C H A P T E R
4
Antioxidant Capacity of Green
Tea (Camellia sinensis)
Richard S. Bruno*, Joshua A. Bomser*, Mario G. Ferruzzi
*Department of Human Sciences, The Ohio State University, Columbus, OH, USA,
Department of Food Science, Purdue University, West Lafayette, IN, USA
CHAPTER POINTS
G  reen tea (Camellia sinensis) is rich in
polyphenolic catechins.
Epidemiological evidence supports the
consumption of green tea for lowering the
risks of cardiovascular disease (CVD) and
nonalcoholic fatty liver disease (NAFLD).
Green tea catechins have antioxidant and anti-
inflammatory activities that mitigate oxidative
stress responses implicated in CVD and NAFLD.
The antioxidant activities of green tea catechins
are likely to be mediated through indirect
mechanisms given the poor bioavailability of
dietary catechins.
Anti-inflammatory activities of green tea,
mediated in part by its antioxidant activities,
reduce nuclear factor kappa B (NFB) activation
and NFB-dependent pro-inflammatory
responses.
Green tea, when consumed at reasonable dietary
intake levels, appears to be safe in humans.
INTRODUCTION
The tea plant (Camellia sinensis) is grown in more than
30 countries, and is the most commonly consumed pre-
pared beverage worldwide. Even in the United States
where tea is not a native crop, total tea imports are esti-
mated to exceed 281 million pounds with sales up to $8.2
billion each year (www.teausa.com). Of the major tea
varieties, green tea is minimally processed, compared to
Processing and Impact on Antioxidants in Beverages
http://dx.doi.org/10.1016/B978-0-12-404738-9.00004-0 2014 Elsevier Inc. All rights reserved.
black tea, such that its high content of monomeric cat-
echins (Figure 4.1) is preserved. Accumulating evidence
from epidemiologic studies as well as controlled studies
invitro and invivo have generated substantial support
for the health benefits of green tea and its catechins in
mitigating the risk of chronic disease. The health ben-
efits of green tea are often attributed to the antioxidant
and anti-inflammatory activities of its catechins that
effectively regulate oxidative stress responses leading to
chronic disease. Paradoxically, green tea catechins have
relatively low bioavailability due to their instability in
near-neutral pH environments, their high involvement
in phase III efflux pathways that limit enterocyte absorp-
tion, and their rapid rate of biotransformation by phase
II xenobiotic metabolism. This suggests that the direct
free radical scavenging activities of green tea catechins
observed invitro may not fully represent the activities
invivo, such that the health benefits of green tea cate-
chins are potentