M
AD - Department of Environmental Medicine and Public Health, Icahn School of
Medicine at Mount Sinai, New York, New York 10029, USA.
AU - Chu J
AD - Department of Pediatrics, Division of Pediatric Hepatology, Icahn School of
Medicine at Mount Sinai, New York, New York 10029, USA.
AU - Sadler KC
AD - Program in Biology, New York University Abu Dhabi, Saadiyat Island Campus, PO
Box 129188 Abu Dhabi, United Arab Emirates Kirsten.Edepli@nyu.edu.
SO - Dis Model Mech. 2018, 02 26. [Disease models & mechanisms]
AB - The rapid increase in fatty liver disease (FLD) incidence is attributed
largely to genetic and lifestyle factors; however, environmental toxicants
are a frequently overlooked factor that can modify the effects of more
common causes of FLD. Chronic exposure to inorganic arsenic (iAs) is
associated with liver disease in humans and animal models, but neither the
mechanism of action nor the combinatorial interaction with other
disease-causing factors has been fully investigated. Here, we examined the
contribution of iAs to FLD using zebrafish and tested the interaction with
ethanol to cause alcoholic liver disease (ALD). We report that zebrafish
exposed to iAs throughout development developed specific phenotypes
beginning at 4&#8197;days post-fertilization (dpf), including the
development of FLD in over 50% of larvae by 5&#8197;dpf. Comparative
transcriptomic analysis of livers from larvae exposed to either iAs or
ethanol revealed the oxidative stress response and the unfolded protein
response (UPR) caused by endoplasmic reticulum (ER) stress as common
pathways in both these models of FLD, suggesting that they target similar
cellular processes. This was confirmed by our finding that arsenic is
synthetically lethal with both ethanol and a well-characterized
ER-stress-inducing agent (tunicamycin), suggesting that these exposures
work together through UPR activation to cause iAs toxicity. Most
significantly, combined exposure to sub-toxic concentrations of iAs and
ethanol potentiated the expression of UPR-associated genes, cooperated to
induce FLD, reduced the expression of as3mt, which encodes an
arsenic-metabolizing enzyme, and significantly increased the concentration
of iAs in the liver. This demonstrates that iAs exposure is sufficient to
cause FLD and that low doses of iAs can potentiate the effects of ethanol
to cause liver disease.This article has an associated First Person
interview with the first author of the paper.
COI - Competing interestsThe authors declare no competing or financial
interests.
KW - *Arsenic
KW - *Environmental exposure
KW - *Ethanol
KW - *Fatty liver disease
LA - eng
IS - 1754-8411 (Electronic)
PT - Journal Article
PT - Research Support, N.I.H., Extramural
TA - Dis Model Mech
YR - 2018
DATE- 20180521
CI - &copy; 2018. Published by The Company of Biologists Ltd.
CITO- NLM
CS - England
FJT - Disease models &amp; mechanisms
EDAT- 20180226
STAT- In-Process
CM - Cites: Indian J Gastroenterol. 2000 Jul-Sep;19(3):112-5 (medline
/10918716)
CM - Cites: BMC Public Health. 2012 Aug 10;12:639 (medline /22883023)
CM - Cites: Sci Prog. 1999;82 ( Pt 1):69-88 (medline /10445007)
CM - Cites: Bioinformatics. 2015 Jan 15;31(2):166-9 (medline /25260700)
CM - Cites: Database (Oxford). 2016 Jun 23;2016: (medline /27337980)
CM - Cites: Toxicol Pathol. 2013 Feb;41(2):343-60 (medline /23262638)
CM - Cites: Toxicol Appl Pharmacol. 2004 Aug 1;198(3):319-26 (medline
/15276411)
CM - Cites: Toxicol Appl Pharmacol. 2009 Mar 15;235(3):338-50 (medline
/19168087)
CM - Cites: Mass Spectrom Rev. 2017 Jan;36(1):47-57 (medline /26398248)
CM - Cites: Philos Trans R Soc Lond B Biol Sci. 2013 Mar 25;368(1617):20110403
(medline /23530257)
CM - Cites: Environ Health Perspect. 2016 Feb;124(2):201-9 (medline /26151952)
CM - Cites: Arch Toxicol. 2014 Feb;88(2):213-26 (medline /23892647)
CM - Cites: Curr Opin Lipidol. 2014 Apr;25(2):125-32 (medline /24565920)
CM - Cites: Ann Epidemiol. 2007 Nov;17(11):863-9 (medline /17728149)
CM - Cites: Toxicol Lett. 2002 Jul 7;133(1):1-16 (medline /12076506)
CM - Cites: Nat Rev Gastroenterol Hepatol. 2015 Apr;12(4):231-42 (medline
/25782093)
CM - Cites: Environ Sci Technol. 2009 Apr 15;43(8):2714-9 (medline /19475939)
CM - Cites: Pharmacol Ther. 2016 May;161:11-21 (medline /27016469)
CM - Cites: Environ Health Perspect. 2012 Jul;120(7):1061-6 (medline /22466225)
CM - Cites: Ann Intern Med. 2013 Nov 19;159(10):649-59 (medline /24061511)
CM - Cites: J Expo Sci Environ Epidemiol. 2006 Mar;16(2):191-205 (medline
/16160703)
CM - Cites: PLoS One. 2016 Mar 11;11(3):e0151225 (medline /26967897)
CM - Cites: Bioinformatics. 2009 May 1;25(9):1105-11 (medline /19289445)
CM - Cites: J Appl Toxicol. 2011 Mar;31(2):95-107 (medline /21321970)
CM - Cites: Hepatology. 2011 Jul;54(1):229-39 (medline /21503947)
CM - Cites: Hepatology. 2010 May;51(5):1593-602 (medline /20222092)
CM - Cites: Mol Cell Biochem. 2004 Jan;255(1-2):57-66 (medline /14971646)
CM - Cites: Toxicol Lett. 2012 Jul 20;212(2):161-8 (medline /22613031)
CM - Cites: PLoS Genet. 2014 May 29;10(5):e1004335 (medline /24874946)
CM - Cites: Environ Health. 2011 Jul 08;10:64 (medline /21740555)
CM - Cites: PLoS One. 2013 Jul 29;8(7):e68737 (medline /23922661)
CM - Cites: Analyst. 2012 Apr 7;137(7):1527-37 (medline /22314636)
CM - Cites: Free Radic Biol Med. 2015 Mar;80:171-82 (medline /25091901)
CM - Cites: Mol Biol Cell. 2010 Sep 1;21(17):2975-86 (medline /20631254)
CM - Cites: Sci Rep. 2017 Mar 17;7:44424 (medline /28303940)
CM - Cites: Bioinformatics. 2014 Aug 1;30(15):2114-20 (medline /24695404)
CM - Cites: Arch Toxicol. 2013 Jun;87(6):969-79 (medline /22811022)
CM - Cites: Hepatology. 2009 Feb;49(2):443-52 (medline /19127516)
CM - Cites: Int J Environ Res Public Health. 2015 Oct 12;12(10):12628-42
(medline /26473898)
CM - Cites: Toxicol Sci. 2016 Nov;154(1):195 (medline /27794142)
CM - Cites: Biol Trace Elem Res. 2017 Mar;176(1):154-175 (medline /27498811)
CM - Cites: Zebrafish. 2013 Jun;10(2):199-210 (medline /23697887)
CM - Cites: Oncol Rep. 2012 Nov;28(5):1851-8 (medline /22922937)
CM - Cites: BMC Mol Biol. 2009 Nov 25;10:104 (medline /19939263)
CM - Cites: Toxicol Appl Pharmacol. 2011 Dec 15;257(3):356-64 (medline
/21983427)
CM - Cites: Genome Biol. 2004;5(10):R80 (medline /15461798)
CM - Cites: J Epidemiol Community Health. 2014 Feb;68(2):176-84 (medline
/24133074)
CM - Cites: Environ Mol Mutagen. 2016 Mar;57(2):137-50 (medline /26581878)
CM - Cites: Front Oncol. 2017 Apr 03;7:55 (medline /28421160)
CM - Cites: Mutat Res. 2016 Oct;809:50-56 (medline /27692299)
CM - Cites: Arch Toxicol. 1988;62(6):473-5 (medline /3250379)
CM - Cites: Dis Model Mech. 2014 Jul;7(7):823-35 (medline /24973751)
CM - Cites: Mol Biosyst. 2014 Apr;10 (4):851-861 (medline /24488121)
CM - Cites: Arch Environ Occup Health. 2016 Nov;71(6):338-346 (medline
/26666397)
CM - Cites: J Cell Sci. 2012 Nov 1;125(Pt 21):5073-83 (medline /22946053)
CM - Cites: Alcohol Clin Exp Res. 2012 Jan;36(1):14-23 (medline /21790674)
CM - Cites: Toxicol Pathol. 2015 Jun;43(4):482-97 (medline /25326588)
CM - Cites: Zebrafish. 2016 Oct;13(5):405-12 (medline /27140519)
CM - Cites: Cancer Cell. 2014 Feb 10;25(2):196-209 (medline /24486181)
CM - Cites: Dis Model Mech. 2013 Sep;6(5):1271-8 (medline /23813869)
CM - Cites: Indian J Gastroenterol. 1999 Oct-Nov;18(4):152-5 (medline
/10531716)
CM - Cites: Toxicol Appl Pharmacol. 2012 Jul 15;262(2):185-93 (medline
/22575231)
CM - Cites: Environ Health Perspect. 2013 Jul;121(7):832-8 (medline /23665672)
CM - Cites: Aquat Toxicol. 2014 Jul;152:152-63 (medline /24768856)
CM - Cites: QJM. 2010 Feb;103(2):71-83 (medline /19914930)
CM - Cites: Curr Top Dev Biol. 2017;124:331-367 (medline /28335863)
CM - Cites: Nature. 2016 Jan 21;529(7586):326-35 (medline /26791723)
CM - Cites: Toxicol Appl Pharmacol. 2007 Apr 15;220(2):146-55 (medline
/17303202)
CM - Cites: Physiol Genomics. 2006 Nov 27;27(3):351-61 (medline /16882884)
CM - Cites: Antioxid Redox Signal. 2007 Dec;9(12):2277-93 (medline /17979528)
CM - Cites: Hepatology. 2011 Aug;54(2):495-508 (medline /21538441)
CM - Cites: Science. 2004 Oct 15;306(5695):457-61 (medline /15486293)
CM - Cites: Free Radic Biol Med. 2008 Mar 1;44(5):723-38 (medline /18078827)
CM - Cites: Aquat Toxicol. 2014 Aug;153:66-72 (medline /24176670)
CM - Cites: Toxicol Appl Pharmacol. 2007 Dec 1;225(2):154-61 (medline
/17905400)
CM - Cites: Environ Health. 2016 Nov 8;15(1):106 (medline /27825389)
CM - Cites: Aquat Toxicol. 2009 Feb 19;91(3):229-37 (medline /19110324)
CM - Cites: Dis Model Mech. 2013 Sep;6(5):1213-26 (medline /23798569)
CM - Cites: Biochemistry. 2009 Jan 20;48(2):424-32 (medline /19102631)
CM - Cites: J Biochem Mol Toxicol. 2015 Jan;29(1):1-9 (medline /25155036)
CM - Cites: Biochemistry. 2015 Jan 20;54(2):612-21 (medline /25506675)
CM - Cites: Gastroenterology. 1998 Apr;114(4):842-5 (medline /9547102)
CM - Cites: J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2007
Jan-Mar;25(1):1-22 (medline /17365340)
CM - Cites: Sci Rep. 2015 Nov 05;5:16093 (medline /26537450)
CM - Cites: J Toxicol Clin Toxicol. 2000;38(4):395-405 (medline /10930056)
CM - Cites: Cell Rep. 2013 Apr 25;3(4):1279-92 (medline /23583182)
CM - Cites: Lancet. 2010 Jul 24;376(9737):252-8 (medline /20646756)
CM - Cites: Semin Liver Dis. 2015 Aug;35(3):270-90 (medline /26378644)
CM - Cites: Environ Toxicol Pharmacol. 2016 Dec;48:214-224 (medline /27829199)
CM - Cites: Aquat Toxicol. 2016 Jul;176:45-52 (medline /27108203)
CM - Cites: Hepatology. 2011 Aug;54(2):452-62 (medline /21488074)
CM - Cites: Environ Health Perspect. 2013 Mar;121(3):295-302 (medline
/23458756)
CM - Cites: Histopathology. 2012 Aug;61(2):141-52 (medline /22372457)
CM -Cites: Cell Death Dis. 2013 Dec 19;4:e968 (medline /24357799)
CM -Cites: Free Radic Res. 2015;49(12):1405-18 (medline /26223319)
CM -Cites: Development. 2015 Feb 1;142(3):510-21 (medline /25564650)
CM -Cites: Environ Health Perspect. 2011 Oct;119(10):1356-63 (medline
/21684831)
CM - Cites: Environ Health Perspect. 2002 Oct;110 Suppl 5:883-6 (medline
/12426152)
CM - Cites: Diabetes Care. 2015 Apr;38(4):620-7 (medline /25583752)
CM - Cites: Environ Res. 2014 Nov;135:120-5 (medline /25262084)
CM - Cites: Antioxid Redox Signal. 2012 May 15;16(10):1077-87 (medline
/21854214)
CM - Cites: PLoS One. 2013;8(1):e53732 (medline /23341986)
CM - Cites: Comp Biochem Physiol C Toxicol Pharmacol. 2015 Jun-Jul;172-173:7-12
(medline /25882832)
CM - Cites: Environ Health Perspect. 1996 Jun;104(6):620-8 (medline /8793350)
CM - Cites: Arch Toxicol. 2013 Feb;87(2):383-96 (medline /22914984)
CM - Cites: Mol Cell Biochem. 2004 Jan;255(1-2):67-78 (medline /14971647)
CM - Cites: Development. 2017 Aug 15;144(16):2925-2939 (medline /28698226)
CM - Cites: Gastroenterology. 2015 Nov;149(6):1361-77 (medline /26319012)
CM - Cites: J Clin Invest. 2004 Jul;114(2):147-52 (medline /15254578)
CM - Cites: Toxicol Appl Pharmacol. 2005 Aug 7;206(2):169-75 (medline
/15967205)
CM - Cites: Dig Dis. 2010;28(6):802-11 (medline /21525766)
CM - Cites: Toxicol Lett. 2006 Jun 1;163(3):191-7 (medline /16376500)
CM - Cites: Environ Health Perspect. 2011 Feb;119(2):182-8 (medline /21247820)
CM - Cites: Genome Biol. 2014;15(12):550 (medline /25516281)
DOCNO- medline/29361514

165 - TOXLINE
TI - Gestational exposure to inorganic arsenic (iAs3+) alters glutamate
disposition in the mouse hippocampus and ionotropic glutamate receptor
expression leading to memory impairment.
AU - Nelson-Mora J
AD - Dep. de Medicina Gen�mica y Toxicolog�a Ambiental, Instituto de
Investigaciones Biom�dicas, Universidad Nacional Aut�noma de M�xico, A.P. 70-228,
Ciudad Universitaria, 04510, Mexico, Mexico.
AU - Escobar ML
AD - Divisi�n de Investigaci�n y Estudios de Posgrado, Facultad de Psicolog�a,
Universidad Nacional Aut�noma de M�xico, 04510, Mexico, Mexico.
AU - Rodr�guez-Dur�n L
AD - Divisi�n de Investigaci�n y Estudios de Posgrado, Facultad de Psicolog�a,
Universidad Nacional Aut�noma de M�xico, 04510, Mexico, Mexico.
AU - Massieu L
AD - Divisi�n de Neurociencias, Departamento de Neuropatolog�a Molecular,
Instituto de Fisiolog�a Celular, Universidad Nacional Aut�noma de M�xico, 04510,
Mexico, Mexico.
AU - Montiel T
AD - Divisi�n de Neurociencias, Departamento de Neuropatolog�a Molecular,
Instituto de Fisiolog�a Celular, Universidad Nacional Aut�noma de M�xico, 04510,
Mexico, Mexico.
AU - Rodr�guez VM
AD - Departamento de Neurobiolog�a Conductual y Cognitiva, Instituto de
Neurobiolog�a, Campus Universidad Nacional Aut�noma de M�xico, Juriquilla, 76230,
Quer�taro, Mexico.
AU - Hern�ndez-Mercado K
AD - Dep. de Medicina Gen�mica y Toxicolog�a Ambiental, Instituto de
Investigaciones Biom�dicas, Universidad Nacional Aut�noma de M�xico, A.P. 70-228,
Ciudad Universitaria, 04510, Mexico, Mexico.
AU - Gonsebatt ME
AD - Dep. de Medicina Gen�mica y Toxicolog�a Ambiental, Instituto de
Investigaciones Biom�dicas, Universidad Nacional Aut�noma de M�xico, A.P. 70-228,
Ciudad Universitaria, 04510, Mexico, Mexico. margen@unam.mx.
SO - Arch Toxicol. 2018, Mar; 92(3):1037-1048. [Archives of toxicology]
AB - Early life exposure to environmental pollutants and toxic chemicals has
been linked to learning and behavioral alterations in children. iAs
exposure is associated with different types neurological disorders such as
memory and learning impairment. iAs is methylated in the brain by the
arsenic III-methyltransferase in a process that requires glutathione
(GSH). The xCT-antiporter cell membrane transporter participates in the
influx of cystine for GSH synthesis in exchange for glutamate in a 1:1
ratio. In CD-1 mice gestationally exposed to 20 ppm of sodium
arsenite in drinking water, we have previously observed up-regulation of
xCT in the male mouse hippocampus which caused glutamatergic synapse
alterations affecting learning and memory processes. Here, we used the
same gestational iAs exposure model to investigate whether the
up-regulation of xCT and down-regulation of GLT-1 transporters were
associated with higher levels of extracellular glutamate and changes in
the expression of the
&alpha;-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)
glutamate receptor, responsible for excitatory fast synaptic transmission.
The induction of LTP in the perforant-dentate gyrus pathway (PP-DG) of the
hippocampus was also studied, as well as learning and memory formation
using the water maze test. Changes in GSH levels were also tested in the
hippocampus of animals exposed to iAs. Results showed increased GSH
synthesis (p&thinsp; < &thinsp;0.05), associated with significantly
higher extracellular glutamate levels in iAs exposed mice. Exposure was
also significantly associated with AMPA subunits down-regulation,
deficient LTP induction, and lower excitability of the PP-DG pathway. In
addition, animals showed deficient learning and memory in the Morris Water
Maze test.
KW - AMPA receptors
KW - Arsenic neurotoxicity
KW - Extracellular glutamate
KW - LTP
KW - Morris water maze
LA - eng
IS - 1432-0738 (Electronic)
PT - Journal Article
TA - Arch Toxicol
YR - 2018
DATE- 20180325
CITO- NLM
CS - Germany
FJT - Archives of toxicology
EDAT- 20171204
STAT- In-Data-Review
DOCNO- medline/29204679

166 - TOXLINE
TI - May humic acids or mineral fertilisation mitigate arsenic mobility and
availability to carrot plants (Daucus carota L.) in a volcanic soil
polluted by As from irrigation water?
AU - Caporale AG
AD - Department of Agricultural Sciences, University of Naples Federico II,
Portici, Naples, Italy. Electronic address: ag.caporale@unina.it.
AU - Adamo P
AD - Department of Agricultural Sciences, University of Naples Federico II,
Portici, Naples, Italy.
AU - Azam SMGG
AD - Department of Agricultural Sciences, University of Naples Federico II,
Portici, Naples, Italy.
AU - Rao MA
AD - Department of Agricultural Sciences, University of Naples Federico II,
Portici, Naples, Italy.
AU - Pigna M
AD - Department of Agricultural Sciences, University of Naples Federico II,
Portici, Naples, Italy.
SO - Chemosphere. 2018, Feb; 193:464-471. [Chemosphere]
AB - Carrot (Daucus carota L.) is a widely consumed root vegetable, whose
growth and safety might be threatened by growing-medium arsenic (As)
contamination. By this work, we evaluated the effects of humic acids from
Leonardite and NPK mineral fertilisation on As mobility and availability
to carrot plants grown for 60 days in a volcanic soil irrigated with
As-contaminated water - representing the most common scenario occurring in
As-affected Italian areas. As expected, the irrigation with
As-contaminated water caused a serious toxic effect on plant growth and
photosynthetic rate; the highest rate of As also inhibited soil enzymatic
activity. In contrast, the organic and mineral fertilisation alleviated,
at least partially, the toxicity of As, essentially by stimulating plant
growth and promoting nutrient uptake. The mobility of As in the volcanic
soil and thus its phytoavailability were differently affected by the
organic and mineral fertilisers; the application of humic acids mitigated
the availability of the contaminant, likely by its partial immobilisation
on humic acid sorption sites - thus raising up the intrinsic anionic
sorption capacity of the volcanic soil; the mineral fertilisation enhanced
the mobility of As in soil, probably due to competition of P for the
anionic sorption sites of the soil variable-charge minerals, very affine
to available P. These findings hence suggest that a proper soil management
of As-polluted volcanic soils and amendment by stable organic matter might
mitigate the environmental risk of these soils, thus minimising the
availability of As to biota.
KW - Arsenic pollution
KW - Arsenic speciation
KW - Carrot
KW - Humic acids
KW - Phosphorus
KW - Volcanic soil
RN - N712M78A8G
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180323
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171109
STAT- MEDLINE
DOCNO- medline/29156331

167 - TOXLINE
TI - Arsenic removal from As-hyperaccumulator Pteris vittata biomass: Coupling
extraction with precipitation.
AU - da Silva EB
AD - Research Institute of Rural Sewage Treatment, South West Forestry University,
Yunnan 650224, China; Soil and Water Sciences Department, University of Florida,
Gainesville, FL 32611, United States.
AU - de Oliveira LM
AD - Soil and Water Sciences Department, University of Florida, Gainesville, FL
32611, United States.
AU - Wilkie AC
AD - Soil and Water Sciences Department, University of Florida, Gainesville, FL
32611, United States.
AU - Liu Y
AD - Research Institute of Rural Sewage Treatment, South West Forestry University,
Yunnan 650224, China. Electronic address: yungenliu@swfu.edu.cn.
AU - Ma LQ
AD - Research Institute of Rural Sewage Treatment, South West Forestry University,
Yunnan 650224, China; Soil and Water Sciences Department, University of Florida,
Gainesville, FL 32611, United States. Electronic address: lqma@ufl.edu.
SO - Chemosphere. 2018, Feb; 193:288-294. [Chemosphere]
AB - Proper disposal of As-hyperaccumulator Pteris vittata biomass (Chinese
brake fern) enhances its application in phytoremediation. The goal of this
study was to optimize As removal from P. vittata (PV) biomass by
testing different particle sizes, extractants, extraction times and
solid-to-liquid ratios. PV biomass was extracted using different
extractants followed by different Mg-salts to recover soluble As via
precipitation. Water-soluble As in PV biomass varied from 6.8% to 61% of
total As depending on extraction time, with 99% of As being arsenate
(AsV). Extraction with 2.1% HCl, 2.1% H3PO4, 1 M NaOH and 50% ethanol
recovered 81, 78, 47 and 14% of As from PV biomass. A follow-up extraction
using HCl recovered 27-32% with ethanol recovering only 5%. Though ethanol
showed the lowest extractable As, residual As in the biomass was also the
lowest. Among the extractants, 35% ethanol was the best to remove As from
PV biomass. Approximately 90% As was removed from PV biomass using
particle size < 1 mm at solid:liquid ratio 1:50 and pH 6 for
2 h. Adding MgCl2 at As:Mg ratio of 1:400 with pH 9.5 was effective
to precipitate soluble As, resulting in 98% removal. Effective removal of
As from PV biomass prior to disposal helps make phytoremediation more
feasible.
KW - Arsenic recovery
KW - Ethanol
KW - Extraction
KW - Magnesium arsenate
KW - Precipitation
KW - Speciation
RN - N712M78A8G
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180322
CI - Published by Elsevier Ltd.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171027
STAT- MEDLINE
DOCNO- medline/29145089

168 - TOXLINE
TI - Geo-Spatial Characterization of Soil Mercury and Arsenic at a
High-Altitude Bolivian Gold Mine.
AU - Johnson GD
AD - Department of Environmental, Occupational and Geospatial Health Sciences,
City University of New York School of Public Health, 55 West 125th St, New York,
NY, 10027, USA. glen.johnson@sph.cuny.edu.
AU - Pavilonis B
AD - Department of Environmental, Occupational and Geospatial Health Sciences,
City University of New York School of Public Health, 55 West 125th St, New York,
NY, 10027, USA.
AU - Caravanos J
AD - Department of Environmental Public Health Sciences, College of Global Public
Health, New York University, 665 Broadway, New York, NY, 10003, USA.
AU - Grassman J
AD - Department of Environmental, Occupational and Geospatial Health Sciences,
City University of New York School of Public Health, 55 West 125th St, New York,
NY, 10027, USA.
SO - Bull Environ Contam Toxicol. 2018, Feb; 100(2):259-264. [Bulletin of
environmental contamination and toxicology]
AB - Soil mercury concentrations at a typical small-scale mine site in the
Bolivian Andes were elevated (28-737 mg/kg or ppm) in localized areas
where mercury amalgams were either formed or vaporized to release gold,
but was not detectable beyond approximately 10 m from its sources.
Arsenic was measurable, exceeding known background levels throughout the
mine site (77-137,022 ppm), and was also measurable through the local
village of Ingenio (36-1803 ppm). Although arsenic levels were high
at all surveyed locations, its spatial pattern followed mercury, being
highest where mercury was high.
KW - Arsenic
KW - Artisanal and small-scale gold mining
KW - Mercury
KW - Soil metal contamination
RN - 7440-57-5
RN - FXS1BY2PGL
RN - N712M78A8G
LA - eng
IS - 1432-0800 (Electronic)
PT - Journal Article
TA - Bull Environ Contam Toxicol
YR - 2018
DATE- 20180515
CITO- NLM
CS - United States
CSET- IM
FJT - Bulletin of environmental contamination and toxicology
EDAT- 20171116
STAT- MEDLINE
DOCNO- medline/29147740

169 - TOXLINE
TI - Concentration of Thyrotropic Hormone in Persons Occupationally Exposed to
Lead, Cadmium and Arsenic.
AU - Jurdziak M
AD - Department of Internal Medicine, Occupational Diseases and Hypertension,
Wroclaw Medical University, Borowska 213, 50-556, Wroclaw, Poland.
AU - Ga&#263; P
AD - Department of Hygiene, Wroclaw Medical University, Mikulicza-Radeckiego 7,
50-368, Wroclaw, Poland. pawelgac@interia.pl.
AU - Por&#281;ba M
AD - Department of Pathophysiology, Wroclaw Medical University, Marcinkowskiego 1,
50-368, Wroclaw, Poland.
AU - Szyma&#324;ska-Chabowska A
AD - Department of Internal Medicine, Occupational Diseases and Hypertension,
Wroclaw Medical University, Borowska 213, 50-556, Wroclaw, Poland.
AU - Mazur G
AD - Department of Internal Medicine, Occupational Diseases and Hypertension,
Wroclaw Medical University, Borowska 213, 50-556, Wroclaw, Poland.
AU - Por&#281;ba R
AD - Department of Internal Medicine, Occupational Diseases and Hypertension,
Wroclaw Medical University, Borowska 213, 50-556, Wroclaw, Poland.
SO - Biol Trace Elem Res. 2018, Apr; 182(2):196-203. [Biological trace element
research]
AB - Thyroid hormones are essential for body homeostasis. The scientific
literature contains restricted proofs for effects of environmental
chemical factors on thyroid function. The present study aimed at
evaluating the relationship between toxicological parameters and
concentration of thyrotropic hormone in persons occupationally exposed to
lead, cadmium and arsenic. The studies were conducted on 102 consecutive
workers occupationally exposed to lead, cadmium and arsenic (mean age
45.08 &plusmn; 9.87 years). The estimated parameters
characterizing occupational exposure to metals included blood cadmium
concentration (Cd-B), blood lead concentration (Pb-B), blood zinc
protoporphyrin concentration (ZnPP) and urine arsenic concentration
(As-U). Thyroid function was evaluated using the parameter employed in
screening studies, the blood thyrotropic hormone concentration (TSH). No
differences were disclosed in mean values of toxicological parameters
between the subgroup of persons occupationally exposed to lead, cadmium
and arsenic with TSH in and out of the accepted normal values. Logistic
regression demonstrated that higher blood total bilirubin concentrations
(ORu = 4.101; p = 0.025) and higher Cd-B
(ORu = 1.532; p = 0.027) represented independent risk
factors of abnormal values of TSH in this group. In conclusion, in the
group of workers exposed to lead, cadmium and arsenic, higher blood
cadmium concentration seems to augment the risk of abnormal hormonal
thyroid function.
KW - Arsenic
KW - Cadmium
KW - Lead
KW - Occupational exposure
KW - Thyroid
KW - Thyrotropic hormone
LA - eng
IS - 1559-0720 (Electronic)
PT - Journal Article
TA - Biol Trace Elem Res
YR - 2018
DATE- 20180311
CITO- NLM
CS - United States
FJT - Biological trace element research
EDAT- 20170719
STAT- In-Process
CM - Cites: Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2005
Dec;149(2):329-33 (medline /16601782)
CM - Cites: J Hazard Mater. 2016 Feb 13;303:76-82 (medline /26513566)
CM - Cites: Hum Reprod Update. 1998 May-Jun;4(3):301-9 (medline /9741713)
CM - Cites: Exp Clin Endocrinol Diabetes. 2017 Feb;125(2):79-85 (medline
/27793066)
CM -Cites: Am J Ind Med. 2016 Jul;59(7):583-90 (medline /27094769)
CM -Cites: Arch Intern Med. 1983 Feb;143(2):220-4 (medline /6600605)
CM -Cites: Environ Health Perspect. 2008 Jun;116(6):806-13 (medline /18560538)
CM -Cites: Environ Health Perspect. 2001 Mar;109(3):245-51 (medline /11333185)
CM -Cites: Biometals. 2000 Jun;13(2):187-92 (medline /11016408)
CM -Cites: Thyroid. 1998 Sep;8(9):827-56 (medline /9777756)
CM -Cites: Neurotoxicology. 2007 Sep;28(5):951-6 (medline /17576015)
CM -Cites: Exp Mol Pathol. 1991 Aug;55(1):97-104 (medline /1884772)
CM -Cites: Int J Clin Exp Med. 2015 May 15;8(5):7160-7 (medline /26221254)
CM -Cites: Environ Res. 2009 Oct;109(7):869-73 (medline /19595304)
CM -Cites: Pharmacol Res. 2000 Dec;42(6):599-602 (medline /11058414)
CM -Cites: Environ Health Perspect. 2006 Dec;114(12):1865-71 (medline
/17185277)
CM - Cites: Med Clin North Am. 2012 Mar;96(2):257-68 (medline /22443974)
CM - Cites: Environ Res. 2008 Feb;106(2):195-202 (medline /17988663)
CM - Cites: J Nutr. 2003 May;133(5 Suppl 1):1536S-8S (medline /12730460)
CM - Cites: J Neuroendocrinol. 2008 Jun;20(6):784-94 (medline /18601701)
CM - Cites: Toxicol Sci. 2007 Jul;98(1):75-86 (medline /17283378)
CM - Cites: Biol Trace Elem Res. 2008 Winter;126(1-3):194-203 (medline
/18685812)
CM - Cites: Biol Trace Elem Res. 2008 Winter;126(1-3):1-12 (medline /18716716)
CM - Cites: Med Clin North Am. 2012 Mar;96(2):235-56 (medline /22443973)
CM - Cites: Toxicology. 2006 Nov 10;228(1):77-84 (medline /16982123)
CM - Cites: Curr Opin Endocrinol Diabetes Obes. 2009 Oct;16(5):385-91 (medline
/19625957)
CM - Cites: J Appl Toxicol. 1998 Sep-Oct;18(5):317-20 (medline /9804431)
CM - Cites: Environ Health Perspect. 2008 Feb;116(2):165-72 (medline /18288313)
CM - Cites: J Environ Sci Health A Tox Hazard Subst Environ Eng. 2003
Jan;38(1):129-39 (medline /12635823)
CM - Cites: Arch Environ Health. 2001 Sep-Oct;56(5):449-55 (medline /11777027)
CM - Cites: Environ Pollut. 2015 Oct;205:145-52 (medline /26057477)
CM - Cites: Int J Hyg Environ Health. 2013 Nov;216(6):624-32 (medline
/23044211)
CM - Cites: Br Med Bull. 1999;55(3):658-68 (medline /10746354)
CM - Cites: Int Arch Occup Environ Health. 1998 Oct;71(7):453-8 (medline
/9826077)
CM - Cites: Environ Health Perspect. 2013 Feb;121(2):181-6 (medline /23164649)
CM - Cites: Environ Res. 2006 May;101(1):140-5 (medline /16360141)
CM - Cites: Biol Trace Elem Res. 2008 Winter;126(1-3):49-55 (medline /18685814)
CM - Cites: Environ Health Perspect. 1992 Jul;97:259-67 (medline /1396465)
CM - Cites: Mol Cell Endocrinol. 2005 Oct 20;242(1-2):10-5 (medline /16150534)
CM - Cites: Mutat Res. 2006 Jun;612(3):215-46 (medline /16574468)
CM - Cites: Biol Trace Elem Res. 2007 Oct;119(1):10-8 (medline /17914214)
CM - Cites: Environ Res. 2008 Jul;107(3):380-92 (medline /18313043)
CM - Cites: Scand J Work Environ Health. 1988 Jun;14(3):175-80 (medline
/3393853)
CM - Cites: Toxicol Ind Health. 2015 Dec;31(12):1258-68 (medline /23796758)
DOCNO- medline/28726072

170 - TOXLINE
TI - Ameliorative role of genistein against age-dependent chronic arsenic
toxicity in murine brains via the regulation of oxidative stress and
inflammatory signaling cascades.
AU - Saha S
AD - Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M,
Kolkata, 700054, India.
AU - Sadhukhan P
AD - Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M,
Kolkata, 700054, India.
AU - Mahalanobish S
AD - Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M,
Kolkata, 700054, India.
AU - Dutta S
AD - Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M,
Kolkata, 700054, India.
AU - Sil PC
AD - Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M,
Kolkata, 700054, India. Electronic address: parames@jcbose.ac.in.
SO - J Nutr Biochem. 2018, May; 55:26-40. [The Journal of nutritional
biochemistry]
AB - Brain is highly prone to oxidative damage due to its huge lipid content
and extensive energy requirements. Exogenous insult in brain via oxidative
injury can lead to severe pathophysiological conditions. Age-dependent
deterioration of normal brain functions is also noteworthy. Genistein, a
polyphenolic isoflavonoid, obtained from the soy plant, is well known to
protect against several diseased conditions. Here, in this study chronic
brain toxicity model was developed using oral administration of arsenic
for 90 days in adult and aged murines. We observed that intraperitoneal
administration of genistein improved the arsenic induced behavioral
abnormalities in the rats. It was also evident from the histopathological
studies that the extent of tissue damage due to arsenic exposure was more
in aged rats compared to the adults. Evaluation of different stress
markers, intracellular ROS level and mitochondrial membrane potential
revealed the involvement of oxidative stress and mitochondrial dysfunction
in inducing brain damage in arsenic exposed murines. It was observed that
genistein can significantly ameliorate the stressed condition in both the
animal groups but the protective effect of genistein was more significant
in the adult animals. The underlying signalling mechanism behind the
cytotoxicity of arsenic was investigated and revealed that genistein
exhibited neuroprotection significantly by modulating the JNK3 mediated
apoptosis, ERK1/2 mediated autophagy and TNF&alpha; associated
inflammatory pathways. Overall study infers that genistein has significant
ameliorative effect of against age-dependent cytotoxicity of arsenic in
murine brains.
KW - Apoptosis
KW - Arsenic
KW - Autophagy
KW - Brain
KW - Genistein
KW - Inflammation
KW - Oxidative stress
LA - eng
IS - 1873-4847 (Electronic)
PT - Journal Article
TA - J Nutr Biochem
YR - 2018
DATE- 20180506
CI - Copyright &copy; 2017 Elsevier Inc. All rights reserved.
CITO- NLM
CS - United States
FJT - The Journal of nutritional biochemistry
EDAT- 20171212
STAT- In-Data-Review
DOCNO- medline/29331881

171 - TOXLINE
TI - Prospective role of indigenous Exiguobacterium profundum PT2 in arsenic
biotransformation and biosorption by planktonic cultures and biofilms.
AU - Saba
AD - The Women University Multan, Multan, Pakistan.
AU - Andreasen R
AD - Department of Geoscience, Aarhus University, Aarhus, Denmark.
AU - Li Y
AD - Bio-Optics Institute, School of Physics and Electronics, Henan University,
Henan, China.
AU - Rehman Y
AD - Department of Microbiology and Molecular Genetics, University of the Punjab,
Lahore, Pakistan.
AU - Ahmed M
AD - Department of Microbiology and Molecular Genetics, University of the Punjab,
Lahore, Pakistan.
AU - Meyer RL
AD - Interdisciplinary Nanoscience Centre, Aarhus University, Aarhus, Denmark.
AU - Sabri AN
AD - Department of Microbiology and Molecular Genetics, University of the Punjab,
Lahore, Pakistan.
SO - J Appl Microbiol. 2018, Feb; 124(2):431-443. [Journal of applied
microbiology]
AB - AIMS: The aim of this study was to analyse arsenic (As) transformation and
biosorption by indigenous As-resistant bacteria both in planktonic and
biofilm modes of growth.
AB - METHODS AND RESULTS: As-resistant bacteria were isolated from industrial
waste water and strain PT2, and identified as Exiguobacterium profundum
through 16S rRNA gene sequencing was selected for further study. As
transformation and biosorption by E. profundumPT2 was determined by
HPLC-ICP-MS analysis. Planktonic cultures reduced
3&middot;73 mmol l-1 As5+ into As3+ from artificial waste water
effluent after 48-h incubation. In case of biosorption, planktonic
cultures and biofilms exhibited 25&middot;2 and
29&middot;4 mg g-1 biomass biosorption, respectively. As
biosorption kinetics followed Freundlich isotherm and pseudo second-order
model. Biofilm formation peaked after 3 days of incubation, and in
the presence of As stress, biofilm formation was significantly affected in
contrast to control (P < 0&middot;05). Homogeneous nature of
mature biofilms with an increased demand of nutrients was revealed by
minimum roughness and maximum surface to biovolume ratio measured through
CLSM analysis.
AB - CONCLUSION: Indigenous As-resistant E. profundumPT2 was found capable of
As transformation and biosorption both in the form of planktonic cultures
and biofilms.
AB - SIGNIFICANCE AND IMPACT OF THE STUDY: Indigenous biofilm forming E.
profundum PT2 revealing As biosorption and biotransformation potential is
presented an eco-friendly and cost-effective source for As remediation
that can be implemented for waste water treatment.
KW - arsenic biotransformation
KW - arsenic resistance
KW - biofilms
KW - bioremediation
KW - wastewater treatment
RN - N712M78A8G
LA - eng
IS - 1365-2672 (Electronic)
PT - Journal Article
TA - J Appl Microbiol
YR - 2018
DATE- 20180514
CI - &copy; 2017 The Society for Applied Microbiology.
DBAN- GENBANK: KX185940: KX185941: KX185938: KX185939
CITO- NLM
CS - England
CSET- IM
FJT - Journal of applied microbiology
EDAT- 20180115
STAT- MEDLINE
DOCNO- medline/29130635

172 - TOXLINE
TI - Transcriptional changes measured in rice roots after exposure to
arsenite-contaminated sediments.
AU - Brinke A
AD - German Federal Institute of Hydrology, Am Mainzer Tor 1, 56068, Koblenz,
Germany. Alexandra.Brinke@bafg.de.
AU - Reifferscheid G
AD - German Federal Institute of Hydrology, Am Mainzer Tor 1, 56068, Koblenz,
Germany.
AU - Klein R
AD - Department VI, Trier University, Biogeography, 54286, Trier, Germany.
AU - Feiler U
AD - German Federal Institute of Hydrology, Am Mainzer Tor 1, 56068, Koblenz,
Germany.
AU - Buchinger S
AD - German Federal Institute of Hydrology, Am Mainzer Tor 1, 56068, Koblenz,
Germany.
SO - Environ Sci Pollut Res Int. 2018, Jan; 25(3):2707-2717. [Environmental
science and pollution research international]
AB - Transcriptional analyses are discussed to provide a deeper understanding
of the molecular mechanisms underlying toxic effects. Thus, they can
complement classic ecotoxicological test methods and potentially allow the
identification of biomarkers associated to the exposure of chemical
stressors and or adverse biological effects. This feasibility study
intended to identify a set of potential gene expression biomarkers for
arsenite-exposure in rice roots that could complement the informative
value of an existing sediment-contact test with rice. A sediment-contact
test with Oryza sativa with the parameters inhibition of root and shoot
elongation as phenotypic endpoints was used as basis. Rice plants were
exposed to arsenite-spiked sediments. Transcriptomic changes in response
to arsenite were observed by means of cDNA-microarray analysis regarding
the whole-transcriptome at two sublethal arsenite concentrations. In order
to identify candidate biomarker genes, differentially expressed genes were
identified. Arsenite-induced differentially expressed genes were
significantly associated with gene ontology (GO)-terms that indicated a
general stress response. Of the differentially expressed genes, five genes
were selected and their expression was measured at seven arsenite
concentrations by means of qPCR in order to obtain their expression
profiles. Three candidate biomarker genes showed a dose-dependent
upregulation, while two showed no clear dose-dependent expression. The
expression of all candidate biomarkers was also assessed in rice plants
grown on two arsenic-contaminated natural sediments, but only one
biomarker gene showed the expected upregulation.
KW - Aquatic plants
KW - Biomarkers
KW - Ecotoxicogenomics
KW - Freshwater toxicology
KW - Sediment toxicity
LA - eng
IS - 1614-7499 (Electronic)
PT - Journal Article
TA - Environ Sci Pollut Res Int
YR - 2018
DATE- 20180131
CITO- NLM
CS - Germany
FJT - Environmental science and pollution research international
EDAT- 20171113
STAT- In-Process
CM - Cites: Plant Physiol. 2000 Mar;122(3):793-801 (medline /10712543)
CM - Cites: Curr Opin Plant Biol. 2009 Jun;12(3):364-72 (medline /19501016)
CM - Cites: Environ Sci Technol. 2013 Aug 6;47(15):8825-34 (medline /23802634)
CM - Cites: J Exp Bot. 2007;58(2):253-65 (medline /17132712)
CM - Cites: Nucleic Acids Res. 2011 Jan;39(Database issue):D1002-4 (medline
/21071405)
CM - Cites: Ecotoxicol Environ Saf. 2015 Apr;114:126-33 (medline /25637747)
CM - Cites: Mol Carcinog. 1999 Mar;24(3):153-9 (medline /10204799)
CM - Cites: Chemosphere. 2009 Feb;74(5):688-702 (medline /18996570)
CM - Cites: Plant J. 2006 Nov;48(4):535-47 (medline /17059409)
CM - Cites: Rice (N Y). 2012 Jul 19;5(1):17 (medline /24279809)
CM - Cites: Environ Sci Pollut Res Int. 2015 Aug;22(16):12664-75 (medline
/25913308)
CM - Cites: Environ Health Perspect. 2003 May;111(6):A338-9 (medline /12760838)
CM - Cites: Aquat Toxicol. 2014 Aug;153:73-88 (medline /24434169)
CM - Cites: Curr Opin Plant Biol. 2002 Jun;5(3):218-23 (medline /11960739)
CM - Cites: Plant Cell Physiol. 2013 Feb;54(2):e6 (medline /23299411)
CM - Cites: Environ Toxicol Chem. 2017 Sep;36(9):2352-2366 (medline /28224655)
CM - Cites: Front Cell Dev Biol. 2017 Jul 18;5:67 (medline /28770198)
CM - Cites: Biochimie. 2006 Nov;88(11):1707-19 (medline /16914250)
CM - Cites: Biotechniques. 2003 Feb;34(2):374-8 (medline /12613259)
CM - Cites: Plant Cell. 2009 Feb;21(2):655-67 (medline /19244140)
CM - Cites: J Exp Bot. 2008;59(8):2267-76 (medline /18453530)
CM - Cites: Trends Plant Sci. 2002 Mar;7(3):106-11 (medline /11906833)
CM - Cites: Biochem Biophys Res Commun. 2006 Jun 30;345(2):646-51 (medline
/16690022)
CM - Cites: Plant Cell Physiol. 2006 Jan;47(1):1-13 (medline /16299003)
CM - Cites: Environ Sci Pollut Res Int. 2017 Apr 8;:null (medline /28391457)
CM - Cites: Genome Biol. 2008;9(2):R40 (medline /18291039)
CM - Cites: Proc Natl Acad Sci U S A. 2010 Dec 7;107(49):20853-4 (medline
/21106757)
CM - Cites: Environ Pollut. 2010 Sep;158(9):2999-3010 (medline /20594629)
CM - Cites: Environ Sci Technol. 2014 Mar 18;48(6):3504-12 (medline /24552435)
CM - Cites: Environ Sci Pollut Res Int. 2015 Apr;22(8):5742-50 (medline
/25827791)
CM - Cites: Proteomics. 2008 Sep;8(17):3561-76 (medline /18752204)
CM - Cites: Environ Sci Pollut Res Int. 2015 Nov;22(22):17280-9 (medline
/24994105)
CM - Cites: Reprod Toxicol. 2012 Apr;33(2):245-53 (medline /22326570)
CM - Cites: Nucleic Acids Res. 2015 Jan;43(Database issue):D204-12 (medline
/25348405)
CM - Cites: BMC Genomics. 2009 Apr 14;10:160 (medline /19366437)
CM - Cites: Rice (N Y). 2016 Dec;9(1):60 (medline /27837430)
CM - Cites: BMC Plant Biol. 2014 Apr 16;14:94 (medline /24734953)
DOCNO- medline/29134529

173 - TOXLINE
TI - Nutritional management can assist a significant role in alleviation of
arsenicosis.
AU - Sharma A
AD - Department of Medicinal Chemistry, National Institute of Pharmaceutical
Education and Research, Raebareli, India.
AU - Flora SJS
AD - Department of Medicinal Chemistry, National Institute of Pharmaceutical
Education and Research, Raebareli, India. Electronic address: sjsflora@hotmail.com.
SO - J Trace Elem Med Biol. 2018, Jan; 45:11-20. [Journal of trace elements in
medicine and biology : organ of the Society for Minerals and Trace
Elements (GMS)]
AB - Consumption of arsenic contaminated water causes serious skin disease and
cancer in a significant number of exposed people. Chelating agents,
consider an expensive therapy, are employed in the treatment of arsenic
intoxication. There are reports which suggest that the poorest suffer the
most from arsenicosis. This may be due to improper diet intake, consist of
low protein and micronutrients which increase the vulnerability to
arsenic-related disorders. Several human studies demonstrated the
associations between malnourishment and the development of arsenic-caused
skin lesions, skin cancer and cardiovascular effects. Thus, there is an
urgent need of implementation of mitigation strategies for improving the
health of exposed populations. Nutrition enhances the detoxification
process so food rich in vitamins, protein, antioxidants help in its
detoxification process. Methylation is the detoxification process which
takes place via S-adenosylmethionine (SAM). It is a methyl group donor and
it derived its methyl group from diet. Nutritional intervention thus may
appear as a practical and inexpensive approach. Nutrition provides
protection from toxic effect of arsenic by two ways (i) methylation of As
(ii) antioxidants which provides protection against free radical species.
The governments and NGOs may run awareness programmes in arsenic affected
area regarding prevention and alternate therapy which can decrease the
susceptibility of the exposed population. They could also help in
distributing cheaper, high protein diets particularly to the masses who
cannot afford such foods. Thus, to prevent arsenicosis alternate therapy
and proper nutrition could be the important strategy for alleviating its
toxic effects. This mini review provides an insight on the importance of
nutrition in preventing adverse effect cause by arsenic to suffer
population.
KW - Arsenic
KW - Dietary
KW - Malnutrition
KW - Micronutrients
KW - Toxicity
KW - Vitamins
LA - eng
IS - 1878-3252 (Electronic)
PT - Journal Article
PT - Review
TA - J Trace Elem Med Biol
YR - 2018
DATE- 20171127
CI - Copyright &copy; 2017 Elsevier GmbH. All rights reserved.
CITO- NLM
CS - Germany
FJT - Journal of trace elements in medicine and biology : organ of the Society
for Minerals and Trace Elements (GMS)
EDAT- 20170914
STAT- In-Process
DOCNO- medline/29173466

174 - TOXLINE
TI - A systematic review and meta-analysis of bidirectional effect of arsenic
on ERK signaling pathway.
AU - Li D
AD - Department of Public Health, School of Medicine, Shihezi University, Shihezi,
Xinjiang 832002, P.R. China.
AU - Wei Y
AD - Department of Cardiothoracic Surgery, First Affiliated Hospital, School of
Medicine, Shihezi University, Shihezi, Xinjiang 832000, P.R. China.
AU - Xu S
AD - Department of Public Health, School of Medicine, Shihezi University, Shihezi,
Xinjiang 832002, P.R. China.
AU - Niu Q
AD - Department of Public Health, School of Medicine, Shihezi University, Shihezi,
Xinjiang 832002, P.R. China.
AU - Zhang M
AD - Department of Public Health, School of Medicine, Shihezi University, Shihezi,
Xinjiang 832002, P.R. China.
AU - Li S
AD - Department of Public Health, School of Medicine, Shihezi University, Shihezi,
Xinjiang 832002, P.R. China.
AU - Jing M
AD - Department of Public Health, School of Medicine, Shihezi University, Shihezi,
Xinjiang 832002, P.R. China.
SO - Mol Med Rep. 2018, Mar; 17(3):4422-4432. [Molecular medicine reports]
AB - Arsenic is a toxic metal, which ultimately leads to cell apoptosis. ERK is
considered a key transcriptional regulator of arsenic&#8209;induced
apoptosis. Due to a few controversial issues about arsenic&#8209;mediated
extracellular signal&#8209;regulated MAP kinases (ERK) signaling, a
meta&#8209;analysis was performed. Subgroup analyses demonstrated that
high doses (&ge;2 &micro;mol/l) of arsenic increased the expression
of Ras, ERK, ERK1, ERK2, phosphorylated (p)&#8209;ERK, p&#8209;ERK1, and
p&#8209;ERK2, while low doses ( < 2 &micro;mol/l) decreased the
expression of Ras, ERK1, p&#8209;ERK, and p&#8209;ERK2 when compared to
control groups. Long term exposure ( > 24 h) to arsenic led to
inhibition of expression of ERK1, p&#8209;ERK1, and p&#8209;ERK2, whereas
short&#8209;term exposure (&le;24 h) triggered the expression of
ERK1, ERK2, p&#8209;ERK, p&#8209;ERK1, and p&#8209;ERK2. Furthermore,
normal cells exposed to arsenic exhibited higher production levels of Ras
and p&#8209;ERK. Conversely, exposure of cancer cells to arsenic showed a
lower level of production of Ras and p&#8209;ERK as well as higher level
of p&#8209;ERK1 and p&#8209;ERK2 as compared to control group.
Short&#8209;term exposure of normal cells to high doses of arsenic may
promote ERK signaling pathway. In contrast, long&#8209;term exposure of
cancer cells to low doses of arsenic may inhibit ERK signaling pathway.
This study may be helpful in providing a theoretical basis for the
diverging result of arsenic adverse effects on one hand and therapeutic
mechanisms on the other concerning arsenic&#8209;induced apoptosis.
LA - eng
IS - 1791-3004 (Electronic)
PT - Journal Article
TA - Mol Med Rep
YR - 2018
DATE- 20180227
CITO- NLM
CS - Greece
FJT - Molecular medicine reports
EDAT- 20180105
STAT- In-Process
CM - Cites: PLoS One. 2013 Dec 31;8(12):e85995 (medline /24392034)
CM - Cites: Toxicol Sci. 2014 Apr;138(2):268-77 (medline /24431212)
CM -Cites: Mol Cell Biochem. 2001 Jan;217(1-2):131-6 (medline /11269657)
CM -Cites: Arch Toxicol. 2016 Sep;90(9):2187-200 (medline /26404762)
CM -Cites: Mol Med Rep. 2015 Nov;12(5):7335-43 (medline /26459009)
CM -Cites: Cell Signal. 2006 Feb;18(2):244-55 (medline /15961274)
CM -Cites: Arch Toxicol. 2011 Jun;85(6):565-75 (medline /21533816)
CM -Cites: Pharmacol Res. 2013 Nov;77:11-21 (medline /24004656)
CM -Cites: Neurotoxicol Teratol. 2011 Sep-Oct;33(5):530-7 (medline /21784148)
CM -Cites: Arch Toxicol. 2012 Jun;86(6):879-96 (medline /22488045)
CM -Cites: Toxicol Appl Pharmacol. 2005 Aug 15;206(3):288-98 (medline
/16039940)
CM - Cites: Toxicol Sci. 2016 Jul;152(1):62-71 (medline /27071941)
CM - Cites: Biochem Pharmacol. 2011 Dec 1;82(11):1619-29 (medline /21889928)
CM - Cites: Toxicol Appl Pharmacol. 2011 Oct 1;256(1):44-51 (medline /21798276)
CM - Cites: J Biomed Sci. 2006 Jan;13(1):113-25 (medline /16283431)
CM - Cites: J Cell Physiol. 2011 Mar;226(3):762-8 (medline /20799280)
CM - Cites: Biotechnol Lett. 2014 Oct;36(10 ):1927-36 (medline /24934751)
CM - Cites: Biochem Pharmacol. 2012 Dec 15;84(12):1604-16 (medline /23041229)
CM - Cites: Carcinogenesis. 2004 Jan;25(1):21-8 (medline /14514659)
CM - Cites: Toxicol Sci. 2006 Jan;89(1):164-72 (medline /16207941)
CM - Cites: Toxicol Appl Pharmacol. 2010 Apr 15;244(2):162-73 (medline
/20045430)
CM - Cites: Toxicol Appl Pharmacol. 2015 Jul 1;286(1):36-43 (medline /25804888)
CM - Cites: Arch Toxicol. 2015 Nov;89(11):1971-9 (medline /25199681)
CM - Cites: J Biol Chem. 1999 May 21;274(21):14595-601 (medline /10329651)
CM - Cites: Int J Cancer. 2001 May 15;92 (4):518-26 (medline /11304686)
CM - Cites: Toxicol Lett. 2010 Oct 5;198(2):263-71 (medline /20654705)
CM - Cites: Biochem Biophys Res Commun. 2015 May 29;461(2):243-8 (medline
/25869069)
CM - Cites: Nan Fang Yi Ke Da Xue Xue Bao. 2008 Apr;28(4):639-41 (medline
/18495609)
CM - Cites: Toxicol Lett. 2014 Jan 3;224(1):130-40 (medline /24157283)
CM - Cites: Toxicol Appl Pharmacol. 2010 Feb 1;242(3):247-55 (medline
/19874834)
DOCNO- medline/29328451

175 - TOXLINE
TI - Arsenite Targets the RING Finger Domain of Rbx1 E3 Ubiquitin Ligase to
Inhibit Proteasome-Mediated Degradation of Nrf2.
AU - Jiang J
AU - Tam LM
AU - Wang P
AU - Wang Y
SO - Chem Res Toxicol. 2018, May 21; 31(5):380-387. [Chemical research in
toxicology]
AB - Activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)
antioxidant response signaling pathway is a major mechanism for the
cellular defense against oxidative stress. Arsenite, a widespread
contaminant in drinking water, is known to induce oxidative stress and
activate the Nrf2-dependent signaling pathway through the stabilization of
the Nrf2 protein by inhibiting its ubiquitination via the Cul3-Rbx1-Keap1
(cullin 3, RING-box 1, and Kelch-like ECH-associated protein 1) E3
ubiquitin ligase, and its degradation by the 26S proteasome, though the
underlying mechanism, remains elusive. In the present study, we
demonstrated that arsenite could bind to the RING finger domain of Rbx1 in
vitro and in cells, which led to the suppression of Cul3-Rbx1 E3 ubiquitin
ligase activity, thereby impairing the Nrf2 ubiquitination and activating
the Nrf2-induced antioxidant signaling pathway. Our finding provided novel
insight into arsenic toxicity by uncovering a distinct mechanism
accounting for arsenite-induced Nrf2 activation.
LA - eng
IS - 1520-5010 (Electronic)
PT - Journal Article
TA - Chem Res Toxicol
YR - 2018
DATE- 20180521
CITO- NLM
CS - United States
FJT - Chemical research in toxicology
EDAT- 20180423
STAT- In-Data-Review
DOCNO- medline/29658272

176 - TOXLINE
TI - Health risk assessment of arsenic in Realgar and NiuHuangJieDu Tablets
based on pharmacokinetic study.
AU - Wu X
AD - Key Laboratory of Drug Quality Control and Pharmacovigilance, Ministry of
Education, Department of Pharmaceutical Analysis, China Pharmaceutical University,
Nanjing 210009, China.
AU - Wu S
AD - Key Laboratory of Drug Quality Control and Pharmacovigilance, Ministry of
Education, Department of Pharmaceutical Analysis, China Pharmaceutical University,
Nanjing 210009, China.
AU - Liu Y
AD - Key Laboratory of Drug Quality Control and Pharmacovigilance, Ministry of
Education, Department of Pharmaceutical Analysis, China Pharmaceutical University,
Nanjing 210009, China.
AU - Guan R
AD - Key Laboratory of Drug Quality Control and Pharmacovigilance, Ministry of
Education, Department of Pharmaceutical Analysis, China Pharmaceutical University,
Nanjing 210009, China.
AU - Liang F
AD - Key Laboratory of Drug Quality Control and Pharmacovigilance, Ministry of
Education, Department of Pharmaceutical Analysis, China Pharmaceutical University,
Nanjing 210009, China.
AU - Song M
AD - Key Laboratory of Drug Quality Control and Pharmacovigilance, Ministry of
Education, Department of Pharmaceutical Analysis, China Pharmaceutical University,
Nanjing 210009, China. Electronic address: cqsongmin@sina.com.
AU - Hang T
AD - Key Laboratory of Drug Quality Control and Pharmacovigilance, Ministry of
Education, Department of Pharmaceutical Analysis, China Pharmaceutical University,
Nanjing 210009, China. Electronic address: hangtj@cpu.edu.cn.
SO - J Trace Elem Med Biol. 2018, Jul; 48:81-86. [Journal of trace elements in
medicine and biology : organ of the Society for Minerals and Trace
Elements (GMS)]
AB - NiuHuangJieDu Tablets (NHJDT), a popular realgar (As4S4) containing
patented traditional Chinese medicine (TCM), is widely used in the
treatment of acute tonsillitis, pharyngitis, periodontitis and mouth
ulcer. However, arsenic is considered as one of the most toxic elements,
leading to growing concerns about the quality and safety of
realgar-containing TCMs recently. In this study, health risk assessment of
arsenic in realgar and NHJDT was conducted through oral administration of
both substances to rats with single and multiple doses, respectively. The
total blood arsenic concentration was used as the health risk indicator
and determined by hydride generation-atomic fluorescence spectrometry
after modified Kjeldahl digestion, and then applied to the pharmacokinetic
study. For single oral dose study in rats, the low, medium, and high doses
of realgar and NHJDT were set equivalent to 1, 5 and 20 times the human
therapeutic dose (1.3&#8239;mg realgar/kg), respectively. Multiple doses
were given at low and high dose levels every 12&#8239;h for seven
consecutive days, respectively. Significant differences in the total blood
arsenic pharmacokinetic profiles were observed between the corresponding
realgar and NHJDT groups. These results indicated that NHJDT significantly
reduced the total blood arsenic exposure present in realgar, and the
detoxification mechanism might be attributed to herb-herb interactions in
NHJDT. However, the accumulation of blood total arsenic was significant
due to the long elimination half-life and high accumulation index in both
realgar and NHJDT groups. Therefore, the potential health risk of arsenic
caused by the administration of realgar-containing TCMs should be taken
into account for excessive or long-term medication. Precautions should be
taken for the clinical application of realgar-containing TCMs.
KW - Arsenic
KW - Health risk assessment
KW - Hydride generation-atomic fluorescence spectrometry
KW - NiuHuangJieDu Tablets
KW - Pharmacokinetics
KW - Realgar
LA - eng
IS - 1878-3252 (Electronic)
PT - Journal Article
TA - J Trace Elem Med Biol
YR - 2018
DATE- 20180518
CI - Copyright &copy; 2018 Elsevier GmbH. All rights reserved.
CITO- NLM
CS - Germany
FJT - Journal of trace elements in medicine and biology : organ of the Society
for Minerals and Trace Elements (GMS)
EDAT- 20180314
STAT- In-Process
DOCNO- medline/29773199

177 - TOXLINE
TI - Arjunolic Acid Improves the Serum Level of Vitamin B12 and Folate in the
Process of the Attenuation of Arsenic Induced Uterine Oxidative Stress.
AU - Maity M
AD - Clinical Nutrition and Dietetics Division (Funded under UGC Innovative
Programme), Vidyasagar University, Midnapore, West Bengal, 721102, India.
AU - Perveen H
AD - Clinical Nutrition and Dietetics Division (Funded under UGC Innovative
Programme), Vidyasagar University, Midnapore, West Bengal, 721102, India.
AU - Dash M
AD - Clinical Nutrition and Dietetics Division (Funded under UGC Innovative
Programme), Vidyasagar University, Midnapore, West Bengal, 721102, India.
AU - Jana S
AD - Clinical Nutrition and Dietetics Division (Funded under UGC Innovative
Programme), Vidyasagar University, Midnapore, West Bengal, 721102, India.
AU - Khatun S
AD - Clinical Nutrition and Dietetics Division (Funded under UGC Innovative
Programme), Vidyasagar University, Midnapore, West Bengal, 721102, India.
AU - Dey A
AD - Clinical Nutrition and Dietetics Division (Funded under UGC Innovative
Programme), Vidyasagar University, Midnapore, West Bengal, 721102, India.
AU - Mandal AK
AD - Chemical Biology Laboratory, Department of Sericulture, Raiganj University,
Uttar Dinajpur, West Bengal, 733134, India.
AU - Chattopadhyay S
AD - Clinical Nutrition and Dietetics Division (Funded under UGC Innovative
Programme), Vidyasagar University, Midnapore, West Bengal, 721102, India.
sandipdoc@mail.vidyasagar.ac.in.
SO - Biol Trace Elem Res. 2018, Mar; 182(1):78-90. [Biological trace element
research]
AB - Continuation of prolonged treatment against arsenicosis with conventional
chelating therapy is a global challenge. The present study was intended to
evaluate the defensive effect of arjunolic acid against arsenic-induced
oxidative stress and female reproductive dysfunction. Wistar strain adult
female rats were given sodium arsenite (10 mg/kg body weight) in
combination with arjunolic acid (10 mg/kg body weight) orally for two
estrous cycles. Electrozymographic analysis explored that arjunolic acid
co-treatment counteracted As3+-induced ROS production in uterine tissue by
stimulating the activities of endogenous enzymatic antioxidants. Arjunolic
acid was able to enhance the protection against mutagenic uterine DNA
breakage, necrosis, and ovarian-uterine tissue damages in arsenicated rats
by improving the ovarian steroidogenesis. The mechanisms might be coupled
with the augmentation of antioxidant defense system, partly through the
elimination of arsenic with the involvement of S-adenosyl methionine pool
where circulating levels of vitamin B12, folic acid, and homocysteine play
critical roles as evidenced from our present investigation.
KW - Arjunolic acid
KW - Arsenic
KW - Folic acid
KW - SAM
KW - Uterine oxidative stress
KW - Vitamin B12
LA - eng
IS - 1559-0720 (Electronic)
PT - Journal Article
TA - Biol Trace Elem Res
YR - 2018
DATE- 20180211
CITO- NLM
CS - United States
FJT - Biological trace element research
EDAT- 20170628
STAT- In-Process
DOCNO- medline/28660490

178 - TOXLINE
TI - Arsenic Uptake, Toxicity, Detoxification, and Speciation in Plants:
Physiological, Biochemical, and Molecular Aspects.
AU - Abbas G
AD - Department of Environmental Sciences, COMSATS Institute of Information
Technology, Vehari-61100, Pakistan. g.a92pk@gmail.com.
AU - Murtaza B
AD - Department of Environmental Sciences, COMSATS Institute of Information
Technology, Vehari-61100, Pakistan. behzadmurtaza@ciitvehari.edu.pk.
AU - Bibi I
AD - MARUM and Department of Geosciences, University of Bremen, D-28359 Bremen,
Germany. irshad.niazi81@gmail.com.
AU - Shahid M
AD - Department of Environmental Sciences, COMSATS Institute of Information
Technology, Vehari-61100, Pakistan. muhammadshahid@ciitvehari.edu.pk.
AU - Niazi NK
AD - Southern Cross GeoScience, Southern Cross University, Lismore 2480,
Australia. nabeelkniazi@gmail.com.
AU - Khan MI
AD - Institute of Soil and Environmental Sciences, University of Agriculture
Faisalabad, Faisalabad 38040, Pakistan. khanimran1173@yahoo.com.
AU - Amjad M
AD - Department of Environmental Sciences, COMSATS Institute of Information
Technology, Vehari-61100, Pakistan. drmuhammadamjad@ciitvehari.edu.pk.
AU - Hussain M
AD - Institute of Soil and Environmental Sciences, University of Agriculture
Faisalabad, Faisalabad 38040, Pakistan. munawarhussain452@yahoo.com.
AU - Natasha
AD - Department of Environmental Sciences, COMSATS Institute of Information
Technology, Vehari-61100, Pakistan. natasha564ag@gmail.com.
SO - Int J Environ Res Public Health. 2018, Jan 02. [International journal of
environmental research and public health]
AB - Environmental contamination with arsenic (As) is a global environmental,
agricultural and health issue due to the highly toxic and carcinogenic
nature of As. Exposure of plants to As, even at very low concentration,
can cause many morphological, physiological, and biochemical changes. The
recent research on As in the soil-plant system indicates that As toxicity
to plants varies with its speciation in plants (e.g., arsenite, As(III);
arsenate, As(V)), with the type of plant species, and with other soil
factors controlling As accumulation in plants. Various plant species have
different mechanisms of As(III) or As(V) uptake, toxicity, and
detoxification. This review briefly describes the sources and global
extent of As contamination and As speciation in soil. We discuss different
mechanisms responsible for As(III) and As(V) uptake, toxicity, and
detoxification in plants, at physiological, biochemical, and molecular
levels. This review highlights the importance of the As-induced generation
of reactive oxygen species (ROS), as well as their damaging impacts on
plants at biochemical, genetic, and molecular levels. The role of
different enzymatic (superoxide dismutase, catalase, glutathione
reductase, and ascorbate peroxidase) and non-enzymatic (salicylic acid,
proline, phytochelatins, glutathione, nitric oxide, and phosphorous)
substances under As(III/V) stress have been delineated via conceptual
models showing As translocation and toxicity pathways in plant species.
Significantly, this review addresses the current, albeit partially
understood, emerging aspects on (i) As-induced physiological, biochemical,
and genotoxic mechanisms and responses in plants and (ii) the roles of
different molecules in modulation of As-induced toxicities in plants. We
also provide insight on some important research gaps that need to be
filled to advance our scientific understanding in this area of research on
As in soil-plant systems.
COI - The authors declare no conflict of interest.
KW - arsenic contamination
KW - bioavailability
KW - oxidative stress
KW - phosphate
KW - plant health
KW - potentially toxic elements
KW - reactive oxygen species
LA - eng
IS - 1660-4601 (Electronic)
PT - Journal Article
PT - Review
TA - Int J Environ Res Public Health
YR - 2018
DATE- 20180207
CITO- NLM
CS - Switzerland
FJT - International journal of environmental research and public health
EDAT- 20180102
STAT- In-Data-Review
CM - Cites: Proc Natl Acad Sci U S A. 2008 Jul 22;105(29):9931-5 (medline
/18626020)
CM - Cites: J Phys Chem A. 2012 Feb 16;116(6):1596-604 (medline /22257280)
CM - Cites: Biochem J. 1974 Jul;142(1):65-74 (medline /4441373)
CM - Cites: Environ Pollut. 2012 Feb;161:1-7 (medline /22230060)
CM - Cites: ScientificWorldJournal. 2014 Jan 09;2014:921581 (medline /24526924)
CM - Cites: Ecotoxicol Environ Saf. 2009 Feb;72(2):626-34 (medline /18262648)
CM - Cites: Ecotoxicol Environ Saf. 2016 Feb;124:68-73 (medline /26473328)
CM - Cites: Nat Mater. 2017 May;16(5):572-579 (medline /27992420)
CM - Cites: Plant Physiol Biochem. 2016 Jun;103:45-52 (medline /26963899)
CM - Cites: Curr Opin Plant Biol. 2009 Jun;12(3):364-72 (medline /19501016)
CM - Cites: Aquat Toxicol. 2008 Jan 31;86(2):205-15 (medline /18096252)
CM - Cites: Ecotoxicol Environ Saf. 2015 Jul;117:164-73 (medline /25881134)
CM - Cites: Acc Chem Res. 2013 Feb 19;46(2):550-9 (medline /23157446)
CM - Cites: J Hazard Mater. 2015 Apr 28;287:384-91 (medline /25677475)
CM - Cites: Plant Cell. 2010 Jun;22(6):2045-57 (medline /20530755)
CM - Cites: Int J Phytoremediation. 2017 Jul 3;19(7):670-678 (medline
/28084797)
CM - Cites: Int J Phytoremediation. 2017 Nov 2;19(11):1037-1046 (medline
/28463566)
CM - Cites: J Hazard Mater. 2015 May 30;289:219-34 (medline /25726907)
CM - Cites: Annu Rev Phytopathol. 2017 Aug 4;55:85-107 (medline /28504920)
CM - Cites: Mutat Res. 2003 Mar 3;535(2):127-39 (medline /12581530)
CM - Cites: Plant Signal Behav. 2012 Nov;7(11):1456-66 (medline /22951402)
CM - Cites: Front Plant Sci. 2015 May 18;6:340 (medline /26042132)
CM - Cites: Plant Physiol. 2008 Sep;148(1):620-41 (medline /18599647)
CM - Cites: Plant Physiol Biochem. 2013 Dec;73:77-82 (medline /24077292)
CM - Cites: Plant J. 2006 Mar;45(6):917-29 (medline /16507083)
CM - Cites: Toxicol Appl Pharmacol. 2008 Oct 15;232(2):252-7 (medline
/18671993)
CM - Cites: Plant Physiol Biochem. 2014 Jul;80:203-10 (medline /24811675)
CM - Cites: J Environ Sci (China). 2013 Dec 1;25(12):2451-9 (medline /24649677)
CM - Cites: Plant Physiol Biochem. 2009 Jun;47(6):448-55 (medline /19136270)
CM - Cites: Chemosphere. 2005 Oct;61(2):293-301 (medline /16168752)
CM - Cites: Chemosphere. 2013 Jun;92(2):157-70 (medline /23466274)
CM - Cites: Sci Total Environ. 2015 Nov 1;532:803-11 (medline /26136157)
CM - Cites: Environ Sci Pollut Res Int. 2017 Apr;24(10 ):9142-9158 (medline
/28160172)
CM - Cites: Environ Sci Technol. 2011 Sep 1;45(17):7135-42 (medline /21797214)
CM - Cites: Nitric Oxide. 2013 Aug 1;32:13-20 (medline /23545403)
CM - Cites: Plant Physiol. 2005 Jul;138(3):1516-26 (medline /15980200)
CM - Cites: Annu Rev Plant Biol. 2010;61:535-59 (medline /20192735)
CM - Cites: Plant Physiol Biochem. 2012 Aug;57:261-7 (medline /22766395)
CM - Cites: Aquat Toxicol. 2000 Aug 1;50(1-2):1-12 (medline /10930646)
CM - Cites: Environ Health Perspect. 2005 Jun;113(6):A378-86 (medline
/15929879)
CM - Cites: Environ Health Perspect. 2012 Dec;120(12):1733-8 (medline
/23060367)
CM - Cites: J Biol Chem. 1989 May 15;264(14):7761-4 (medline /2542241)
CM - Cites: Biol Trace Elem Res. 2012 Jun;146(3):360-8 (medline /22124861)
CM - Cites: Chemosphere. 2017 Aug;181:44-54 (medline /28419900)
CM - Cites: Plant Cell. 1999 Jun;11(6):1153-64 (medline /10368185)
CM - Cites: Environ Int. 2009 Apr;35(3):485-90 (medline /18793803)
CM - Cites: J Biotechnol. 2013 Jan 10;163(1):1-9 (medline /23108027)
CM - Cites: J Exp Bot. 2002 May;53(372):1255-72 (medline /11997374)
CM - Cites: Environ Int. 2012 Oct 1;46:16-22 (medline /22664651)
CM - Cites: Int J Phytoremediation. 2010 Jul;12(5):487-502 (medline /21166290)
CM - Cites: Plant Physiol Biochem. 2016 Feb;99:86-96 (medline /26741538)
CM - Cites: Trends Plant Sci. 2006 Aug;11(8):392-7 (medline /16839801)
CM - Cites: Sci Rep. 2017 Jun 15;7(1):3592 (medline /28620222)
CM - Cites: Annu Rev Plant Biol. 2007;58:459-81 (medline /17288534)
CM - Cites: Biochim Biophys Acta. 2006 Aug;1758(8):1165-75 (medline /16716251)
CM - Cites: Ecotoxicology. 2013 Apr;22(3):584-96 (medline /23430410)
CM - Cites: New Phytol. 2009;183(2):340-8 (medline /19402874)
CM - Cites: J Hazard Mater. 2015 Nov 15;298:241-51 (medline /26073379)
CM - Cites: Indian J Microbiol. 2011 Jan;51(1):44-7 (medline /22282627)
CM - Cites: Chem Res Toxicol. 2012 Jul 16;25(7):1423-34 (medline /22624971)
CM - Cites: Environ Pollut. 2006 May;141(2):238-46 (medline /16257102)
CM - Cites: Int J Environ Res Public Health. 2015 Oct 05;12(10):12371-90
(medline /26445051)
CM - Cites: Science. 2006 Feb 3;311(5761):622-7 (medline /16456071)
CM - Cites: J Biol Chem. 1983 May 25;258(10):6266-71 (medline /6853484)
CM - Cites: Nitric Oxide. 2009 Jun;20(4):289-97 (medline /19233306)
CM - Cites: Int J Environ Res Public Health. 2017 Jan 19;14 (1): (medline
/28106848)
CM - Cites: Sci Total Environ. 2014 Aug 1;488-489:176-87 (medline /24830930)
CM - Cites: New Phytol. 2009;184(1):41-7 (medline /19656300)
CM - Cites: Plant Physiol Biochem. 2016 Jan;98:119-27 (medline /26686284)
CM - Cites: FEMS Microbiol Rev. 1994 Dec;15(4):355-67 (medline /7848659)
CM - Cites: Plant Physiol Biochem. 2017 Feb;111:144-154 (medline /27930927)
CM - Cites: Sci Total Environ. 2017 Oct 17;:null (medline /29054629)
CM - Cites: J Exp Bot. 2006;57(8):1711-8 (medline /16595577)
CM - Cites: Ecotoxicol Environ Saf. 2015 Feb;112:247-70 (medline /25463877)
CM - Cites: Chem Biol Interact. 2010 Nov 5;188(2):334-9 (medline /20637748)
CM - Cites: Redox Rep. 2017 Nov;22(6):353-360 (medline /28073323)
CM - Cites: Front Physiol. 2012 Jun 06;3:182 (medline /22685440)
CM - Cites: Environ Pollut. 2017 Apr;223:230-237 (medline /28108165)
CM - Cites: J Biol Chem. 1992 Oct 25;267(30):21802-7 (medline /1400489)
CM - Cites: Plant Physiol Biochem. 2013 Oct;71:307-14 (medline /24007815)
CM - Cites: Environ Technol. 2017 May 27;:1-12 (medline /28488470)
CM - Cites: J Plant Physiol. 2009 Oct 15;166(15):1694-9 (medline /19446917)
CM - Cites: Plant Physiol. 2007 Nov;145(3):919-24 (medline /17905867)
CM - Cites: Rev Environ Contam Toxicol. 2013;221:107-27 (medline /23090631)
CM - Cites: Arch Biochem Biophys. 2010 May;497(1-2):13-20 (medline /20193657)
CM - Cites: Toxicology. 2011 May 10;283(2-3):65-87 (medline /21414382)
CM - Cites: ISRN Toxicol. 2013 Jul 22;2013:340925 (medline /23970978)
CM - Cites: Annu Rev Plant Biol. 2004;55:373-99 (medline /15377225)
CM - Cites: New Phytol. 2016 Jan;209(2):762-72 (medline /26010225)
CM - Cites: New Phytol. 2009 Mar;181(4):777-94 (medline /19207683)
CM - Cites: Sci Total Environ. 2017 Apr 15;584-585:631-641 (medline /28131446)
CM - Cites: Curr Environ Health Rep. 2015 Mar;2(1):52-68 (medline /26231242)
CM - Cites: Biomed Res Int. 2016;2016:1423828 (medline /27022603)
CM - Cites: Chemosphere. 2015 Sep;134:1-6 (medline /25880602)
CM - Cites: Chem Biol Interact. 1994 Feb;90(2):139-55 (medline /8156604)
CM - Cites: J Environ Sci (China). 2007;19(6):725-32 (medline /17969647)
CM - Cites: New Phytol. 2005 Dec;168(3):551-8 (medline /16313638)
CM - Cites: J Chem Ecol. 2007 Feb;33(2):251-64 (medline /17216362)
CM - Cites: Chemosphere. 2017 Jul;178:513-533 (medline /28347915)
CM - Cites: Rev Environ Contam Toxicol. 2014;232:1-44 (medline /24984833)
CM - Cites: Free Radic Biol Med. 2011 Jul 15;51(2):257-81 (medline /21554949)
CM - Cites: Plant Physiol. 1990 Aug;93(4):1449-52 (medline /16667638)
CM - Cites: Biochem J. 2008 Mar 15;410(3):621-9 (medline /18039180)
CM - Cites: Proteomics. 2006 Apr;6 Suppl 1:S156-62 (medline /16534746)
CM - Cites: Environ Pollut. 2017 Jul;226:212-218 (medline /28432964)
CM - Cites: J Environ Biol. 2015 Jan;36(1):249-54 (medline /26536800)
CM - Cites: Plant Physiol Biochem. 2017 Mar;112:74-86 (medline /28049059)
CM - Cites: Plant Physiol. 2005 Jun;138(2):790-802 (medline /15908592)
CM - Cites: Environ Geochem Health. 2009 Apr;31 Suppl 1:179-87 (medline
/19142738)
CM - Cites: Plant Physiol. 2009 Aug;150(4):2071-80 (medline /19542298)
CM - Cites: Environ Pollut. 2017 Apr;223:137-145 (medline /28153415)
CM - Cites: Angew Chem Int Ed Engl. 2007;46(15):2594-7 (medline /17352440)
CM - Cites: Plant Physiol Biochem. 2015 Jul;92:11-8 (medline /25900420)
CM - Cites: Biometals. 2014 Apr;27(2):219-28 (medline /24509935)
CM - Cites: Environ Pollut. 2007 Feb;145(3):839-49 (medline /16777300)
CM - Cites: Environ Sci Technol. 2007 Apr 15;41(8):2930-6 (medline /17533860)
CM - Cites: J Hazard Mater. 2013 Nov 15;262:1123-31 (medline /22917495)
CM - Cites: Int J Environ Res Public Health. 2010 Nov;7(11):4050-61 (medline
/21139876)
CM - Cites: Nitric Oxide. 2017 Jul 1;67:39-52 (medline /28456602)
CM - Cites: J Plant Physiol. 2004 Jul;161(7):867-72 (medline /15310076)
CM - Cites: Mutat Res. 2011 Feb 3;719(1-2):29-34 (medline /20970520)
CM - Cites: J Plant Physiol. 2015 Jun 1;181:20-9 (medline /25974366)
CM - Cites: Plant Physiol. 2010 Apr;152(4):2211-21 (medline /20130102)
CM - Cites: Environ Pollut. 2016 Nov;218:111-117 (medline /27552044)
CM - Cites: Plant Cell. 2007 Mar;19(3):1123-33 (medline /17400898)
CM - Cites: Water Res. 2010 Nov;44(19):5789-802 (medline /20684969)
CM - Cites: Bioresour Technol. 2013 May;136:604-9 (medline /23567737)
CM - Cites: J Biol Chem. 1981 Jun 25;256(12):5981-3 (medline /7240187)
CM - Cites: J Plant Physiol. 2006 Sep;163(9):927-36 (medline /16949956)
CM - Cites: Chemosphere. 2007 Jun;68(6):989-1003 (medline /17349677)
CM - Cites: Biol Trace Elem Res. 2014 Jun;158(3):410-21 (medline /24699829)
CM - Cites: Plant Physiol. 2010 Nov;154(3):1505-13 (medline /20870777)
CM - Cites: Sci Rep. 2017 Sep 11;7(1):11231 (medline /28894204)
CM - Cites: Rev Environ Contam Toxicol. 2011;213:113-36 (medline /21541849)
CM - Cites: Environ Int. 2015 Jan;74:221-30 (medline /25454239)
CM - Cites: Ecotoxicol Environ Saf. 2015 Oct;120:59-65 (medline /26036416)
CM - Cites: J Environ Qual. 2003 May-Jun;32(3):767-72 (medline /12809277)
CM - Cites: J Bacteriol. 1995 Apr;177(8):2050-6 (medline /7721697)
CM - Cites: Biol Trace Elem Res. 2011 Jun;140(3):354-67 (medline /20455031)
CM - Cites: J Agric Food Chem. 2008 Sep 24;56(18):8580-7 (medline /18795759)
CM - Cites: Plant Physiol Biochem. 2016 Jul;104:266-77 (medline /27061371)
CM - Cites: J Exp Bot. 2011 Aug;62(12):4391-8 (medline /21586431)
CM - Cites: J Biosci Bioeng. 2014 Jul;118(1):1-9 (medline /24507904)
CM - Cites: Front Microbiol. 2017 Sep 06;8:1706 (medline /28932218)
CM - Cites: Int J Environ Res Public Health. 2013 Apr 12;10(4):1527-46 (medline
/23583964)
CM - Cites: Chemosphere. 2015 Jan;119:697-703 (medline /25150973)
CM - Cites: Plant Physiol Biochem. 2014 Sep;82:76-84 (medline /24907527)
CM - Cites: J Hazard Mater. 2017 May 15;330:68-75 (medline /28212511)
CM - Cites: Annu Rev Plant Biol. 2013;64:429-50 (medline /23451784)
CM - Cites: Ecotoxicol Environ Saf. 2013 Apr;90:28-34 (medline /23321366)
CM - Cites: Sci Total Environ. 2015 Dec 15;538:306-16 (medline /26312405)
CM - Cites: Nitric Oxide. 2014 May 30;39:35-45 (medline /24731839)
CM - Cites: Environ Pollut. 2018 Jan;232:31-41 (medline /28966026)
CM - Cites: Environ Geochem Health. 2016 Dec;38(6):1283-1301 (medline
/26825060)
CM - Cites: Chemosphere. 2016 Apr;149:366-72 (medline /26874625)
CM - Cites: Environ Sci Technol. 2010 Dec 15;44(24):9542-9 (medline /21077666)
CM - Cites: Plant Physiol. 2004 Mar;134(3):1113-22 (medline /15001701)
CM - Cites: Biodegradation. 2018 Feb;29(1):59-69 (medline /29143902)
CM - Cites: Environ Pollut. 2017 Dec 15;234:915-934 (medline /29253832)
CM - Cites: J Exp Bot. 2011 Jun;62(10):3321-38 (medline /21357767)
CM - Cites: Mutat Res. 2009 Mar 31;674(1-2):85-92 (medline /18984063)
CM - Cites: Sci Total Environ. 2015 Feb 1;505:423-34 (medline /25461044)
CM - Cites: New Phytol. 2012 Jul;195(2):356-71 (medline /22578268)
CM - Cites: Ecotoxicol Environ Saf. 2015 May;115:119-25 (medline /25700090)
CM - Cites: Environ Sci Pollut Res Int. 2017 Jul;24(19):16097-16106 (medline
/28537029)
CM - Cites: Ecotoxicology. 2010 Jun;19(5):983-93 (medline /20221688)
CM - Cites: Plant Cell. 2002 Nov;14 (11):2837-47 (medline /12417705)
CM - Cites: Int J Phytoremediation. 2017 Jul 3;19(7):662-669 (medline
/28084804)
CM - Cites: J Phys Chem B. 2014 Jan 9;118(1):37-47 (medline /24328335)
CM - Cites: Free Radic Biol Med. 1998 Sep;25(4-5):576-85 (medline /9741595)
CM - Cites: Clin Chem. 2006 Apr;52(4):601-23 (medline /16484333)
CM - Cites: J Exp Bot. 2002 May;53(372):1331-41 (medline /11997379)
CM - Cites: Plant Physiol Biochem. 2017 Jun;115:163-173 (medline /28371690)
CM - Cites: Int J Mol Sci. 2012;13(3):3145-75 (medline /22489146)
CM - Cites: Transgenic Res. 2012 Dec;21(6):1265-77 (medline /22350764)
CM - Cites: Chemosphere. 2016 Jul;154:283-288 (medline /27058920)
CM - Cites: Plant Physiol Biochem. 2014 Jul;80:278-84 (medline /24813727)
CM - Cites: Environ Health Perspect. 2013 Mar;121(3):295-302 (medline
/23458756)
CM - Cites: Cold Spring Harb Perspect Biol. 2013 Feb 01;5(2):null (medline
/23378590)
CM - Cites: Sci Total Environ. 2015 Sep 15;527-528:552-60 (medline /26006052)
CM - Cites: Ecotoxicology. 2013 May;22(4):656-70 (medline /23479061)
CM - Cites: ScientificWorldJournal. 2015;2015:756120 (medline /25688377)
CM - Cites: J Hazard Mater. 2017 Mar 5;325:36-58 (medline /27915099)
CM - Cites: Biochemistry. 2011 Feb 22;50(7):1128-34 (medline /21214261)
CM - Cites: Environ Sci Pollut Res Int. 2012 Sep;19(8):3506-15 (medline
/22529007)
CM - Cites: Trends Plant Sci. 2004 Dec;9(12):606-13 (medline /15564128)
CM - Cites: Cytoskeleton (Hoboken). 2012 Jan;69(1):1-21 (medline /21976360)
CM - Cites: Physiol Mol Biol Plants. 2015 Jan;21(1):61-9 (medline /25648550)
CM - Cites: Biochim Biophys Acta. 2016 Aug;1864(8):932-44 (medline /26940747)
CM - Cites: J Hazard Mater. 2012 May 30;217-218:141-8 (medline /22459980)
CM - Cites: Environ Sci Technol. 2005 Jul 15;39(14):5241-6 (medline /16082952)
CM - Cites: Mutagenesis. 2007 Jul;22(4):255-61 (medline /17369186)
CM - Cites: Int J Phytoremediation. 2016;18(5):442-9 (medline /26552612)
CM - Cites: Plant Physiol Biochem. 2010 Dec;48(12):909-30 (medline /20870416)
CM - Cites: Ecotoxicol Environ Saf. 2014 Aug;106:126-35 (medline /24836887)
CM - Cites: Annu Rev Plant Biol. 2016 Apr 29;67:489-512 (medline /27128467)
CM - Cites: J Exp Bot. 2005 May;56(415):1335-42 (medline /15781440)
CM - Cites: Environ Pollut. 2012 Jun;165:18-24 (medline /22398017)
CM - Cites: Plant J. 2004 Aug;39(4):629-42 (medline /15272879)
CM - Cites: Plant Physiol. 2011 Jul;156(3):1149-63 (medline /21628630)
CM - Cites: Ecotoxicol Environ Saf. 2011 Jan;74(1):78-84 (medline /20851467)
CM - Cites: Plant Signal Behav. 2012 Jul;7(7):771-8 (medline /22751303)
CM - Cites: Plant Physiol. 2006 Jun;141(2):357-66 (medline /16760488)
CM - Cites: Anal Chem. 2014 Oct 21;86(20):10422-8 (medline /25300934)
CM - Cites: Front Physiol. 2012 Jul 23;3:275 (medline /22934029)
CM - Cites: J Exp Bot. 2002 Dec;53(379):2381-92 (medline /12432030)
CM - Cites: Mutat Res. 2010 Jan;695(1-2):2-8 (medline /19800024)
CM - Cites: Plant Physiol Biochem. 2013 Oct;71:155-63 (medline /23917073)
CM - Cites: Biometals. 2012 Dec;25(6):1155-65 (medline /22886388)
CM - Cites: J Hazard Mater. 2012 Jun 15;219-220:1-12 (medline /22502897)
CM - Cites: Annu Rev Plant Biol. 2008;59:595-624 (medline /18444909)
CM - Cites: Chem Res Toxicol. 2008 May;21(5):1120-4 (medline /18447394)
CM - Cites: Plant Physiol Biochem. 2013 Feb;63:254-61 (medline /23313792)
CM - Cites: C R Biol. 2010 Nov-Dec;333(11-12):814-24 (medline /21146138)
CM - Cites: Rev Environ Contam Toxicol. 2017;241:73-137 (medline /27300014)
CM - Cites: J Hazard Mater. 2012 Nov 30;241-242:307-15 (medline /23062509)
CM - Cites: Front Plant Sci. 2011 Nov 30;2:83 (medline /22645553)
CM - Cites: Front Plant Sci. 2016 Jan 12;6:1272 (medline /26793232)
CM - Cites: Plant J. 2004 Dec;40(6):909-19 (medline /15584956)
DOCNO- medline/29301332

179 - TOXLINE
TI - Chronic arsenicosis and cadmium exposure in wild snowshoe hares (Lepus
americanus) breeding near Yellowknife, Northwest Territories (Canada),
part 1: Evaluation of oxidative stress, antioxidant activities and hepatic
damage.
AU - Amuno S
AD - School of Environment and Sustainability, University of Saskatchewan,
Saskatoon, Canada. Electronic address: soa882@mail.usask.ca.
AU - Jamwal A
AD - Department of Biology, University of Saskatchewan, Saskatoon, Canada.
AU - Grahn B
AD - Western College of Veterinary Medicine, University of Saskatchewan,
Saskatoon, Canada.
AU - Niyogi S
AD - Department of Biology, University of Saskatchewan, Saskatoon, Canada;
Toxicology Centre, University of Saskatchewan, Saskatoon, Canada.
SO - Sci Total Environ. 2018, Mar 15; 618:916-926. [The Science of the total
environment]
AB - Previous gold mining activities and arsenopyrite ore roasting activities
at the Giant mine site (1948 to 2004) resulted in the release of high
amounts of arsenic and trace metals into the terrestrial and aquatic
ecosystems of Yellowknife, Northwest Territories, Canada. While elevated
levels of arsenic has been consistently reported in surface soils and
vegetation near the vicinity of the Giant mine area and in surrounding
locations, systematic studies evaluating the overall health status of
terrestrial small mammals endemic to the area are lacking. The purpose of
this present study was to evaluate and comparatively assess the
biochemical responses and histopathological effects induced by chronic
arsenic and cadmium exposure in wild snowshoe hares breeding near the city
of Yellowknife, specifically around the vicinity of the abandoned Giant
mine site and in reference locations. Analysis included measurement of
total arsenic and cadmium concentration in nails, livers, kidneys, bones,
stomach content of hares, in addition to histopathological evaluation of
hepatic and ocular lesions. Biochemical responses were determined through
measurement of lipid peroxidation levels and antioxidant enzymes
activities (catalase, superoxide dismutase, glutathione peroxidase, and
glutathione disulfide). The results revealed that arsenic concentration
was 17.8 to 48.9 times higher in the stomach content, and in the range of
4 to 23 times elevated in the nails of hares from the mine area compared
to the reference location. Arsenic and cadmium levels were also noted to
be increased in the bones, renal and hepatic tissues of hares captured
near the mine area compared to the reference site. Specifically, hares
from the mine area showed nail cadmium levels that was 2.3 to 17.6 times
higher than those from the reference site. Histopathological examination
of the eyes revealed no specific ocular lesions, such as lens opacity
(cataracts) or conjunctivitis; however, hares from both locations
exhibited hepatic steatosis (fatty liver change). Lipid peroxidation
levels were relatively increased and accompanied with reduced antioxidant
enzyme activities in hares from the mine area compared to the hares from
the reference site. The results of this preliminary study suggest that the
snowshoe hares breeding near the vicinity of Yellowknife, including near
the Giant mine area have been chronically exposed to elevated levels of
arsenic and cadmium, which consequently led to the increased levels of
oxidative stress and perturbation of antioxidant defense system in exposed
animals. The results of this present study constitute the first
observation of chronic arsenicosis in wild small mammal species in Canada.
KW - Arsenic
KW - Arsenicosis
KW - Giant mine
KW - Small mammals
KW - Snowshoe hares
LA - eng
IS - 1879-1026 (Electronic)
PT - Journal Article
TA - Sci Total Environ
YR - 2018
DATE- 20180118
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - The Science of the total environment
EDAT- 20171014
STAT- In-Process
DOCNO- medline/29037475

180 - TOXLINE
TI - Granulated Bog Iron Ores as Sorbents in Passive (Bio)Remediation Systems
for Arsenic Removal.
AU - Debiec K
AD - Laboratory of Environmental Pollution Analysis, Faculty of Biology,
University of Warsaw, Warsaw, Poland.
AU - Rzepa G
AD - Department of Mineralogy, Petrography and Geochemistry, Faculty of Geology,
Geophysics and Environmental Protection, AGH University of Science and Technology,
Krakow, Poland.
AU - Bajda T
AD - Department of Mineralogy, Petrography and Geochemistry, Faculty of Geology,
Geophysics and Environmental Protection, AGH University of Science and Technology,
Krakow, Poland.
AU - Uhrynowski W
AD - Laboratory of Environmental Pollution Analysis, Faculty of Biology,
University of Warsaw, Warsaw, Poland.
AU - Sklodowska A
AD - Laboratory of Environmental Pollution Analysis, Faculty of Biology,
University of Warsaw, Warsaw, Poland.
AU - Krzysztoforski J
AD - Faculty of Chemical and Process Engineering, Warsaw University of Technology,
Warsaw, Poland.
AU - Drewniak L
AD - Laboratory of Environmental Pollution Analysis, Faculty of Biology,
University of Warsaw, Warsaw, Poland.
SO - Front Chem. 2018; 6:54. [Frontiers in chemistry]
AB - The main element of PbRS (passive (bio)remediation systems) are sorbents,
which act as natural filters retaining heavy metals and carriers of
microorganisms involved in water treatment. Thus, the effectiveness of
PbRS is determined by the quality of the (ad)sorbents, which should be
stable under various environmental conditions, have a wide range of
applications and be non-toxic to (micro)organisms used in these systems.
Our previous studies showed that bog iron ores (BIOs) meet these
requirements. However, further investigation of the physical and chemical
parameters of BIOs under environmental conditions is required before their
large-scale application in PbRS. The aim of this study was (i) to
investigate the ability of granulated BIOs (gBIOs) to remove arsenic from
various types of contaminated waters, and (ii) to estimate the application
potential of gBIOs in technologies dedicated to water treatment. These
studies were conducted on synthetic solutions of arsenic and environmental
samples of arsenic contaminated water using a set of adsorption columns
filled with gBIOs. The experiments performed in a static system revealed
that gBIOs are appropriate arsenic and zinc adsorbent. Dynamic adsorption
studies confirmed these results and showed, that the actual sorption
efficiency of gBIOs depends on the adsorbate concentration and is directly
proportional to them. Desorption analysis showed that As-loaded gBIOs are
characterized by high chemical stability and they may be reused for the
(ad)sorption of other elements, i.e., zinc. It was also shown that gBIOs
may be used for remediation of both highly oxygenated waters and
groundwater or settling ponds, where the oxygen level is low, as both
forms of inorganic arsenic (arsenate and arsenite) were effectively
removed. Arsenic concentration after treatment was < 100 &mu;g/L, which
is below the limit for industrial water.
KW - arsenic
KW - bog iron ores (BIOs)
KW - dynamic sorption
KW - in situ remediation
KW - mineral sorbents
KW - water treatment
LA - eng
IS - 2296-2646 (Print)
PT - Journal Article
TA - Front Chem
YR - 2018
DATE- 20180408
CITO- NLM
CS - Switzerland
FJT - Frontiers in chemistry
EDAT- 20180316
STAT- PubMed-not-MEDLINE
CM - Cites: Water Res. 2007 Feb;41(3):591-602 (medline /17173951)
CM - Cites: J Environ Manage. 2010 Nov;91(11):2238-47 (medline /20598797)
CM - Cites: Sci Total Environ. 2016 Oct 1;566-567:76-85 (medline /27213673)
CM - Cites: J Environ Sci Health A Tox Hazard Subst Environ Eng.
2011;46(13):1491-502 (medline /21961559)
CM - Cites: Water Res. 2005 Aug;39(13):2944-54 (medline /15979686)
CM - Cites: J Hazard Mater. 2008 Mar 1;151(2-3):811-20 (medline /17658682)
CM - Cites: J Environ Manage. 2012 Aug 15;104:93-100 (medline /22484707)
CM - Cites: J Hazard Mater. 2009 Dec 30;172(2-3):1591-6 (medline /19733972)
CM - Cites: Sci Total Environ. 2006 Feb 1;354(2-3):179-90 (medline /16398994)
CM - Cites: J Hazard Mater. 2007 Oct 1;149(1):226-33 (medline /17560022)
CM - Cites: J Hazard Mater. 2008 Jun 15;154(1-3):184-91 (medline /18031930)
CM - Cites: Water Res. 2004 Apr;38(7):1893-9 (medline /15026244)
CM - Cites: Environ Sci Technol. 2001 Jul 1;35(13):2778-84 (medline /11452609)
CM - Cites: Environ Sci Technol. 2016 Aug 2;50(15):8255-62 (medline /27351211)
CM - Cites: Environ Sci Technol. 2007 May 1;41(9):3322-8 (medline /17539544)
CM - Cites: Environ Toxicol Chem. 2009 Mar;28(3):509-15 (medline /18939890)
CM - Cites: Bioresour Technol. 2014 Apr;157:316-26 (medline /24559743)
CM - Cites: J Hazard Mater. 2008 Mar 1;151(2-3):628-35 (medline /17640801)
CM - Cites: Water Sci Technol. 2004;50(8):23-32 (medline /15566183)
CM - Cites: J Hazard Mater. 2007 Apr 2;142(1-2):1-53 (medline /17324507)
CM - Cites: Chemosphere. 2014 Sep;111:243-59 (medline /24997925)
CM - Cites: Water Res. 2005 Oct;39(17):4153-63 (medline /16181656)
CM - Cites: J Environ Manage. 2011 Oct;92(10):2786-93 (medline /21737198)
CM - Cites: Water Res. 2013 Jun 1;47(9):2938-48 (medline /23566332)
CM - Cites: J Hazard Mater. 2009 Mar 15;162(2-3):1007-13 (medline /18614286)
CM - Cites: Toxicol Ind Health. 2016 Jan;32(1):1-6 (medline /23344825)
CM - Cites: Environ Sci Technol. 2006 Oct 1;40(19):6015-20 (medline /17051793)
CM - Cites: Appl Environ Microbiol. 1993 Sep;59(9):2851-6 (medline /8215359)
CM - Cites: Environ Sci Technol. 2008 Jan 1;42(1):147-52 (medline /18350889)
CM - Cites: J Colloid Interface Sci. 2015 Sep 1;453:132-141 (medline /25982936)
CM - Cites: Chemosphere. 2017 Dec;188:99-109 (medline /28881245)
CM - Cites: Environ Geochem Health. 2006 Jun;28(3):197-214 (medline /16607568)
CM - Cites: Water Res. 2015 Mar 15;71:32-41 (medline /25589434)
DOCNO- medline/29616211

181 - TOXLINE
TI - Arsenic impairs insulin signaling in differentiated neuroblastoma SH-SY5Y
cells.
AU - Niyomchan A
AD - Laboratory of Pharmacology, Chulabhorn Research Institute, Thailand;
Chulabhorn Graduate Institute, 54 Kamphaeng Phet 6 Rd, Bangkok, 10210, Thailand.
AU - Visitnonthachai D
AD - Laboratory of Pharmacology, Chulabhorn Research Institute, Thailand.
AU - Suntararuks S
AD - Laboratory of Pharmacology, Chulabhorn Research Institute, Thailand.
AU - Ngamsiri P
AD - Laboratory of Pharmacology, Chulabhorn Research Institute, Thailand.
AU - Watcharasit P
AD - Laboratory of Pharmacology, Chulabhorn Research Institute, Thailand;
Chulabhorn Graduate Institute, 54 Kamphaeng Phet 6 Rd, Bangkok, 10210, Thailand;
Center of Excellence on Environmental Health and Toxicology (EHT), Office of the
Higher Education Commission, Thailand. Electronic address: Piyajit@cri.or.th.
AU - Satayavivad J
AD - Laboratory of Pharmacology, Chulabhorn Research Institute, Thailand;
Chulabhorn Graduate Institute, 54 Kamphaeng Phet 6 Rd, Bangkok, 10210, Thailand;
Center of Excellence on Environmental Health and Toxicology (EHT), Office of the
Higher Education Commission, Thailand.
SO - Neurotoxicology. 2018, May; 66:22-31. [Neurotoxicology]
AB - A strong correlation between chronic arsenic exposure and
neuropsychological disorders leads to a growing concern about a potential
risk of arsenic related neurodegeneration. Evidently, brain insulin
signaling contributes to physiological effects, including energy
homeostasis, and learning and memory. Arsenic has been shown to impair
insulin signaling in adipocytes and myocytes, however, this impairment has
not yet been explored in neurons. Here we showed that NaAsO2 caused
significant reduction in basal levels of glucose, plasma membrane glucose
transporter, GLUT 3 and Akt phosphorylation in differentiated human
neuroblastoma SH-SY5Y cells. NaAsO2 significantly decreased
insulin-mediated glucose uptake, as well as GLUT1 and 3 membrane
translocation. Furthermore, the ability of insulin to increase Akt
phosphorylation, a well-recognized insulin signaling response, was
significantly lessened by NaAsO2 treatment. In addition, the classical
tyrosine phosphorylation response of insulin was reduced by NaAsO2, as
evidenced by reduction of insulin-induced tyrosine phosphorylation of
insulin receptor (IR) and insulin receptor substrate-1(IRS-1). Moreover,
NaAsO2 lowered the ratio of p110, a catalytic subunit to p85, a regulatory
subunit of PI3K causing an imbalance between p110 and p85, the conditions
reported to contribute to insulin sensitivity. Additionally, increment of
IRS-1 interaction with GSK3&beta;, and p85-PI3K were observed in NaAsO2
treated cells. These molecular modulations may be mechanistically
attributed to neuronal insulin signaling impairment by arsenic.
KW - Akt
KW - Arsenic
KW - Insulin
KW - Insulin receptor (IR)
KW - Insulin receptor substrate (IRS)
KW - PI3K
LA - eng
IS - 1872-9711 (Electronic)
PT - Journal Article
TA - Neurotoxicology
YR - 2018
DATE- 20180508
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Neurotoxicology
EDAT- 20180308
STAT- In-Data-Review
DOCNO- medline/29526746

182 - TOXLINE
TI - Arsenic in groundwater of West Bengal, India: A review of human health
risks and assessment of possible intervention options.
AU - Bhowmick S
AD - Kolkata Zonal Center, CSIR-National Environmental Engineering Research
Institute (NEERI), Kolkata, West Bengal 700107, India. Electronic address:
subhamoy081984@gmail.com.
AU - Pramanik S
AD - Kolkata Zonal Center, CSIR-National Environmental Engineering Research
Institute (NEERI), Kolkata, West Bengal 700107, India.
AU - Singh P
AD - Kolkata Zonal Center, CSIR-National Environmental Engineering Research
Institute (NEERI), Kolkata, West Bengal 700107, India.
AU - Mondal P
AD - Ceramic Membrane Division, CSIR-Central Glass and Ceramic Research Institute
(CGCRI), Raja S.C. Mullick Road, Kolkata 700032, India.
AU - Chatterjee D
AD - Department of Chemistry, University of Kalyani, Kalyani, Nadia, West Bengal
741235, India.
AU - Nriagu J
AD - Department of Environmental Health Sciences, School of Public Health,
University of Michigan, 109 Observatory Street, Ann Arbor, MI 48109-2029, USA.
SO - Sci Total Environ. 2018, Jan 15; 612:148-169. [The Science of the total
environment]
AB - This paper reviews how active research in West Bengal has unmasked the
endemic arsenism that has detrimental effects on the health of millions of
people and their offspring. It documents how the pathways of exposure to
this toxin/poison have been greatly expanded through intensive application
of groundwater in agriculture in the region within the Green Revolution
framework. A goal of this paper is to compare and contrast the
similarities and differences in arsenic occurrence in West Bengal with
those of other parts of the world and assess the unique socio-cultural
factors that determine the risks of exposure to arsenic in local
groundwater. Successful intervention options are also critically reviewed
with emphasis on integrative strategies that ensure safe water to the
population, proper nutrition, and effective ways to reduce the transfer of
arsenic from soil to crops. While no universal model may be suited for the
vast areas of the world affected with by natural contamination of
groundwater with arsenic, we have emphasized community-specific
sustainable options that can be adapted. Disseminating scientifically
correct information among the population coupled with increased community
level participation and education are recognized as necessary adjuncts for
an engineering intervention to be successful and sustainable.
KW - Biomarkers
KW - Groundwater
KW - Mitigation
KW - Rice
KW - Sustainable management
LA - eng
IS - 1879-1026 (Electronic)
PT - Journal Article
PT - Review
TA - Sci Total Environ
YR - 2018
DATE- 20180103
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - The Science of the total environment
EDAT- 20170901
STAT- In-Process
DOCNO- medline/28850835

183 - TOXLINE
TI - Arsenic biokinetics and bioavailability in deposit-feeding clams and
polychaetes.
AU - Zhang W
AD - Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong
Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of
Oceanology, Chinese Academy of Sciences, Guangzhou 510301, China; Division of Life
Science, Hong Kong University of Science and Technology (HKUST), Clearwater Bay,
Kowloon, Hong Kong.
AU - Wang WX
AD - Division of Life Science, Hong Kong University of Science and Technology
(HKUST), Clearwater Bay, Kowloon, Hong Kong; Marine Environmental Laboratory, HKUST
Shenzhen Research Institute, Shenzhen 518057, China. Electronic address:
wwang@ust.hk.
SO - Sci Total Environ. 2018, Mar; 616-617:594-601. [The Science of the total
environment]
AB - In the present study, the arsenic (As) biokinetics and bioavailability in
two deposit-feeding invertebrates (clams Gafrarium tumidum and polychaetes
Nereis succinea) were quantified. Radiotracer techniques were applied to
measure the dissolved uptake rate, dietary assimilation efficiency and
efflux of As by the clams and polychaetes. Simultaneously, arsenic species
analysis was conducted to examine the As biotransformation following
dietary uptake. The radiotracer results showed that the uptake rate
constant and efflux rate constant were 0.068L/g/d and 0.07d-1, and
0.173L/g/d and 0.09d-1, in the clams and polychaetes, respectively.
Sediments labeled for different times (1.5-60 d) with different
inorganic/organic As percentages led to diverse assimilation efficiencies
of As (35.1-56.1% in the clams, and 51.6-72.6% in the polychaetes).
Modeling calculations showed that sediment was a significant source for As
bioaccumulation in the two deposit-feeders. After feeding on the spiked
sediments, inorganic As (75.6%) was initially the predominant form, but
arsenobetaine (AsB) became the predominant compound ( > 90%) in the clams
and polychaetes during depuration, suggesting biotransformation of
inorganic As. Combined with the biokinetics and biotransformation
measurements, we showed that AsB was more efficiently assimilated and
tended to be accumulated, whereas As(III) was less efficiently assimilated
and more rapidly eliminated by the two invertebrates. This study
demonstrated that As speciation in the sediments as a significant source
for As bioaccumulation caused different bioavailability in deposit-feeding
clams and polychaetes.
KW - Arsenic
KW - Bioavailability
KW - Biokinetics
KW - Biotransformation
KW - Deposit-feeding invertebrates
RN - N712M78A8G
LA - eng
IS - 1879-1026 (Electronic)
PT - Journal Article
TA - Sci Total Environ
YR - 2018
DATE- 20180515
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - The Science of the total environment
STAT- MEDLINE
DOCNO- medline/29100693

184 - TOXLINE
TI - Treatment of Arsenite Intoxication-Induced Peripheral Vasculopathy with
Mesenchymal Stem Cells.
AU - Chiang YH
AD - Department of Orthopaedics, National Yang-Ming University Hospital, Yilan
260, Taiwan. chiang340@gmail.com.
AU - Lin CC
AD - Department of Biotechnology and Animal Science, National Yilan University,
Yilan 260, Taiwan. Lincc@niu.edu.tw.
AU - Chen YC
AD - Department of Pathology, National Yang-Ming University Hospital, Yilan 260,
Taiwan. 999liquor999@gmail.com.
AU - Lee OK
AD - Department of Orthopaedics and Traumatology, Taipei Veterans General
Hospital, Taipei 11217, Taiwan. DAV47@tpech.gov.tw.
SO - Int J Mol Sci. 2018, Mar 29. [International journal of molecular sciences]
AB - Arsenite (As), a notorious toxic metal, is ubiquitously distributed in the
earth and poses a serious threat to human health. Histopathological
lesions of As intoxication are known as thromboangiitis obliterans, which
are resistant to current treatment and often lead to lower limb
amputation. In this study, we attempt to find that treatment with
mesenchymal stem cells (MSCs) may be effective for As-induced
vasculopathy. We first conducted an in vitro study with a co-culture
system containing human MSCs and human umbilical vein endothelial cells
(HUVECs) and treated individual and co-cultured cells with various
concentrations of arsenite. We also designed an in vivo study in which
Sprague Dawley (SD) rats received periodic intraperitoneal (IP) injections
of 16 ppm arsenite for 12 weeks. MSCs were harvested from BALB/c mice that
were transplanted via tail vein injection. We found that there was
significantly higher cellular viability in human mesenchymal stem cells
(hMSCs) than in HUVECs under concentrations of arsenite between 15 and 25
&mu;M. The Annexin V apoptosis assay further confirmed this finding.
Cytokine array assay for As-conditioned media revealed an elevated
vascular endothelial growth factor (VEGF) level secreted by MSCs, which is
crucial for HUVEC survival and was evaluated by an siRNA VEGF knockdown
test. In the in vivo study, we demonstrated early apoptotic changes in the
anterior tibial vessels of As-injected SD rats with a Terminal
deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, but
these apoptotic changes were less frequently observed upon MSCs
transplantation, indicating that the cytoprotective effect of MSCs
successfully protected against As-induced peripheral vasculopathy. The
feasibility of MSCs to treat and /or prevent the progression of As-induced
vasculopathy is justified. Further clinical studies are required to
demonstrate the therapeutic efficacy of MSCs in patients suffering from As
intoxication with vasculopathy.
COI - The authors declare no conflict of interest.
KW - arsenite
KW - mesenchymal stem cells
KW - peripheral vascular disease
LA - eng
IS - 1422-0067 (Electronic)
PT - Journal Article
TA - Int J Mol Sci
YR - 2018
DATE- 20180611
CITO- NLM
CS - Switzerland
FJT - International journal of molecular sciences
EDAT- 20180329
STAT- In-Process
CM - Cites: Atherosclerosis. 2010 Feb;208(2):461-6 (medline /19720375)
CM - Cites: Atherosclerosis. 2008 Jul;199(1):12-8 (medline /18367191)
CM - Cites: Toxicol Sci. 2008 Apr;102(2):207-18 (medline /17947343)
CM - Cites: J Environ Sci Health C Environ Carcinog Ecotoxicol Rev.
2005;23(1):55-74 (medline /16291522)
CM - Cites: Nat Med. 2003 Jun;9(6):702-12 (medline /12778169)
CM - Cites: J Cell Biochem. 2006 Aug 1;98(5):1076-84 (medline /16619257)
CM - Cites: Cell Stem Cell. 2008 Sep 11;3(3):301-13 (medline /18786417)
CM - Cites: J Biol Chem. 1998 Nov 13;273(46):30336-43 (medline /9804796)
CM - Cites: J Cell Mol Med. 2010 Sep;14(9):2190-9 (medline /20716123)
CM - Cites: Cytotherapy. 2014 May;16(5):579-85 (medline /24113425)
CM - Cites: J Cell Physiol. 2009 Jun;219(3):563-71 (medline /19170074)
CM - Cites: PLoS One. 2013;8(1):e54747 (medline /23359810)
CM - Cites: Am J Blood Res. 2013 Aug 19;3(3):225-38 (medline /23997985)
CM - Cites: Proc Natl Acad Sci U S A. 1995 May 23;92(11):4857-61 (medline
/7761413)
CM - Cites: Biomaterials. 2014 Apr;35(11):3607-17 (medline /24462361)
CM - Cites: Nat Med. 1999 Mar;5(3):309-13 (medline /10086387)
CM - Cites: Rev Environ Health. 2011;26(1):71-8 (medline /21714384)
CM - Cites: Cell Transplant. 2009;18(3):371-80 (medline /19500466)
CM - Cites: Nature. 2002 Jul 4;418(6893):41-9 (medline /12077603)
CM - Cites: Diabetes. 2013 Apr;62(4):1041-53 (medline /23520284)
CM - Cites: Am J Physiol Renal Physiol. 2010 Dec;299(6):F1288-98 (medline
/20844023)
CM - Cites: PLoS One. 2014 Sep 08;9(9):e107001 (medline /25198551)
CM - Cites: Int J Hyg Environ Health. 2001 Mar;203(3):249-62 (medline
/11279822)
CM - Cites: Mol Ther. 2002 Jul;6(1):127-33 (medline /12095313)
CM - Cites: N Engl J Med. 2010 Jul 8;363(2):147-55 (medline /20573916)
CM - Cites: Drug Discov Today. 2008 Mar;13(5-6):268-74 (medline /18342804)
CM - Cites: Environ Toxicol. 2008 Apr;23(2):263-8 (medline /18214907)
CM - Cites: Toxicol Sci. 2011 Jul;122(1):211-21 (medline /21512104)
CM - Cites: PLoS One. 2014 Oct 31;9(10):e109916 (medline /25360519)
CM - Cites: Toxicol Appl Pharmacol. 2010 May 1;244(3):263-72 (medline
/20083129)
CM -Cites: Endocrinology. 2008 May;149(5):2433-42 (medline /18187555)
CM -Cites: Annu Rev Pharmacol Toxicol. 2007;47:243-62 (medline /17002598)
CM -Cites: Science. 1999 Apr 2;284(5411):143-7 (medline /10102814)
CM -Cites: Environ Health Perspect. 2001 Oct;109(10):1011-7 (medline
/11675266)
CM - Cites: J Vasc Surg. 2015 Sep;62(3):673-80 (medline /26304481)
CM - Cites: Nat Med. 2003 Jun;9(6):653-60 (medline /12778163)
CM - Cites: Cell Stem Cell. 2012 Jun 14;10(6):709-16 (medline /22704511)
CM - Cites: Transplantation. 1968 Mar;6(2):230-47 (medline /5654088)
CM - Cites: J Prev Med Public Health. 2014 Sep;47(5):253-7 (medline /25284196)
CM - Cites: Oncotarget. 2015 Oct 13;6(31):30453-71 (medline /26421711)
CM - Cites: Stem Cells. 2007 Sep;25(9):2363-70 (medline /17540857)
CM - Cites: Toxicol In Vitro. 2016 Sep;35:188-201 (medline /27327130)
CM - Cites: Transfus Med Hemother. 2008;35(4):279-285 (medline /21512643)
DOCNO- medline/29596344

185 - TOXLINE
TI - Myco-phytoremediation of arsenic- and lead-contaminated soils by
Helianthus annuus and wood rot fungi, Trichoderma sp. isolated from
decayed wood.
AU - Govarthanan M
AD - Department of Energy and Environmental System Engineering, University of
Seoul, Seoul 02504, Republic of Korea; PG &amp; Research Department of
Biotechnology, Mahendra Arts and Science College (Autonomous), Kalippatti, Namakkal
637501, Tamil Nadu, India. Electronic address: gova.muthu@gmail.com.
AU - Mythili R
AD - PG &amp; Research Department of Biotechnology, Mahendra Arts and Science
College (Autonomous), Kalippatti, Namakkal 637501, Tamil Nadu, India.
AU - Selvankumar T
AD - PG &amp; Research Department of Biotechnology, Mahendra Arts and Science
College (Autonomous), Kalippatti, Namakkal 637501, Tamil Nadu, India.
AU - Kamala-Kannan S
AD - Division of Biotechnology, Advanced Institute of Environment and Bioscience,
College of Environmental and Bioresource Sciences, Chonbuk National University,
Iksan 570 752, South Korea.
AU - Kim H
AD - Department of Energy and Environmental System Engineering, University of
Seoul, Seoul 02504, Republic of Korea. Electronic address: h_kim@uos.ac.kr.
SO - Ecotoxicol Environ Saf. 2018, Apr 30; 151:279-284. [Ecotoxicology and
environmental safety]
AB - In the present study, Helianthus annuus grown in arsenic- (As) and lead-
(Pb) contaminated soil were treated with plant-growth promoting fungi
Trichoderma sp. MG isolated from decayed wood and assessed for their
phytoremediation efficiency. The isolate MG exhibited a high tolerance to
As (650mg/L) and Pb (500mg/L), and could remove > 70% of metals in
aqueous solution with an initial concentration of 100mg/L each. In
addition, the isolate MG was screened for plant-growth-promoting factors
such as siderophores, 1-aminocyclopropane-1-carboxylic acid (ACC)
deaminase, indole acetic acid (IAA) synthesis, and phosphate
solubilisation. Phytoremediation studies indicated that treatment of H.
annuus with the isolate MG had the maximum metal-accumulation in shoots
(As; 67%, Pb; 59%). Furthermore, a significant increase in the soil
extracellular enzyme-activities was observed in myco-phytoremediated
soils. The activities of phosphatase (35 U/g dry soil), dehydrogenase
(41mg TPF/g soil), cellulase (37.2mg glucose/g/2h), urease (55.4mgN/g
soil/2h), amylase (49.3mg glucose/g/2h) and invertase (45.3mg
glucose/g/2h) significantly increased by 12%, 14%, 12%, 22%, 19% and 14%
in As contaminated soil, respectively. Similarly, the activities of
phosphatase (31.4U/g dry soil), dehydrogenase (39.3mg TPF/g soil),
cellulase (37.1mg glucose/g/2h), urease (49.8mgN/g soil/2h), amylase
(46.3mg glucose/g/2h), and invertase (42.1mg glucose/g/2h) significantly
increased by 11%, 15%, 11%, 18%, 20% and 14% in Pb contaminated soil,
respectively. Obtained results indicate that the isolate MG could be a
potential strain for myco-phytoremediation of As and Pb contaminated soil.
KW - Arsenic
KW - Helianthus annuus
KW - Phytoremediation
KW - Soil enzymes
KW - Trichoderma
RN - 2P299V784P
RN - 3K9EJ633GL
RN - 6U1S09C61L
RN - N712M78A8G
LA - eng
IS - 1090-2414 (Electronic)
PT - Journal Article
TA - Ecotoxicol Environ Saf
YR - 2018
DATE- 20180530
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Ecotoxicology and environmental safety
EDAT- 20180203
STAT- MEDLINE
DOCNO- medline/29407561

186 - TOXLINE
TI - Influence of the Chemical Form of Antimony on Soil Microbial Community
Structure and Arsenite Oxidation Activity.
AU - Kataoka T
AD - Center for Marine Environmental Studies (CMES), Ehime University.
AU - Mitsunobu S
AD - Department of Bioresources, Faculty of Agriculture, Ehime University.
AU - Hamamura N
AD - Department of Biology, Faculty of Science, Kyushu University.
SO - Microbes Environ. 2018, Jun 09. [Microbes and environments]
AB - In the present study, the influence of the co-contamination with various
chemical forms of antimony (Sb) with arsenite (As[III]) on soil microbial
communities was investigated. The oxidation of As(III) to As(V) was
monitored in soil columns amended with As(III) and three different
chemical forms of Sb: antimony potassium tartrate (Sb[III]-tar),
antimony(III) oxide (Sb2O3), and potassium antimonate (Sb[V]). Soil
microbial communities were examined qualitatively and quantitatively using
16S rDNA- and arsenite oxidase gene (aioA)-targeted analyses. Microbial
As(III) oxidation was detected in all soil columns and 90-100% of added
As(III) (200 &mu; mol L-1) was oxidized to As(V) in 9 d, except in the
Sb(III)-tar co-amendments that only oxidized 30%. 16S rDNA- and
aioA-targeted analyses showed that the presence of different Sb chemical
forms significantly affected the selection of distinct As(III)-oxidizing
bacterial populations. Most of the 16S rRNA genes detected in soil columns
belonged to Betaproteobacteria and Gammaproteobacteria, and some sequences
were closely related to those of known As(III) oxidizers. Co-amendments
with Sb(III)-tar and high concentrations of Sb2O3 significantly increased
the ratios of aioA-possessing bacterial populations, indicating the
enrichment of As(III) oxidizers resistant to As and Sb toxicity. Under Sb
co-amendment conditions, there was no correlation between aioA gene
abundance and the rates of As(III) oxidation. Collectively, these results
demonstrated that the presence of different Sb chemical forms imposed a
strong selective pressure on the soil bacterial community and, thus, the
co-existing metalloid is an important factor affecting the redox
transformation of arsenic in natural environments.
KW - advective flow cultivation
KW - antimony
KW - arsenite oxidase gene (aio)
KW - multiple metalloid contamination
KW - soil microbial community
LA - eng
IS - 1347-4405 (Electronic)
PT - Journal Article
TA - Microbes Environ
YR - 2018
DATE- 20180611
CITO- NLM
CS - Japan
FJT - Microbes and environments
EDAT- 20180609
STAT- Publisher
DOCNO- medline/29887548

187 - TOXLINE
TI - Vermiremediation of metal(loid)s via Eichornia crassipes phytomass
extraction: A sustainable technique for plant amelioration.
AU - Majumdar A
AD - Earth and Environmental Science Research Laboratory, Department of Earth
Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur,
West Bengal 741246, India.
AU - Barla A
AD - Earth and Environmental Science Research Laboratory, Department of Earth
Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur,
West Bengal 741246, India.
AU - Upadhyay MK
AD - Institute of Environment &amp; Sustainable Development, Banaras Hindu
University, Varanasi 221005, India.
AU - Ghosh D
AD - Department of Environmental Science, University of Calcutta, Ballygunge
Circular Road, Kolkata 700019, India.
AU - Chaudhuri P
AD - Department of Environmental Science, University of Calcutta, Ballygunge
Circular Road, Kolkata 700019, India.
AU - Srivastava S
AD - Institute of Environment &amp; Sustainable Development, Banaras Hindu
University, Varanasi 221005, India.
AU - Bose S
AD - Earth and Environmental Science Research Laboratory, Department of Earth
Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur,
West Bengal 741246, India. Electronic address: sutaparai@gmail.com.
SO - J Environ Manage. 2018, Aug 15; 220:118-125. [Journal of environmental
management]
AB - Eichhornia crassipes (water hyacinth), imparts deficiency of soluble
arsenic and other toxic metal (loid)s through rhizofiltration and
phytoaccumulation. Without proper management strategy, this
phytoremediation of metal (loid)s might fail and get reverted back to the
environment, contaminating the nearby water bodies. This study, focused on
bio-conversion of phytoremediating hyacinths, spiked with 100 times and
greater arsenic, lead and cadmium concentrations than the average water
contamination, ranging in 58.81&#8239;&plusmn;&#8239;0.394,
16.74&#8239;&plusmn;&#8239;0.367,
12.18&#8239;&plusmn;&#8239;0.153&#8239;mg Kg-1arsenic,
18.95&#8239;&plusmn;&#8239;0.212, 9.53&#8239;&plusmn;&#8239;0.054,
6.83&#8239;&plusmn;&#8239;0.306&#8239;mg&#8239;kg-1 lead and
2.79&#8239;&plusmn;&#8239;0.033, 1.39&#8239;&plusmn;&#8239;0.025,
0.92&#8239;&plusmn;&#8239;0.045&#8239;mg&#8239;kg-1 cadmium, respectively
in root, shoot and leaves, proving it's phytoaccumulation capacity. Next,
these hyacinths has been used as a source of organic supplement for
preparing vermicompost using Eisenia fetida following analysis of total
metal content and sequential extraction. Control soil was having
134.69&#8239;&plusmn;&#8239;2.47&#8239;mg&#8239;kg-1 arsenic in compare to
44.6&#8239;&plusmn;&#8239;0.91&#8239;mg&#8239;kg-1 at premature stage of
compost to 23.9&#8239;&plusmn;&#8239;1.55&#8239;mg&#8239;kg-1 at mature
compost indicating sustainable fate of phytoremediated vermicompost. This
vermiremediation of arsenic and other toxic elements, restricted the
bioavailability of soil pollutants. Furthermore, processed compost amended
as organic fertilizer, growing chickpea, coriander, tomato and chilli
plant, resulted in negligible metal(loid)s in treated samples, enhancing
also plant's growth and production.
KW - Arsenic
KW - Bio-conversion
KW - Phytoaccumulation
KW - Plant growth promotion
KW - Vermiremediation
LA - eng
IS - 1095-8630 (Electronic)
PT - Journal Article
TA - J Environ Manage
YR - 2018
DATE- 20180531
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Journal of environmental management
EDAT- 20180526
STAT- In-Process
DOCNO- medline/29775821

188 - TOXLINE
TI - Provenance, prevalence and health perspective of co-occurrences of
arsenic, fluoride and uranium in the aquifers of the Brahmaputra River
floodplain.
AU - Das N
AD - Department of Environmental Science, Tezpur University, Napaam 784028, Assam,
India.
AU - Das A
AD - Department of Environmental Science, Tezpur University, Napaam 784028, Assam,
India.
AU - Sarma KP
AD - Department of Environmental Science, Tezpur University, Napaam 784028, Assam,
India.
AU - Kumar M
AD - Department of Earth Sciences, Indian Institute of Technology Gandhinagar,
382355, Gujarat, India. Electronic address: manish.env@gmail.com.
SO - Chemosphere. 2018, Mar; 194:755-772. [Chemosphere]
AB - The present work focuses on understanding the provenance, prevalence and
health perspective of As and F- along with possible co-occurrence of
uranium (U) in the aquifers of the Brahmaputra floodplains (BFP), India.
Groundwater (n = 164) and sediment samples (n = 5)
were obtained from the upper, middle and lower BFP. Energy dispersive
spectroscopy (EDX) revealed the presence of As, U and Fe in the sediment
matrix. Regression analysis showed a weaker relationship between As and F-
co-occurrence. Hierarchical cluster analysis (HCA) and principal component
analysis (PCA) suggested reductive dissolution of Fe (hydr)oxides
responsible for As release in the BFP, especially in the upper and lower
BFP. Bicarbonate appeared to compete with As oxyanions for adsorption on
positively charged surfaces leading to As release. Arsenic desorption in
presence of PO43-, F- and HCO3- at elevated pH appeared greatest in the
upper BFP, suggesting the highest potential for co-occurrence.
Co-occurrence, were mainly in isolated aquifers of the upper BFP owing to
desorption of adsorbed As and F- from Fe (hydr)oxides at higher pH.
Weathering and dissolution of clay minerals in the upper BFP, and
competitive desorption in presence of HCO3- and PO43- in the middle and
lower BFP, respectively, explain variabilities in F- release. Amorphous Fe
(hydr)oxides like ferrihydrite act as sinks of U. Concentrations of As and
F- will likely increase in the future as projected from the saturated
levels of goethite and ferrihydrite. Hazard indices (HI) revealed that
children (3-8 years) were at greater health risk than adults.
KW - Arsenic
KW - Brahmaputra
KW - Fluoride
KW - Groundwater
KW - Health
KW - Uranium
RN - 1310-14-1
RN - 4OC371KSTK
RN - 87PZU03K0K
RN - N712M78A8G
RN - Q80VPU408O
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180228
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171205
STAT- MEDLINE
DOCNO- medline/29247935

189 - TOXLINE
TI - Arbuscular mycorrhizal fungi alleviate arsenic toxicity to Medicago sativa
by influencing arsenic speciation and partitioning.
AU - Li J
AD - State Key Laboratory of Urban and Regional Ecology, Research Center for Eco-
Environmental Sciences, Chinese Academy of Sciences, No. 18, Shuangqing Road,
Haidian District, Beijing 100085, China; University of Chinese Academy of Sciences,
Beijing 100049, China.
AU - Sun Y
AD - State Key Laboratory of Urban and Regional Ecology, Research Center for Eco-
Environmental Sciences, Chinese Academy of Sciences, No. 18, Shuangqing Road,
Haidian District, Beijing 100085, China; University of Chinese Academy of Sciences,
Beijing 100049, China.
AU - Jiang X
AD - State Key Laboratory of Urban and Regional Ecology, Research Center for Eco-
Environmental Sciences, Chinese Academy of Sciences, No. 18, Shuangqing Road,
Haidian District, Beijing 100085, China.
AU - Chen B
AD - State Key Laboratory of Urban and Regional Ecology, Research Center for Eco-
Environmental Sciences, Chinese Academy of Sciences, No. 18, Shuangqing Road,
Haidian District, Beijing 100085, China; University of Chinese Academy of Sciences,
Beijing 100049, China.
AU - Zhang X
AD - State Key Laboratory of Urban and Regional Ecology, Research Center for Eco-
Environmental Sciences, Chinese Academy of Sciences, No. 18, Shuangqing Road,
Haidian District, Beijing 100085, China. Electronic address: xinzhang@rcees.ac.cn.
SO - Ecotoxicol Environ Saf. 2018, Aug 15; 157:235-243. [Ecotoxicology and
environmental safety]
AB - In a pot experiment, Medicago sativa inoculated with/without arbuscular
mycorrhizal (AM) fungus Rhizophagus irregularis were grown in four levels
(0, 10, 25, and 75&#8239;mg/kg) of arsenic (As)-polluted soil to
investigate the influences of AM symbiosis on plant As tolerance. The
results showed that mycorrhizal inoculation significantly increased plant
biomass, while As addition decreased mycorrhizal colonization and hyphal
length density. Mycorrhizal inoculation dramatically improved plant
phosphorus (P) nutrition, restricted As uptake and retained more As in
roots by upregulating the expression of the AM-induced P transporter gene
MsPT4 and the metallothionein gene MsMT2. High soil As content
downregulated MsPT4 expression. Dimethylarsenic acid (DMA) was detected
only in the shoots of mycorrhizal plants, indicating that AM fungi likely
play an essential role in As detoxification by biological methylation. The
present investigation allowed deeper insights into the As detoxification
mechanisms of AM associations and demonstrated the important role of AM
fungi in plant resistance under As-contaminated conditions.
KW - Arbuscular mycorrhiza
KW - As partitioning
KW - As speciation
KW - Gene expression
KW - Medicago sativa
KW - P acquisition
LA - eng
IS - 1090-2414 (Electronic)
PT - Journal Article
TA - Ecotoxicol Environ Saf
YR - 2018
DATE- 20180424
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Ecotoxicology and environmental safety
EDAT- 20180403
STAT- In-Process
DOCNO- medline/29625397

190 - TOXLINE
TI - Pathological and Clinical Pathological Changes Induced by Four-week,
Repeated-dose, Oral Administration of the Wood Preservative Chromated
Copper Arsenate in Wistar Rats.
AU - Takahashi N
AD - 1 The Institute of Environmental Toxicology, Joso-shi, Ibaraki, Japan.
AU - Yoshida T
AD - 2 Laboratory of Veterinary Pathology, Tokyo University of Agriculture and
Technology, Fuchu-shi, Tokyo, Japan.
AU - Kojima S
AD - 1 The Institute of Environmental Toxicology, Joso-shi, Ibaraki, Japan.
AU - Yamaguchi S
AD - 1 The Institute of Environmental Toxicology, Joso-shi, Ibaraki, Japan.
AU - Ohtsuka R
AD - 1 The Institute of Environmental Toxicology, Joso-shi, Ibaraki, Japan.
AU - Takeda M
AD - 1 The Institute of Environmental Toxicology, Joso-shi, Ibaraki, Japan.
AU - Kosaka T
AD - 1 The Institute of Environmental Toxicology, Joso-shi, Ibaraki, Japan.
AU - Harada T
AD - 1 The Institute of Environmental Toxicology, Joso-shi, Ibaraki, Japan.
SO - Toxicol Pathol. 2018, Apr; 46(3):312-323. [Toxicologic pathology]
AB - Chromated copper arsenate (CCA) is used as a wood preservative worldwide.
Exposure to it may adversely affect human health. Some events have
increased human exposure to CCA, including the Great East Japan
Earthquake, which generated a large amount of lumber debris from
CCA-treated woods. We elucidated the toxicity due to daily exposure to CCA
over a 4-week period at doses of 0, 8, 40, and 80 mg/kg/day in Wistar
Hannover rats. Chromium (Cr) and arsenic (As), but not copper, were
detected in the plasma samples of rats treated with various doses of CCA.
Males and females showed sedation, and males had poor body weight gain.
The clinical pathologies observed in both sexes included hypochromic and
microcytic anemia, hepatic and renal dysfunction, and changes in lipid and
glucose levels. Histopathologically, males and females showed forestomach
hyperkeratosis, mucosal epithelial hyperplasia in the small intestine,
rectal goblet cell hypertrophy, and lipofuscin deposition in the proximal
renal tubule. Females showed diffuse hepatocellular hypertrophy with
increased 8-hydroxydeoxyguanosine levels. These results indicated that
oral administration of CCA mainly affected hematopoietic,
gastrointestinal, hepatic, and renal systems owing to the toxic effects of
As and/or Cr. Major toxic effects were observed in both sexes receiving 40
and 80 mg/kg/day.
KW - anemia
KW - chromated copper arsenate
KW - hyperplasia
KW - oxidative stress
KW - small intestine
LA - eng
IS - 1533-1601 (Electronic)
PT - Journal Article
TA - Toxicol Pathol
YR - 2018
DATE- 20180423
CITO- NLM
CS - United States
FJT - Toxicologic pathology
EDAT- 20180327
STAT- In-Data-Review
DOCNO- medline/29587599

191 - TOXLINE
TI - Effect of titanium dioxide nanoparticles on the accumulation and
distribution of arsenate in Daphnia magna in the presence of an algal
food.
AU - Luo Z
AD - Key Laboratory of Urban Environment and Health, Institute of Urban
Environment, Chinese Academy of Sciences, Xiamen, 361021, China. zxluoire@163.com.
AU - Li M
AD - Key Laboratory of Urban Environment and Health, Institute of Urban
Environment, Chinese Academy of Sciences, Xiamen, 361021, China.
AU - Wang Z
AD - Key Laboratory of Urban Environment and Health, Institute of Urban
Environment, Chinese Academy of Sciences, Xiamen, 361021, China.
AU - Li J
AD - Key Laboratory of Urban Environment and Health, Institute of Urban
Environment, Chinese Academy of Sciences, Xiamen, 361021, China.
AU - Guo J
AD - Key Laboratory of Urban Environment and Health, Institute of Urban
Environment, Chinese Academy of Sciences, Xiamen, 361021, China.
AU - Rosenfeldt RR
AD - nEcoTox, An der Neumuehle 2, 76855, Annweiler, Germany.
AU - Seitz F
AD - nEcoTox, An der Neumuehle 2, 76855, Annweiler, Germany.
AU - Yan C
AD - Key Laboratory of Urban Environment and Health, Institute of Urban
Environment, Chinese Academy of Sciences, Xiamen, 361021, China. czyan@iue.ac.cn.
SO - Environ Sci Pollut Res Int. 2018, May 15. [Environmental science and
pollution research international]
AB - The impact of titanium dioxide nanoparticles (nano-TiO2) on the
bioavailability of metals in aquatic filter-feeding organisms has rarely
been investigated, especially in the presence of algae as a food source.
In this study, we quantified the accumulation and subcellular distribution
of arsenate (AsV) in Daphnia magna in the presence of nano-TiO2 and a
green alga (Scenedesmus obliquus) food source. Results showed that S.
obliquus significantly increased the accumulation of total arsenic (As)
and titanium (Ti) in D. magna. The presence of this food source increased
As in metal-sensitive fractions (MSF) and as biologically detoxified
metals (BDM), while it decreased Ti levels in MSF but increased levels as
BDM. The difference in the subcellular distribution of As and Ti
demonstrates the dissociation of As from nano-TiO2 during digestion at
subcellular partitioning irrespective of food availability. In turn, the
presence of algae was shown to increase metal-based toxicity in D. magna
due to the transfer of As from BMD to MSF. Furthermore, S. obliquus
significantly increased the concentration of As and Ti in soluble
fractions, indicating that As and nano-TiO2 ingested by D. magna could be
transferred more readily to their predators in the presence of S.
obliquus. Our study shows the potential of algae to increase the toxicity
and biomagnification of As V . Furthermore, it highlights food as an
important factor in the toxicity assessment of nanomaterials and
co-existing pollutants.
KW - Algae
KW - Arsenic
KW - Bioavailability
KW - Nanoparticles
KW - Subcellular distribution
LA - eng
IS - 1614-7499 (Electronic)
PT - Journal Article
TA - Environ Sci Pollut Res Int
YR - 2018
DATE- 20180516
CITO- NLM
CS - Germany
FJT - Environmental science and pollution research international
EDAT- 20180515
STAT- Publisher
DOCNO- medline/29766424

192 - TOXLINE
TI - Simultaneous influence of indigenous microorganism along with abiotic
factors controlling arsenic mobilization in Brahmaputra floodplain, India.
AU - Sathe SS
AD - Department of Civil Engineering, Indian Institute of Technology Guwahati,
Guwahati 781039, Assam, India. Electronic address: s.sathe@iitg.ernet.in.
AU - Mahanta C
AD - Department of Civil Engineering, Indian Institute of Technology Guwahati,
Guwahati 781039, Assam, India.
AU - Mishra P
AD - Department of Computer Science and Engineering, Sri Ramswaroop Memorial
College of Engineering and Management, Lucknow 227105, Uttar Pradesh, India.
SO - J Contam Hydrol. 2018, Jun; 213:1-14. [Journal of contaminant hydrology]
AB - In the dynamic cycling of oxic and anoxic aqueous alluvial aquifer
environments, varying Arsenic (As) concentrations are controlled by both
abiotic and biotic factors. Studies have shown a significant form of toxic
As (III) being released through the reductive dissolution of
iron-oxy/hydroxide minerals and microbial reduction mechanisms, which
leads to a serious health concern. The present study was performed in
order to assess the abiotic and biotic factors influencing As release into
the alluvial aquifer groundwater in Brahmaputra floodplain, India. The
groundwater chemistry, characterization of the sediments, isolation,
identification and characterization of prominent As releasing indigenous
bacterium were conducted. The measured solid and liquid phases of total As
concentration were ranged between 0.02 and 17.2&#8239;mg&#8239;kg-1 and 8
to 353&#8239;&mu;g&#8239;L-1, respectively. The morphology and mineralogy
showed the presence of detrital and authigenic mineral assemblages whereas
primary and secondary As bearing Realgar and Claudetite minerals were
identified, respectively. Furthermore, significant non-labile As fraction
was found associated with the amorphous oxides of Fe, Mn and Al. The
observed groundwater chemistry and sediment color, deduced a sub-oxic
reducing aquifer conditions in As-contaminated regions. In addition, 16S
rDNA sequencing results of the isolated bacterium showed the prominent
Pseudomonas aeruginosa responsible for the mobilization of As, reducing
condition, biomineralization and causing grey color to the sediments at
the shallower and deeper aquifers in the study area. These findings
suggest that microbial metabolic activities are equally responsible in
iron-oxy/hydroxide reductive dissolution, controlling As mobilization in
dynamic fluvial flood plains.
KW - Arsenate-reducing bacteria
KW - Arsenic
KW - Hydrogeochemistry
KW - Minerals
KW - Pseudomonas aeruginosa
KW - Sequential extraction
LA - eng
IS - 1873-6009 (Electronic)
PT - Journal Article
TA - J Contam Hydrol
YR - 2018
DATE- 20180528
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Journal of contaminant hydrology
EDAT- 20180305
STAT- In-Data-Review
DOCNO- medline/29598853

193 - TOXLINE
TI - Arsenic-phosphorus interactions in the soil-plant-microbe system: Dynamics
of uptake, suppression and toxicity to plants.
AU - Anawar HM
AD - School of Earth and Environment (M087), The University of Western Australia,
Crawley, WA 6009, Australia. Electronic address: anawar4@hotmail.com.
AU - Rengel Z
AD - School of Earth and Environment (M087), The University of Western Australia,
Crawley, WA 6009, Australia.
AU - Damon P
AD - School of Earth and Environment (M087), The University of Western Australia,
Crawley, WA 6009, Australia.
AU - Tibbett M
AD - Centre for Agri-Environmental Research &amp; Soil Research Centre, School of
Agriculture, Policy and Development, University of Reading, RG6 6AR Reading, UK.
SO - Environ Pollut. 2018, Feb; 233:1003-1012. [Environmental pollution
(Barking, Essex : 1987)]
AB - High arsenic (As) concentrations in the soil, water and plant systems can
pose a direct health risk to humans and ecosystems. Phosphate (Pi) ions
strongly influence As availability in soil, its uptake and toxicity to
plants. Better understanding of As(V)-Pi interactions in soils and plants
will facilitate a potential remediation strategy for As contaminated
soils, reducing As uptake by crop plants and toxicity to human populations
via manipulation of soil Pi content. However, the As(V)-Pi interactions in
soil-plant systems are complex, leading to contradictory findings among
different studies. Therefore, this review investigates the role of soil
type, soil properties, minerals, Pi levels in soil and plant, Pi
transporters, mycorrhizal association and microbial activities on As-Pi
interactions in soils and hydroponics, and uptake by plants, elucidate the
key mechanisms, identify key knowledge gaps and recommend new research
directions. Although Pi suppresses As uptake by plants in hydroponic
systems, in soils it could either increase or decrease As availability and
toxicity to plants depending on the soil types, properties and charge
characteristics. In soil, As(V) availability is typically increased by the
addition of Pi. At the root surface, the Pi transport system has high
affinity for Pi over As(V). However, Pi concentration in plant influences
the As transport from roots to shoots. Mycorrhizal association may reduce
As uptake via a physiological shift to the mycorrhizal uptake pathway,
which has a greater affinity for Pi over As(V) than the root epidermal
uptake pathway.
KW - Arsenic toxicity
KW - As-Pi interactions
KW - As-Pi uptake by plants
KW - Mycorrhizal association
KW - Soil mineralogy
KW - Soil types
RN - 059QF0KO0R
RN - 27YLU75U4W
RN - N712M78A8G
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180418
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Environmental pollution (Barking, Essex : 1987)
EDAT- 20171013
STAT- MEDLINE
DOCNO- medline/29033177

194 - TOXLINE
TI - Copper (II) and/or arsenite-induced oxidative stress cascades apoptosis
and autophagy in the skeletal muscles of chicken.
AU - Wang Y
AD - College of Wildlife Resources, Northeast Forestry University, Harbin, 150040,
Heilongjiang, PR China.
AU - Zhao H
AD - College of Wildlife Resources, Northeast Forestry University, Harbin, 150040,
Heilongjiang, PR China.
AU - Shao Y
AD - College of Wildlife Resources, Northeast Forestry University, Harbin, 150040,
Heilongjiang, PR China.
AU - Liu J
AD - College of Wildlife Resources, Northeast Forestry University, Harbin, 150040,
Heilongjiang, PR China.
AU - Li J
AD - College of Wildlife Resources, Northeast Forestry University, Harbin, 150040,
Heilongjiang, PR China.
AU - Luo L
AD - College of Wildlife Resources, Northeast Forestry University, Harbin, 150040,
Heilongjiang, PR China. Electronic address: luoly@nefu.edu.cn.
AU - Xing M
AD - College of Wildlife Resources, Northeast Forestry University, Harbin, 150040,
Heilongjiang, PR China. Electronic address: xingmingwei@nefu.edu.cn.
SO - Chemosphere. 2018, Sep; 206:597-605. [Chemosphere]
AB - Arsenic (As) is a ubiquitous environmental toxin and robust inducer of
oxidative stress (OxS). Copper (Cu) is an essential microelement, which
participates in OxS as a cofactor for certain enzymes, with narrow optimal
range between essential and toxic concentrations. However, their effects
are rarely studied in chicken skeletal muscles, which have soaring per
capita consumption andare susceptible to oxidative damage. In the present
study, we demonstrated that the administration of copper sulfate
(300&#8239;mg&#8239;kg-1) or arsenite (30&#8239;mg&#8239;kg-1)
individually or their co-administration leads to varying degrees of OxS in
the skeletal muscles of chickens. Corresponding to the protein expression
pattern, the mRNA levels of caspase, B-cell lymphoma-2 (Bcl-2) families,
and autophagy-related genes were also compromised in the experimental
groups, indicating the involvement of both apoptotic and autophagic cell
death. Additionally, rampant mitochondrial fission caused the vicious
cycle between imbalanced mitochondrial dynamics and OxS, thus tethering
intracellular homeostasis. The abovementioned muscle damage and index
anomalies were time dependent, and more deteriorated effects were observed
in Cu2+ and arsenite co-administered groups than those in groups
administered Cu2+ and arsenite alone. Intriguingly, in the studied
skeletal muscles, namely wing biceps brachii and leg gastrocnemius, there
were conspicuous differences in oxidative toxicity susceptibility, which
needs further study. The present study showed that Cu and/or As induce
oxidative damage in chicken skeletal muscles and discussed its mechanism
in terms of apoptosis, autophagy, and mitochondrial dynamics, thus voicing
concerns about poultry breeding areas cross-contaminated with Cu2+ and
arsenite.
KW - Apoptosis
KW - Arsenite
KW - Autophagy
KW - Copper (II)
KW - Oxidative stress
KW - Skeletal muscles
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
TA - Chemosphere
YR - 2018
DATE- 20180609
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
FJT - Chemosphere
EDAT- 20180511
STAT- In-Process
DOCNO- medline/29778937

195 - TOXLINE
TI - The dual role of mitochondrial superoxide in arsenite toxicity: Signaling
at the boundary between apoptotic commitment and cytoprotection.
AU - Fiorani M
AD - Dipartimento di Scienze Biomolecolari, Universit� degli Studi di Urbino
"Carlo Bo", 61029 Urbino, Italy. Electronic address: mara.fiorani@uniurb.it.
AU - Guidarelli A
AD - Dipartimento di Scienze Biomolecolari, Universit� degli Studi di Urbino
"Carlo Bo", 61029 Urbino, Italy. Electronic address: andrea.guidarelli@uniurb.it.
AU - Capellacci V
AD - Dipartimento di Scienze Biomolecolari, Universit� degli Studi di Urbino
"Carlo Bo", 61029 Urbino, Italy. Electronic address:
valentina.capellacci@uniurb.it.
AU - Cerioni L
AD - Dipartimento di Scienze Biomolecolari, Universit� degli Studi di Urbino
"Carlo Bo", 61029 Urbino, Italy. Electronic address: liana.cerioni@uniurb.it.
AU - Crinelli R
AD - Dipartimento di Scienze Biomolecolari, Universit� degli Studi di Urbino
"Carlo Bo", 61029 Urbino, Italy. Electronic address: rita.crinelli@uniurb.it.
AU - Cantoni O
AD - Dipartimento di Scienze Biomolecolari, Universit� degli Studi di Urbino
"Carlo Bo", 61029 Urbino, Italy. Electronic address: orazio.cantoni@uniurb.it.
SO - Toxicol Appl Pharmacol. 2018, Apr 15; 345:26-35. [Toxicology and applied
pharmacology]
AB - Arsenite toxicity is in numerous cellular systems dependent on the
formation of reactive oxygen and or nitrogen species. This is also true in
U937 cells in which the metalloid selectively promotes the formation of
mitochondrial superoxide (mitoO2-) rapidly converted to diffusible H2O2.
We tested the hypothesis that, under the same conditions, mitoO2- also
mediates the triggering of a parallel survival signaling. We found that a
low concentration of the metalloid causes an early activation of nuclear
factor erythroid 2 p45-related factor 2 (Nrf2), and a downstream signaling
leading to enhanced GSH biosynthesis, via a mechanism sensitive to various
treatments/strategies selectively preventing mitoO2- formation. Under the
same conditions, the toxic effects mediated by arsenite, leading to
delayed mitochondrial permeability transition (MPT)-dependent apoptosis,
were also prevented. Additional studies revealed remarkable similarities
in the kinetics of mitoO2- formation, MPT induction, Nrf2 activation and
GSH biosynthesis, prior to the onset of apoptosis in a small portion of
the cells. Importantly, mitoO2- formation, as well as the ensuing toxic
events, were significantly potentiated and anticipated under conditions
associated with inhibition of de novo GSH biosynthesis triggered by the
metalloid through Nrf2 activation. We conclude that, in the arsenite
toxicity paradigm under investigation, mitoO2- represents the only trigger
of two opposite pathways leading to activation of the Nrf2 signaling
and/or to a MPT-dependent apoptotic death. The first pathway, through
enhanced GSH biosynthesis, mitigates the extent of further mitoO2-
formation, thereby limiting and delaying an otherwise rapid and massive
apoptotic death.
KW - Apoptosis
KW - Arsenite
KW - Mitochondrial permeability transition
KW - Mitochondrial superoxide
KW - Nrf2, GSH
LA - eng
IS - 1096-0333 (Electronic)
PT - Journal Article
TA - Toxicol Appl Pharmacol
YR - 2018
DATE- 20180402
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - United States
FJT - Toxicology and applied pharmacology
EDAT- 20180308
STAT- In-Data-Review
DOCNO- medline/29526526

196 - TOXLINE
TI - Silicon Decreases Dimethylarsinic Acid Concentration in Rice Grain and
Mitigates Straighthead Disorder.
AU - Limmer MA
AD - Department of Plant &amp; Soil Sciences University of Delaware , Newark ,
Delaware 19716 , United States.
AU - Wise P
AD - Department of Plant &amp; Soil Sciences University of Delaware , Newark ,
Delaware 19716 , United States.
AU - Dykes GE
AD - Department of Plant &amp; Soil Sciences University of Delaware , Newark ,
Delaware 19716 , United States.
AU - Seyfferth AL
AD - Department of Plant &amp; Soil Sciences University of Delaware , Newark ,
Delaware 19716 , United States.
SO - Environ Sci Technol. 2018, Apr 17; 52(8):4809-4816. [Environmental science
& technology]
AB - While root Si transporters play a role in the uptake of arsenite and
organic As species dimethylarsinic acid (DMA) and monomethylarsonic acid
(MMA) in rice ( Oryza sativa L.), the impact of Si addition on the
accumulation of DMA and MMA in reproductive tissues has not been directly
evaluated, particularly in isolation from inorganic As species.
Furthermore, DMA and MMA are suspected causal agents of straighthead
disorder. We performed a hydroponic study to disentangle the impact of Si
on accumulation of DMA and MMA in rice grain. At 5 &mu;M, MMA was toxic to
rice, regardless of Si addition, although Si significantly decreased root
MMA concentrations. Plants dosed with 5 &mu;M DMA grew well vegetatively
but exhibited straighthead disorder at the lowest Si dose, and this
DMA-induced yield loss reversed with increasing solution Si. Increasing Si
also significantly decreased DMA concentrations in roots, straw, husk, and
grain, particularly in mature plants. Si restricted grain DMA through
competition for root uptake and downregulation of root Si transporters
particularly at later stages of growth when Si uptake was greatest. Our
finding that DMA causes straighthead disorder under low Si availability
but not under high Si availability suggests Si as a straighthead
management strategy.
LA - eng
IS - 1520-5851 (Electronic)
PT - Journal Article
TA - Environ Sci Technol
YR - 2018
DATE- 20180417
CITO- NLM
CS - United States
FJT - Environmental science &amp; technology
EDAT- 20180409
STAT- In-Data-Review
DOCNO- medline/29608840

197 - TOXLINE
TI - Bioaccumulation and Toxicity of Uranium, Arsenic and Nickel to Juveniles
and Adults Hyalella azteca in Spiked Sediment Bioassays.
AU - Goulet RR
AD - Department of Earth Sciences, University of Ottawa, Louis Pasteur, Ottawa,
Ontario, Canada.
AU - Thompson PA
AD - Canadian Nuclear Safety Commission, Slater, Ottawa, Ontario, Canada.
SO - Environ Toxicol Chem. 2018, May 26. [Environmental toxicology and
chemistry]
AB - Uranium mining and milling release arsenic (As), nickel (Ni) and uranium
(U) to receiving waters, which accumulate in sediments. The objective of
this study was to investigate if As, Ni and U concentrations in tissue
residue of Hyalella azteca, overlying water, sediment pore water and
solids could predict juvenile and adult survival and growth in similar
conditions to lake sediments downstream of Uranium mines and mills. We
conducted 14 day, static sediment toxicity tests spiked with uranium,
arsenic and nickel salts. For uranium, we spiked uranyl nitrate with
sodium bicarbonate to limit U precipitation once in contact with
circumneutral sediment. LC50 for As, Ni and U of juveniles and adults
based on measured concentrations in sediments were 1.8 and
2.2&thinsp;&micro;mol As/g dw, 6.3 and 13.4&thinsp;&micro;mol Ni/g dw and
0.2 and 0.9&thinsp;&micro;mol U/g dw, respectively. Adult survival and
growth linearly decreased with increasing bioaccumulation. For juveniles,
metal accumulation linearly predicted survival. We calculated lethal body
concentrations (LBC50 ) for juveniles and adults of 70 and 485 nmol As/g
dw, 246 and 832 nmol Ni/g dw and 1.7 and 4.4 nmol U/g dw, respectively.
The concentrations of As, Ni and U in tissue residue leading to a 20%
decrease in growth were 427 nmol As/g, 755 nmol Ni/g and 5 nmol U/g.
Overall, this study showed that Uranium was the most toxic element
followed by As and Ni, that juveniles were more sensitive to the three
metals tested than adults and that threshold body concentrations can
support assessment of benthic invertebrate community impairment. This
article is protected by copyright. All rights reserved.
KW - Hyalella azteca
KW - Lethal body concentration
KW - Life stage
KW - Nickel, Arsenic
KW - Uranium
LA - eng
IS - 1552-8618 (Electronic)
PT - Journal Article
TA - Environ Toxicol Chem
YR - 2018
DATE- 20180526
CI - This article is protected by copyright. All rights reserved.
CITO- NLM
CS - United States
FJT - Environmental toxicology and chemistry
EDAT- 20180526
STAT- Publisher
DOCNO- medline/29802730

198 - TOXLINE
TI - Association between serum arsenic levels and gestational diabetes
mellitus: A population-based birth cohort study.
AU - Xia X
AD - Department of Maternal, Child and Adolescent Health, School of Public Health,
Anhui Medical University, Hefei, People's Republic of China.
AU - Liang C
AD - Department of Maternal, Child and Adolescent Health, School of Public Health,
Anhui Medical University, Hefei, People's Republic of China; Anhui Provincial Key
Laboratory of Population Health &amp; Aristogenics, Hefei, People's Republic of
China.
AU - Sheng J
AD - Anhui Provincial Key Laboratory of Population Health &amp; Aristogenics,
Hefei, People's Republic of China.
AU - Yan S
AD - Ma'anshan Maternal and Child Health (MCH) Center, Ma'anshan, People's
Republic of China.
AU - Huang K
AD - Department of Maternal, Child and Adolescent Health, School of Public Health,
Anhui Medical University, Hefei, People's Republic of China; Anhui Provincial Key
Laboratory of Population Health &amp; Aristogenics, Hefei, People's Republic of
China.
AU - Li Z
AD - Department of Maternal, Child and Adolescent Health, School of Public Health,
Anhui Medical University, Hefei, People's Republic of China.
AU - Pan W
AD - Ma'anshan Maternal and Child Health (MCH) Center, Ma'anshan, People's
Republic of China.
AU - Tao R
AD - Department of Maternal, Child and Adolescent Health, School of Public Health,
Anhui Medical University, Hefei, People's Republic of China.
AU - Hao J
AD - Department of Maternal, Child and Adolescent Health, School of Public Health,
Anhui Medical University, Hefei, People's Republic of China; Anhui Provincial Key
Laboratory of Population Health &amp; Aristogenics, Hefei, People's Republic of
China.
AU - Zhu B
AD - Department of Maternal, Child and Adolescent Health, School of Public Health,
Anhui Medical University, Hefei, People's Republic of China; Anhui Provincial Key
Laboratory of Population Health &amp; Aristogenics, Hefei, People's Republic of
China.
AU - Tong S
AD - Department of Maternal, Child and Adolescent Health, School of Public Health,
Anhui Medical University, Hefei, People's Republic of China; School of Public
Health and Social Work and Institute of Health and Biomedical Innovation,
Queensland University of Technology, Brisbane, Australia; Shanghai Children's
Medical Centre, Shanghai JiaoTong University, Shanghai, People's Republic of China.
Electronic address: s.tong@qut.edu.au.
AU - Tao F
AD - Department of Maternal, Child and Adolescent Health, School of Public Health,
Anhui Medical University, Hefei, People's Republic of China; Anhui Provincial Key
Laboratory of Population Health &amp; Aristogenics, Hefei, People's Republic of
China. Electronic address: taofangbiao@126.com.
SO - Environ Pollut. 2018, Apr; 235:850-856. [Environmental pollution (Barking,
Essex : 1987)]
AB - Gestational diabetes mellitus (GDM) is a common obstetric complication
with adverse effects on both mothers and their children. Previous studies
revealed the link between Arsenic (As) exposure and incidence of diabetes
mellitus (DM), but the data on the association between maternal As
exposure and GDM is scarce. We examined this association among a
population-based birth cohort. As concentrations were determined at
multiple time points during pregnancy by ICP-MS. The association between
As levels and GDM prevalence was examined using logistic regression model
after adjustment for confounders. A total of 419 (12.85%) women were
diagnosed with GDM. The incidences of GDM gradually increased with
increasing quartiles of As levels with significant trend. As levels were
associated with the GDM (95%CI: 1.29-2.43) at only the 4th quartile in the
first trimester. After adjustment for maternal age, prepregnancy body mass
index (BMI), monthly income, gestational age and parity, the association
remains significant (95%CI: 1.22-2.38). Stratified analyses showed the
associations were largely limited to normal maternal age (95%CI:
1.19-3.04) and normal weight women (95%CI: 1.18-2.66). Our study showed an
association between As and GDM in a birth cohort and explored first
trimester may be the critical period for As associated GDM. This
association was universal in the general pregnant population of normal age
and of normal weight.
KW - Arsenic
KW - Birth cohort
KW - Gestational diabetes
KW - Prenatal exposure
RN - N712M78A8G
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180524
CI - Copyright &copy; 2018 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Environmental pollution (Barking, Essex : 1987)
EDAT- 20180221
STAT- MEDLINE
DOCNO- medline/29348076

199 - TOXLINE
TI - Effect on human health of the arsenic pollution and hydrogeochemistry of
the Yaz&#305;r Lake wetland (�avd&#305;r-Burdur/Turkey).
AU - Varol S
AD - Water Institute, Suleyman Demirel University, Isparta, Turkey.
simgevarol@sdu.edu.tr.
AU - K�se &#304;
AD - Department of Geology Engineering, Suleyman Demirel University, Isparta,
Turkey.
SO - Environ Sci Pollut Res Int. 2018, Jun; 25(16):16217-16235. [Environmental
science and pollution research international]
AB - In this study, the physicochemical parameters, major ions and arsenic (As)
contents of water resources in the Yaz&#305;r lake wetland, were
evaluated. In addition, water resources in this region were investigated
from the point of water quality and health risk assessment. Thirty water
samples were collected from the area in dry and wet seasons. Ca-Mg-HCO3
and Ca-HCO3 were the dominant water types. The Gibbs diagram suggests that
most of the samples fall in rock-dominance zone, which indicates the
groundwater interaction between rock chemistry. When compared to drinking
water guidelines established by World Health Organization and Turkey, much
greater attention should be paid to As, Fe, and Mn through varied
chemicals above the critical values. According to the pH-ORP diagram, the
predominant species is arsenate (H2AsO4-2). The high concentrations of As
in the surface water and groundwater are related to oxidative and
reductive dissolution reaction of Fe and Mn hydroxides within the
K&#305;z&#305;lcada&#287; ophiolite and melange. In addition, the seasonal
changes in As concentrations depend on the increase in pH of water
samples. The major toxic and carcinogenic chemical within water samples is
As for groundwater and surface water. From the results of hazard index, it
is verified that As which is taken by ingestion of water was the main
contaminant, and toxic human risk in the study area. The obtained results
will help define strategies for As problems in the water resources in
future.
KW - Arsenic
KW - Health risk assessment
KW - Hydrogeochemistry
KW - Wetland
KW - Yazır Lake
LA - eng
IS - 1614-7499 (Electronic)
PT - Journal Article
TA - Environ Sci Pollut Res Int
YR - 2018
DATE- 20180608
CITO- NLM
CS - Germany
FJT - Environmental science and pollution research international
EDAT- 20180329
STAT- In-Process
CM - Cites: Water Res. 2011 Nov 1;45(17):5535-44 (medline /21917287)
CM - Cites: Nature. 1998 Sep 24;395(6700):338 (medline /9759723)
CM - Cites: Water Res. 2003 Jul;37(12):2929-36 (medline /12767295)
CM - Cites: J Water Health. 2016 Jun;14(3):471-88 (medline /27280612)
CM - Cites: Environ Int. 2009 Apr;35(3):466-72 (medline /18809211)
CM - Cites: Science. 1970 Dec 4;170(3962):1088-90 (medline /17777828)
CM - Cites: Environ Monit Assess. 2010 Dec;171(1-4):289-308 (medline /20072811)
CM - Cites: Food Chem Toxicol. 2010 Oct;48(10):2855-64 (medline /20643180)
CM - Cites: Sci Total Environ. 2004 Oct 15;333(1-3):267-81 (medline /15364534)
CM - Cites: Environ Pollut. 2008 Apr;152(3):686-92 (medline /17720286)
CM - Cites: Int J Hyg Environ Health. 2009 Mar;212(2):216-27 (medline
/18602865)
DOCNO- medline/29594885

200 - TOXLINE
TI - Poisoning histories in the Italian renaissance: The case of Pico Della
Mirandola and Angelo Poliziano.
AU - Gallello G
AD - Department of Archaeology, University of York, King's Manor, Exhibition
Square, YO1 7EP, York, UK. Electronic address: gianni.gallello@york.ac.uk.
AU - Cilli E
AD - Department of Cultural Heritage, Alma Mater Studiorum University of Bologna,
1 Ariani Street, 48121 Ravenna, Italy.
AU - Bartoli F
AD - Department of Biology University of Pisa, 13 Luca Ghini Street, 56126 Pisa,
Italy.
AU - Andretta M
AD - School of Engineering and Architecture, Alma Mater Studiorum University of
Bologna, CIRSA, 163 S. Alberto Street, 40123 Ravenna, Italy.
AU - Calcagnile L
AD - Department of Mathematics and Physics "Ennio De Giorgi", University of
Salento, Via per Arnesano Street, 73100 Lecce, Italy.
AU - Pastor A
AD - Department of Analytical Chemistry University of Valencia, 50 Dr. Moliner
Street, 46100 Burjassot, Valencia, Spain.
AU - de la Guardia M
AD - Department of Analytical Chemistry University of Valencia, 50 Dr. Moliner
Street, 46100 Burjassot, Valencia, Spain.
AU - Serventi P
AD - Department of Cultural Heritage, Alma Mater Studiorum University of Bologna,
1 Ariani Street, 48121 Ravenna, Italy; Department of Biological, Geological &amp;
Environmental Sciences, Alma Mater Studiorum University of Bologna, 3 Selmi Street,
Bologna, Italy.
AU - Marino A
AD - Reparto Investigazioni Scientifiche (RIS), Arma dei Carabinieri, Parma,
Italy.
AU - Benazzi S
AD - Department of Cultural Heritage, Alma Mater Studiorum University of Bologna,
1 Ariani Street, 48121 Ravenna, Italy; Department of Human Evolution, Max Planck
Institute for Evolutionary Anthropology, Deutscher Platz 6, 04103 Leipzig, Germany.
AU - Gruppioni G
AD - Department of Cultural Heritage, Alma Mater Studiorum University of Bologna,
1 Ariani Street, 48121 Ravenna, Italy.
SO - J Forensic Leg Med. 2018, May; 56:83-89. [Journal of forensic and legal
medicine]
AB - Giovanni Pico della Mirandola and Angelo Poliziano were two of the most
important humanists of the Italian Renaissance. They died suddenly in 1494
and their deaths have been for centuries a subject of debate. The
exhumation of their remains offered the opportunity to study the cause of
their death through a multidisciplinary research project. Anthropological
analyses, together with documentary evidences, radiocarbon dating and
ancient DNA analysis supported the identification of the remains
attributed to Pico. Macroscopic examination did not reveal
paleopathological lesions or signs related to syphilis. Heavy metals
analysis, carried out on bones and mummified tissues, showed that in
Pico's remains there were potentially lethal levels of arsenic, supporting
the philosopher's poisoning theory reported by documentary sources. The
arsenic concentrations obtained from analysis of Poliziano's remains, are
probably more related to an As chronic exposure or diagenetic processes
rather than poisoning.
KW - Ancient DNA
KW - Angelo Poliziano
KW - Arsenic poisoning
KW - Girolamo benivieni
KW - Pico della Mirandola
KW - Radiocarbon dating
RN - N712M78A8G
LA - eng
IS - 1878-7487 (Electronic)
PT - Historical Article
PT - Journal Article
TA - J Forensic Leg Med
YR - 2018
DATE- 20180524
CI - Copyright &copy; 2018 Elsevier Ltd and Faculty of Forensic and Legal
Medicine. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Journal of forensic and legal medicine
EDAT- 20180328
STAT- MEDLINE
DOCNO- medline/29609050

201 - TOXLINE
TI - Arsenic uptake and accumulation in rice (Oryza sativa L.) with selenite
fertilization and water management.
AU - Wan Y
AD - Beijing Key Laboratory of Farmland Soil Pollution Prevention and Remediation,
Key Laboratory of Plant-Soil Interactions of the Ministry of Education, China
Agricultural University, Beijing 100193, People's Republic of China.
AU - Camara AY
AD - Beijing Key Laboratory of Farmland Soil Pollution Prevention and Remediation,
Key Laboratory of Plant-Soil Interactions of the Ministry of Education, China
Agricultural University, Beijing 100193, People's Republic of China; Department of
Water/Forest and Environment, Higher Institute of Agronomy and Veterinary of
Faranah, B.P. 131, Republic of Guinea.
AU - Huang Q
AD - Beijing Key Laboratory of Farmland Soil Pollution Prevention and Remediation,
Key Laboratory of Plant-Soil Interactions of the Ministry of Education, China
Agricultural University, Beijing 100193, People's Republic of China; Gro-
Environmental Protection Institute, Ministry of Agriculture, Tianjin 300191,
People's Republic of China.
AU - Yu Y
AD - Beijing Key Laboratory of Farmland Soil Pollution Prevention and Remediation,
Key Laboratory of Plant-Soil Interactions of the Ministry of Education, China
Agricultural University, Beijing 100193, People's Republic of China.
AU - Wang Q
AD - Beijing Key Laboratory of Farmland Soil Pollution Prevention and Remediation,
Key Laboratory of Plant-Soil Interactions of the Ministry of Education, China
Agricultural University, Beijing 100193, People's Republic of China.
AU - Li H
AD - Beijing Key Laboratory of Farmland Soil Pollution Prevention and Remediation,
Key Laboratory of Plant-Soil Interactions of the Ministry of Education, China
Agricultural University, Beijing 100193, People's Republic of China. Electronic
address: lihuafen@cau.edu.cn.
SO - Ecotoxicol Environ Saf. 2018, Jul 30; 156:67-74. [Ecotoxicology and
environmental safety]
AB - The accumulation of arsenic (As) in rice grain is a potential threat to
human health. Our study investigated the possible mediatory role of
selenite fertilization on As uptake and accumulation by rice (Oryza sativa
L.) under different water management regimes (aerobic or flooded) in a pot
experiment. Soil solutions were also extracted during the growing season
to monitor As dynamics. Results showed that As contents in the soil
solutions, seedlings, and mature rice were higher under flooded than under
aerobic water management. Under aerobic conditions, selenite additions
slightly increased As concentrations in soil solutions (in the last two
samplings), but decreased As levels in rice plants. Relative to the
control, 0.5&#8239;mg&#8239;kg-1 selenite decreased rice grain As by
27.5%. Under flooded conditions, however, selenite additions decreased As
in soil solutions, while increased As in rice grain. Tendencies also
showed that selenite additions decreased the proportion of As in rice
shoots both at the seedling stage and maturity, and were more effective in
aerobic soil. Our results demonstrate that the effect of selenite
fertilizer on As accumulation by rice is related to water management.
KW - Arsenic
KW - Arsenic uptake and accumulation
KW - Rice (Oryza sativa L.)
KW - Selenite
KW - Water management
LA - eng
IS - 1090-2414 (Electronic)
PT - Journal Article
TA - Ecotoxicol Environ Saf
YR - 2018
DATE- 20180407
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Ecotoxicology and environmental safety
EDAT- 20180309
STAT- In-Process
DOCNO- medline/29529515

202 - TOXLINE
TI - Effect of microbially mediated iron mineral transformation on temporal
variation of arsenic in the Pleistocene aquifers of the central Yangtze
River basin.
AU - Deng Y
AD - Geological Survey, China University of Geosciences, Wuhan, China; State Key
Laboratory of Biogeology and Environmental Geology, China University of
Geosciences, Wuhan, China. Electronic address: yamin.deng@cug.edu.cn.
AU - Zheng T
AD - Geological Survey, China University of Geosciences, Wuhan, China.
AU - Wang Y
AD - State Key Laboratory of Biogeology and Environmental Geology, China
University of Geosciences, Wuhan, China; School of Environmental Studies, China
University of Geosciences, Wuhan, China. Electronic address: yx.wang@cug.edu.cn.
AU - Liu L
AD - Geological Survey, China University of Geosciences, Wuhan, China.
AU - Jiang H
AD - State Key Laboratory of Biogeology and Environmental Geology, China
University of Geosciences, Wuhan, China.
AU - Ma T
AD - State Key Laboratory of Biogeology and Environmental Geology, China
University of Geosciences, Wuhan, China; School of Environmental Studies, China
University of Geosciences, Wuhan, China.
SO - Sci Total Environ. 2018, Apr 01; 619-620:1247-1258. [The Science of the
total environment]
AB - Significant seasonal variation of groundwater arsenic (As) concentrations
in shallow aquifers of the Jianghan Plain, central Yangtze River Basin has
been reported recently, but the underlying mechanisms remain not well
understood. To elaborate biogeochemical processes responsible for the
observed As concentration variation, 42-day incubation experiments were
done using sediment samples collected respectively from the depth of 26,
36 and 60m of the As-affected aquifer which were labeled respectively as
JH26, JH36, JH60. Where JH denotes Jianghan Plain, and the number
indicates the depth of the sediment sample. The results indicated that As
could be mobilized from the sediments of 26m and 36m depth under the
stimulation of exogenous organic carbon, with the maximum As release
amount of 1.60 and 1.03mgkg-1, respectively, while the sediments at 60m
depth did not show As mobilization. The microbially mediated reductive
dissolution of amorphous iron oxides and reduction of As(V) to As(III)
could account for the observed As mobilization. The 16S rRNA
high-throughput sequencing results indicated that the variation of
microbial community correlated with the released As concentration (R=0.7,
P < 0.05) and the iron-reducing bacteria, including Pseudomonas,
Clostridium and Geobacter, were the main drivers for the As mobilization
from the sediments at 26m and 36m depth. The increase of arsC gene
abundance (up to 1.4&times;105 copies g-1) during As release suggested
that As reduction was mediated by the resistant reduction mechanism. By
contrast, in the 60m sediments where the Fe and As release was absent, the
iron-reducing bacteria accounted for a very minor proportion and
sulfate-reducing bacteria were predominant in the microbial community. In
addition, after 30days of incubation, the released As in the 26m sediments
was immobilized via co-precipitation with or adsorption onto the
Fe-sulfide mineral newly-formed by the bacterial sulfate reduction. These
results are consistent with the results of our previous field monitoring,
indicating that the bacterial sulfate reduction could lead to the temporal
decrease in groundwater As concentrations. This study provides insights
into the mechanism for As mobilization and seasonal As concentration
variation in the Pleistocene aquifers from alluvial plains.
KW - Arsenic mobilization
KW - Groundwater
KW - Iron mineral transformation
KW - Jianghan plain
KW - Sulfate reduction
KW - Temporal variation
RN - E1UOL152H7
RN - N712M78A8G
LA - eng
IS - 1879-1026 (Electronic)
PT - Journal Article
TA - Sci Total Environ
YR - 2018
DATE- 20180607
CI - Copyright &copy; 2017 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - The Science of the total environment
EDAT- 20171129
STAT- MEDLINE
DOCNO- medline/29734603

203 - TOXLINE
TI - Effects of lead, cadmium, arsenic, and mercury co-exposure on children's
intelligence quotient in an industrialized area of southern China.
AU - Pan S
AD - State Key Laboratory of Organic Geochemistry and Guangdong Key Laboratory of
Environmental Protection and Resources Utilization, Guangzhou Institute of
Geochemistry, and Guangzhou Key Laboratory of Environmental Pollution and Health
Risk Assessment, Chinese Academy of Sciences, Guangzhou 510640, China; Guangdong
Provincial Center for Disease Control and Prevention, Guangzhou 511430, China;
University of Chinese Academy of Sciences, Beijing 100049, China.
AU - Lin L
AD - Guangdong Provincial Center for Disease Control and Prevention, Guangzhou
511430, China.
AU - Zeng F
AD - Center for Disease Control and Prevention of Qujiang District, Shaoguan
512100, China.
AU - Zhang J
AD - Guangdong Provincial Center for Disease Control and Prevention, Guangzhou
511430, China.
AU - Dong G
AD - Department of Preventive Medicine, School of Public Health, Sun Yat-sen
University, Guangzhou 510080, China.
AU - Yang B
AD - Department of Preventive Medicine, School of Public Health, Sun Yat-sen
University, Guangzhou 510080, China.
AU - Jing Y
AD - School of Environment, Guangzhou Key Laboratory of Environmental Exposure and
Health, and Guangdong Key Laboratory of Environmental Pollution and Health, Jinan
University, Guangzhou 510632, China.
AU - Chen S
AD - State Key Laboratory of Organic Geochemistry and Guangdong Key Laboratory of
Environmental Protection and Resources Utilization, Guangzhou Institute of
Geochemistry, and Guangzhou Key Laboratory of Environmental Pollution and Health
Risk Assessment, Chinese Academy of Sciences, Guangzhou 510640, China.
AU - Zhang G
AD - State Key Laboratory of Organic Geochemistry and Guangdong Key Laboratory of
Environmental Protection and Resources Utilization, Guangzhou Institute of
Geochemistry, and Guangzhou Key Laboratory of Environmental Pollution and Health
Risk Assessment, Chinese Academy of Sciences, Guangzhou 510640, China.
AU - Yu Z
AD - State Key Laboratory of Organic Geochemistry and Guangdong Key Laboratory of
Environmental Protection and Resources Utilization, Guangzhou Institute of
Geochemistry, and Guangzhou Key Laboratory of Environmental Pollution and Health
Risk Assessment, Chinese Academy of Sciences, Guangzhou 510640, China.
AU - Sheng G
AD - State Key Laboratory of Organic Geochemistry and Guangdong Key Laboratory of
Environmental Protection and Resources Utilization, Guangzhou Institute of
Geochemistry, and Guangzhou Key Laboratory of Environmental Pollution and Health
Risk Assessment, Chinese Academy of Sciences, Guangzhou 510640, China.
AU - Ma H
AD - State Key Laboratory of Organic Geochemistry and Guangdong Key Laboratory of
Environmental Protection and Resources Utilization, Guangzhou Institute of
Geochemistry, and Guangzhou Key Laboratory of Environmental Pollution and Health
Risk Assessment, Chinese Academy of Sciences, Guangzhou 510640, China. Electronic
address: mahuimin@gig.ac.cn.
SO - Environ Pollut. 2018, Apr; 235:47-54. [Environmental pollution (Barking,
Essex : 1987)]
AB - Exposure to metal(loid)s can lead to adverse effects on nervous system in
children. However, little is known about the possible interaction effects
of simultaneous exposure to multiple metal(loid)s on children's
intelligence. In addition, relationship between blood lead concentrations
( < 100&#8239;&mu;g/L) and the intelligence of children over 5 years
needs further epidemiological evidence. We recruited 530 children aged
9-11 years, including 266 living in a town near an industrialized area and
264 from another town in the same city in South China as a reference. The
levels of lead (Pb), cadmium (Cd), arsenic (As) and mercury (Hg) in blood
(BPb, BCd, BAs, BHg) and urine (UPb, UCd, UAs, UHg) were assessed, as well
as children's intelligence quotient (IQ). A significant decrease in IQ
scores was identified in children from the industrialized town
(p&#8239; < &#8239;.05), who had statistically higher geometric mean
concentrations of BPb, BCd, UPb, UCd and UHg (65.89, 1.93, 4.04, 1.43 and
0.37&#8239;&mu;g/L, respectively) compared with children from the
reference town (37.21, 1.07, 2.14, 1.02 and 0.30&#8239;&mu;g/L,
respectively, p&#8239; < &#8239;.05). After adjusting confounders, only
BPb had a significant negative association with IQ (B&#8239;=&#8239;-0.10,
95% confidence interval: -0.15 to -0.05,
p&#8239; < &#8239;.001), which indicated that IQ decreased 0.10 points
when BPb increased 1&#8239;&mu;g/L. Significant negative interactions
between BAs and BHg, positive interaction between UPb and UCd on IQ were
observed (p&#8239; < &#8239;.10), and BPb < 100&#8239;&mu;g/L still
negatively affected IQ (p&#8239; < &#8239;.05). Our findings suggest that
although only BPb causes a decline in children's IQ when simultaneously
exposed to these four metal(loid)s at relatively low levels, interactions
between metal(loid)s on children's IQ should be paid special attention,
and the reference standard in China of 100&#8239;&mu;g/L BPb for children
above 5 years old should be revised.
KW - Arsenic
KW - Cadmium
KW - Intelligence quotient scores
KW - Lead
KW - Mercury
RN - 00BH33GNGH
RN - 2P299V784P
RN - FXS1BY2PGL
RN - N712M78A8G
LA - eng
IS - 1873-6424 (Electronic)
PT - Journal Article
TA - Environ Pollut
YR - 2018
DATE- 20180523
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Environmental pollution (Barking, Essex : 1987)
EDAT- 20171220
STAT- MEDLINE
DOCNO- medline/29274537

204 - TOXLINE
TI - Investigation on stability and leaching characteristics of mixtures of
biogenic arsenosulphides and iron sulphides formed under reduced
conditions.
AU - Shakya AK
AD - Department of Civil Engineering, Indian Institute of technology Guwahati,
781039, India.
AU - Rajput P
AD - Atomic &amp; Molecular Physics Division, Bhabha Atomic Research Centre,
Trombay, Mumbai, 400085, India.
AU - Ghosh PK
AD - Department of Civil Engineering, Indian Institute of technology Guwahati,
781039, India. Electronic address: pkghosh@iitg.ernet.in.
SO - J Hazard Mater. 2018, Jul 05; 353:320-328. [Journal of hazardous
materials]
AB - Arsenic is removed from aqueous phase through precipitation as
arsenosulphides and/or co-precipitation and adsorption on iron sulphides.
Studies were carried out to ascertain the stability of reduced biogenic
arsenic and iron sulphide precipitates formed in an attached growth
reactor (AGR) through a series of experiments based on Toxicity
Characteristic Leaching Procedure (TCLP), aging and long term leaching
tests. About half of the AGR was initially added with waste activated
carbon (WAC) to support the growth of mixed microbial consortia and used
for treatment of arsenic and iron contaminated simulated groundwater. The
X-ray diffraction (XRD), X-ray absorption near-edge structure (XANES) and
extended X-ray absorption fine structure (EXAFS) spectroscopy results
indicated that the biosolids were mainly composed of arsenosulphides and
iron sulphides. While TCLP and aging tests were conducted in anoxic as
well as oxic conditions with the aim to evaluate stability of biomass
containing biogenic sulphides, long term leaching test was conducted
through supply of aerated distilled water to evaluate the stability of
spent WAC as well. Results generated from the research indicate that the
concentration of leached arsenic never exceeded 123&#8239;&mu;g/L under
all conditions tested, thus biosolids not imposing an environmental
hazard.
KW - Arsenic
KW - Biogenic sulphides
KW - Iron
KW - Stability
KW - TCLP
LA - eng
IS - 1873-3336 (Electronic)
PT - Journal Article
TA - J Hazard Mater
YR - 2018
DATE- 20180615
CI - Copyright &copy; 2018 Elsevier B.V. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Journal of hazardous materials
EDAT- 20180416
STAT- In-Data-Review
DOCNO- medline/29680690

205 - TOXLINE
TI - Opportunities and challenges in the use of mineral nutrition for
minimizing arsenic toxicity and accumulation in rice: A critical review.
AU - Saifullah
AD - Department of Environmental Health, College of Public Health, Imam
Abdulrahman Bin Faisal University, Dammam, Saudi Arabia; Institute for Research and
Medical Consultation (IRMC), Imam Abdulrehman Bin Faisal University, P.O. Box 1982,
Dammam, 31441, Saudi Arabia. Electronic address: smferoz@uod.edu.sa.
AU - Dahlawi S
AD - Department of Environmental Health, College of Public Health, Imam
Abdulrahman Bin Faisal University, Dammam, Saudi Arabia; Institute for Research and
Medical Consultation (IRMC), Imam Abdulrehman Bin Faisal University, P.O. Box 1982,
Dammam, 31441, Saudi Arabia.
AU - Naeem A
AD - Institute of Soil and Environmental Sciences, University of Agriculture,
Faisalabad, Pakistan; Nuclear Institute of Agriculture and Biology, Jhang Road,
Faisalabad, Pakistan.
AU - Iqbal M
AD - Department of Botany, Jamia Hamdard (Hamdard University), New Delhi, India.
AU - Farooq MA
AD - Institute of Soil and Environmental Sciences, University of Agriculture,
Faisalabad, Pakistan.
AU - Bibi S
AD - Institute of Soil and Environmental Sciences, University of Agriculture,
Faisalabad, Pakistan.
AU - Rengel Z
AD - School of Agriculture and Environment, University of Western Australia, 35
Stirling Highway, Perth, WA, 6009, Australia.
SO - Chemosphere. 2018, Mar; 194:171-188. [Chemosphere]
AB - Growing rice on arsenic (As)-contaminated soil or irrigating with
As-contaminated water leads to significant accumulation of As in grains.
Moreover, rice accumulates more As into grains than other cereal crops.
Thus, rice consumption has been identified as a major route of human
exposure to As in many countries. Inorganic As species are carcinogenic
and could pose a considerable health risk to humans even at low dietary
concentration. Genotypic variation and concentration of nutrients such as
iron, manganese, phosphate, sulfur and silicon are the two main factors
that affect As accumulation in rice grains. Therefore, in addition to
better growth and yield of plants, application of specific nutrients in
optimum quantities offers an added benefit of decreasing As content in
rice grains. These nutrient elements influence speciation of As in
rhizosphere, compete with As for root uptake and interfere with As
translocations to the shoot and ultimately accumulation in grains. This
papers critically appraises the methods, forms and rate of application,
mechanisms and extent of efficiency of different mineral nutrients in
decreasing As accumulation in rice grains.
KW - Arsenic
KW - Grain accumulation
KW - Immobilization
KW - Plant nutrition
KW - Uptake
RN - N712M78A8G
LA - eng
IS - 1879-1298 (Electronic)
PT - Journal Article
PT - Review
TA - Chemosphere
YR - 2018
DATE- 20180402
CI - Copyright &copy; 2017 Elsevier Ltd. All rights reserved.
CITO- NLM
CS - England
CSET- IM
FJT - Chemosphere
EDAT- 20171205
STAT- MEDLINE
DOCNO- medline/29202269

206 - TOXLINE
TI - Arsenic-containing hydrocarbons: effects on gene expression, epigenetics,
and biotransformation in HepG2 cells.
AU - M�ller SM
AD - Heinrich-Stockmeyer Foundation, Parkstra&szlig;e 44-46, 49214, Bad
Rothenfelde, Germany.
AU - Finke H
AD - Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-
Allee 114-116, 14558, Nuthetal, Germany.
AU - Ebert F
AD - Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-
Allee 114-116, 14558, Nuthetal, Germany.
AU - Kopp JF
AD - Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-
Allee 114-116, 14558, Nuthetal, Germany.
AU - Schumacher F
AD - Department of Molecular Biology, University of Duisburg-Essen, Hufelandstr.
55, 45122, Essen, Germany.
AU - Kleuser B
AD - Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-
Allee 114-116, 14558, Nuthetal, Germany.
AU - Francesconi KA
AD - Institute of Chemistry, NAWI Graz, University of Graz, Universitaetsplatz 1,
8010, Graz, Austria.
AU - Raber G
AD - Institute of Chemistry, NAWI Graz, University of Graz, Universitaetsplatz 1,
8010, Graz, Austria.
AU - Schwerdtle T
AD - Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-
Allee 114-116, 14558, Nuthetal, Germany. tanja.schwerdtle@uni-potsdam.de.
SO - Arch Toxicol. 2018, May; 92(5):1751-1765. [Archives of toxicology]
AB - Arsenic-containing hydrocarbons (AsHCs), a subgroup of arsenolipids found
in fish and algae, elicit substantial toxic effects in various human cell
lines and have a considerable impact on cellular energy levels. The
underlying mode of action, however, is still unknown. The present study
analyzes the effects of two AsHCs (AsHC 332 and AsHC 360) on the
expression of 44 genes covering DNA repair, stress response, cell death,
autophagy, and epigenetics via RT-qPCR in human liver (HepG2) cells. Both
AsHCs affected the gene expression, but to different extents. After
treatment with AsHC 360, flap structure-specific endonuclease 1 (FEN1) as
well as xeroderma pigmentosum group A complementing protein (XPA) and
(cytosine-5)-methyltransferase 3A (DNMT3A) showed time- and
concentration-dependent alterations in gene expression, thereby indicating
an impact on genomic stability. In the subsequent analysis of epigenetic
markers, within 72 h, neither AsHC 332 nor AsHC 360 showed an impact
on the global DNA methylation level, whereas incubation with AsHC 360
increased the global DNA hydroxymethylation level. Analysis of cell
extracts and cell media by HPLC-mass spectrometry revealed that both AsHCs
were considerably biotransformed. The identified metabolites include not
only the respective thioxo-analogs of the two AsHCs, but also several
arsenic-containing fatty acids and fatty alcohols, contributing to our
knowledge of biotransformation mechanisms of arsenolipids.
KW - Arsenic speciation
KW - Arsenic-containing hydrocarbons
KW - Arsenolipids
KW - Gene expression
KW - Global DNA methylation
KW - Metabolism
LA - eng
IS - 1432-0738 (Electronic)
PT - Journal Article
TA - Arch Toxicol
YR - 2018
DATE- 20180522
CITO- NLM
CS - Germany
FJT - Archives of toxicology
EDAT- 20180330
STAT- In-Data-Review
DOCNO- medline/29602950

207 - TOXLINE
TI - Effects of kinetin on plant growth and chloroplast ultrastructure of two
Pteris species under arsenate stress.
AU - Li Q
AD - Faculty of Environmental Science and Engineering, Kunming University of
Science and Technology, Kunming 650500, Yunnan, China.
AU - Wang H
AD - Faculty of Environmental Science and Engineering, Kunming University of
Science and Technology, Kunming 650500, Yunnan, China. Electronic address:
whb1974@126.com.
AU - Wang H
AD - Faculty of Environmental Science and Engineering, Kunming University of
Science and Technology, Kunming 650500, Yunnan, China.
AU - Zheng W
AD - Faculty of Environmental Science and Engineering, Kunming University of
Science and Technology, Kunming 650500, Yunnan, China.
AU - Wu D
AD - Faculty of Environmental Science and Engineering, Kunming University of
Science and Technology, Kunming 650500, Yunnan, China.
AU - Wang Z
AD - Faculty of Environmental Science and Engineering, Kunming University of
Science and Technology, Kunming 650500, Yunnan, China.
SO - Ecotoxicol Environ Saf. 2018, Aug 30; 158:37-43. [Ecotoxicology and
environmental safety]
AB - Cytokinins (CTKs) are effective in alleviating abiotic stresses on plants,
but little information is available regarding the effects of CTKs on
arsenic (As) accumulation and changes of chloroplast ultrastructure in
plants with different As-accumulating ability. Here a hydroponic
experiment was designed to evaluate the effects of different concentration
of kinetin (KT, 0-40&#8239;mg/L) on growth and chloroplast ultrastructure
of As hyperaccumulator Pteris cretica var. nervosa and
non-hyperaccumulator Pteris ensiformis treated by 5&#8239;mg/L arsenate
for 14 days. The growth parameters, As accumulation, contents of
photosynthetic pigments and chloroplast ultrastructure were examined. The
results showed that KT promoted the growth of two plants, and
significantly increased As accumulation and translocation in P. cretica
var. nervosa and P. ensiformis at 5 and 20&#8239;mg/L, respectively.
Additionally, the contents of chlorophyll a and carotenoid in two plants
showed no significant difference at 20&#8239;mg/L KT compared to the
control. Chloroplast ultrastructure of P. cretica var. nervosa was
integral with KT application. Comparatively, the swollen chloroplasts were
increased, plasmolysis appeared, and chloroplast grana slice layers and
stroma lamellas were clearly separated or distorted at 5&#8239;mg/L KT in
P. ensiformis. The length and width of chloroplasts in P. cretica var.
nervosa were significantly increased with KT addition compared to the
control. However, the length of chloroplasts in P. ensiformis was
significantly decreased but their width showed no significant change.
Furthermore, the deterioration of chloroplast ultrastructure in P.
ensiformis was ameliorated by 40&#8239;mg/L KT. These results suggested
that KT increased As accumulation and was beneficial to maintain the
photosynthetic pigments for a good growth of plants. Therefore, KT could
maintain and reorganize the ultrastructure integrality of As-stressed
chloroplasts to some extent for the two plants, especially at high
concentration.
KW - Arsenic
KW - Chloroplast
KW - Cytokinins
KW - Kinetin
KW - Ultrastructure
LA - eng
IS - 1090-2414 (Electronic)
PT - Journal Article
TA - Ecotoxicol Environ Saf
YR - 2018
DATE- 20180522
CI - Copyright &copy; 2018 Elsevier Inc. All rights reserved.
CITO- NLM
CS - Netherlands
FJT - Ecotoxicology and environmental safety
EDAT- 20180412
STAT- In-Process
DOCNO- medline/29656162

208 - TOXLINE
TI - Purifying arsenic and fluoride-contaminated water by a novel
graphene-based nanocomposite membrane of enhanced selectivity and
sustained flux.
AU - Pal M
AD - Environment and Membrane Technology Laboratory, Department of Chemical
Engineering, National Institute of Technology, Durgapur, 713209, India.
AU - Mondal MK
AD - Environment and Membrane Technology Laboratory, Department of Chemical
Engineering, National Institute of Technology, Durgapur, 713209, India.
AU - Paine TK
AD - Department of Inorganic Chemistry, Indian Association for the Cultivation of
Science, Jadavpur, Kolkata, 700032, India.
AU - Pal P
AD - Environment and Membrane Technology Laboratory, Department of Chemical
Engineering, National Institute of Technology, Durgapur, 713209, India.
parimalpal2000@yahoo.com.
SO - Environ Sci Pollut Res Int. 2018, Mar 29. [Environmental science and
pollution research international]
AB - A novel graphene-based nanocomposite membrane was synthesized by
interfacial polymerization (IP) through chemical bonding of the graphene
oxide (GO) layer to polyethersulfone surface. Detailed characterization of
the composite membrane through AFM, SEM, ATR-FTIR, XRD analysis, and Raman
spectroscopy indicates strong potential of the membrane in highly
selective removal of the toxic contaminants like arsenic and fluoride
while permeating the essential minerals like calcium and magnesium. This
makes the membrane suitable for production of safe drinking water from
contaminated water. The membrane applied in a flat-sheet cross-flow module
succeeded in removal of more than 98% arsenic and around 80% fluoride from
contaminated water while selectively retaining the useful calcium and
magnesium minerals in drinking water. A sustained pure water flux of
around 150 LMH (liter per square meter per hour) during operation over
long hours ( > &thinsp;150 h) with only 3-5% drop in flux indicates
antifouling character of the membrane module.
KW - Arsenic removal
KW - Enhanced selectivity
KW - Novel nanocomposite membrane
KW - Sustained flux
KW - Water contaminant
LA - eng
IS - 1614-7499 (Electronic)
PT - Journal Article
TA - Environ Sci Pollut Res Int
YR - 2018
DATE- 20180329
CITO- NLM
CS - Germany
FJT - Environmental science and pollution research international
EDAT- 20180329
STAT- Publisher
DOCNO- medline/29594887

209 - TOXLINE
TI - Prenatal arsenic exposure and dietary folate and methylcobalamin
supplementation alter the metabolic phenotype of C57BL/6J mice in a
sex-specific manner.
AU - Huang MC
AD - Curriculum in Toxicology, School of Medicine, University of North Carolina at
Chapel Hill, Chapel Hill, NC, USA.
AU - Douillet C
AD - Department of Nutrition, Gillings School of Global Public Health, University
of North Carolina at Chapel Hill, CB# 7461, Chapel Hill, NC, USA.
AU - Dover EN
AD - Curriculum in Toxicology, School of Medicine, University of North Carolina at
Chapel Hill, Chapel Hill, NC, USA.
AU - St�blo M
AD - Department of Nutrition, Gillings School of Global Public Health, University
of North Carolina at Chapel Hill, CB# 7461, Chapel Hill, NC, USA.
styblo@med.unc.edu.
SO - Arch Toxicol. 2018, Jun; 92(6):1925-1937. [Archives of toxicology]
AB - Inorganic arsenic (iAs) is an established environmental diabetogen. The
link between iAs exposure and diabetes is supported by evidence from adult
human cohorts and adult laboratory animals. The contribution of prenatal
iAs exposure to the development of diabetes and underlying mechanisms are
understudied. The role of factors that modulate iAs metabolism and
toxicity in adults and their potential to influence diabetogenic effects
of prenatal iAs exposure are also unclear. The goal of this study was to
determine if prenatal exposure to iAs impairs glucose metabolism in mice
and if maternal supplementation with folate and methylcobalamin (B12) can
modify this outcome. C57BL/6J dams were exposed to iAs in drinking water
(0, 100, and 1000 &micro;g As/L) and fed a folate/B12 adequate or
supplemented diet from before mating to birth of offspring. After birth,
dams and offspring drank deionized water and were fed the folate/B12
adequate diet. The metabolic phenotype of offspring was assessed over the
course of 14 weeks. Male offspring from iAs-exposed dams fed the
folate/B12-adequate diet developed fasting hyperglycemia and insulin
resistance. Maternal folate/B12 supplementation rescued this phenotype but
had only marginal effects on iAs metabolism in dams. The diabetogenic
effects of prenatal iAs exposure in male offspring were not associated
with changes in global DNA methylation in the liver. Only minimal effects
of prenatal iAs exposure or maternal supplementation were observed in
female offspring. These results suggest that prenatal iAs exposure impairs
glucose metabolism in a sex-specific manner and that maternal folate/B12
supplementation may improve the metabolic phenotype in offspring. Further
studies are needed to identify the mechanisms underlying these effects.
KW - Arsenic
KW - Diabetes
KW - Dietary supplementation
KW - Folate
KW - Methylcobalamin
KW - Prenatal exposure
KW - Vitamin
LA - eng
IS - 1432-0738 (Electronic)
PT - Journal Article
TA - Arch Toxicol
YR - 2018
DATE- 20180615
CITO- NLM
CS - Germany
FJT - Archives of toxicology
EDAT- 20180502
STAT- In-Data-Review
DOCNO- medline/29721587

210 - TOXLINE
TI - Rates and processes affecting As speciation and mobility in lake sediments
during aging.
AU - Lock A
AD - Environmental and Life Sciences Graduate Program, Trent University,
Peterborough, Ontario, Canada. Electronic address: alock@laurentian.ca.
AU - Wallschl�ger D
AD - School of the Environment, Department of Chemistry and Water Quality Centre,
Trent University, Peterborough, Ontario, Canada.
AU - Belzile N
AD - Department of Chemistry, Laurentian University, Sudbury, Ontario, Canada.
AU - Spiers G
AD - School of the Environment, Departments of Earth Sciences and Biology,
Laurentian University, Sudbury, Ontario, Canada.
AU - Gueguen C
AD - School of the Environment and Chemistry Department, Trent University,
Peterborough, Ontario, Canada.
SO - J Environ Sci (China). 2018, Apr; 66:338-347. [Journal of environmental
sciences (China)]
AB - Sediments from an arsenic (As) contaminated groundwater vent site were
used to investigate As(III) binding, transformation and redistribution in
native and iron oxide amended lake sediments using aging spiked batch
reactions and a sequential extraction procedure that maintains As(V) and
As(III) speciation. In the native sediments, fractionation analysis
revealed that 10% of the spiked As(III) remained intact after a 32-day
aging experiment and was predominantly adsorbed to the strongly sorbed
(NH4H2PO4 extractable) and amorphous Fe oxide bound (H3PO4 extractable)
fractions. Kinetic modelling of the experimental results allowed
identifying the dominant reaction path for depletion of dissolved As(III)
to As(III) absorbed on to the solid phase, followed by oxidation in the
solid phase. Arsenite was initially adsorbed primarily to the easily
exchangeable fraction ((NH4)2SO4 extractable), then rapidly transformed
into As(V) and redistributed to the strongly sorbed and amorphous Fe oxide
bound fractions. Oxidation of As(III) in recalcitrant fractions was less
efficient. The iron oxide amendments illustrated the controls that iron
oxides can have on As(III) binding and transformation rates. In goethite
amended samples As(III) oxidation was faster and primarily occurred in the
strongly sorbed and amorphous Fe oxide bound fractions. In these samples,
19.3&mu;g Mn was redistributed (compared to the native sediment) from the
easily exchangeable and crystalline Fe oxide bound fractions to the
strongly sorbed and amorphous Fe oxide bound fractions, indicating that
goethite may act as a catalyst for Mn(II) oxidation, thereby producing
sorbed Mn(III/IV), which then appears to be involved in rapidly oxidizing
As(III).
KW - Arsenite
KW - Fractionation
KW - Modelling
KW - Oxidation
KW - Redistribution
RN - N712M78A8G
LA - eng
IS - 1001-0742 (Print)
PT - Journal Article
TA - J Environ Sci (China)
YR - 2018
DATE- 20180419
CI - Copyright &copy; 2017. Published by Elsevier B.V.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Journal of environmental sciences (China)
EDAT- 20170510
STAT- MEDLINE
DOCNO- medline/29628103

211 - TOXLINE
TI - Genetic characterization, micropropagation, and potential use for arsenic
phytoremediation of Dittrichia viscosa (L.) Greuter.
AU - Guarino F
AD - Department of Chemistry and Biology "A. Zambelli" University of Salerno, Via
Giovanni Paolo II, 132, 84084 Fisciano, Salerno, Italy. Electronic address:
fguarino@unisa.it.
AU - Conte B
AD - Department of Science and Technology, University of Sannio, Via Port'Arsa,
11, 82100 Benevento, Italy. Electronic address: bbconte@yahoo.it.
AU - Improta G
AD - Department of Public Health, University of Napoli Federico II, Via Pansini 5,
80131 Napoli, Italy. Electronic address: ing.improta@gmail.com.
AU - Sciarrillo R
AD - Department of Science and Technology, University of Sannio, Via Port'Arsa,
11, 82100 Benevento, Italy. Electronic address: sciarrillo@unisannio.it.
AU - Castiglione S
AD - Department of Chemistry and Biology "A. Zambelli" University of Salerno, Via
Giovanni Paolo II, 132, 84084 Fisciano, Salerno, Italy. Electronic address:
scastiglione@unisa.it.
AU - Cicatelli A
AD - Department of Chemistry and Biology "A. Zambelli" University of Salerno, Via
Giovanni Paolo II, 132, 84084 Fisciano, Salerno, Italy. Electronic address:
acicatelli@unisa.it.
AU - Guarino C
AD - Department of Science and Technology, University of Sannio, Via Port'Arsa,
11, 82100 Benevento, Italy. Electronic address: guarino@unisannio.it.
SO - Ecotoxicol Environ Saf. 2018, Feb; 148:675-683. [Ecotoxicology and
environmental safety]
AB - In the last decade, many scientists have focused their attention on the
search for new plant species that can offer improved capacities to reclaim
polluted soils and waters via phytoremediation. In this study, seed
batches from three natural populations of Dittrichia viscosa, harvested in
rural, urban, and industrial areas of central and southern Italy, were
used to: (i) evaluate the genetic and morphological diversity of the
populations; (ii) develop an efficient protocol for in-vitro propagation
from seedling microcuttings; (iii) achieve optimal acclimatization of
micropropagated plants to greenhouse conditions; (iv) test the response to
arsenic (As) soil contamination of micropropagated plants. The genetic
biodiversity study, based on Random Amplification of Polymorphic DNA
(RAPD), as well as the morphometric analysis of 20 seedlings from each
population revealed some degree of differentiation among populations.
Based on these data, the most biodiverse plants from the three populations
(10 lines each) were clonally multiplied by micropropagation using
microcuttings of in-vitro grown seedlings. Three culture media were tested
and Mureshige and Skoog medium was chosen for both seedling growth and
micropropagation. The micropropagated plants responded well to greenhouse
conditions and over 95% survived the acclimatization phase. Four clones
were tested for their capacity to grow on soil spiked with NaAsO2 and to
absorb and accumulate the metalloid. All clones tolerated up to 1.0mg As.
At the end of the trial (five weeks), As was detectable only in leaves of
As-treated plants and concentration varied significantly among clones. The
amount of As present in plants (leaves) corresponded to ca. 0.10-1.7% of
the amount supplied. However, As was no longer detectable in soil
suggesting that the metalloid was taken up, translocated and probably
phytovolatilized.
KW - Arsenic pollution
KW - Dittrichia viscosa
KW - Genetic study
KW - In vitro culture
KW - Phytotechnology
RN - N712M78A8G
LA - eng
IS - 1090-2414 (Electronic)
PT - Journal Article
TA - Ecotoxicol Environ Saf
YR - 2018
DATE- 20180518
CI - Copyright &copy; 2017 Elsevier Inc. All rights reserved.
CITO- NLM
CS - Netherlands
CSET- IM
FJT - Ecotoxicology and environmental safety
EDAT- 20171121
STAT- MEDLINE
DOCNO- medline/29172148

212 - TOXLINE
TI - Comparison of DGT with traditional extraction methods for assessing
arsenic bioavailability to Brassica chinensis in different soils.
AU - Dai Y
AD - College of Natural Resources and Environment, Northwest A&amp;F University,
Yangling, 712100, China; Key Laboratory of Plant Nutrition and Agri-environment in
Northwest China, Ministry of Agriculture, China.
AU - Nasir M
AD - College of Natural Resources and Environment, Northwest A&amp;F University,
Yangling, 712100, China; Key Laboratory of Plant Nutrition and Agri-environment in
Northwest China, Ministry of Agriculture, China.
AU - Zhang Y
AD - College of Natural Resources and Environment, Northwest A&amp;F University,
Yangling, 712100, China.
AU - Gao J
AD - College of Natural Resources and Environment, Northwest A&amp;F University,
Yangling, 712100, China; Key Laboratory of Plant Nutrition and Agri-environment in
Northwest China, Ministry of Agriculture, China.
AU - Lv Y
AD - College of Natural Resources and Environment, Northwest A&amp;F University,
Yangling, 712100, China; Key Laboratory of Plant Nutrition and Agri-environment in
Northwest China, Ministry of Agriculture, China.
AU - Lv J
AD - College of Natural Resources and Environment, Northwest A&amp;F University,
Yangling, 712100, China; Key Laboratory of Plant Nutrition and Agri-environment in
Northwest China, Ministry of Agriculture, China. Electronic address:
ljlll@nwsuaf.edu.cn.
SO - Chemosphere. 2018, Jan; 191(10):183-189. [Chemosphere]
AB - Several predictive models and methods have been used for heavy metals
bioavailability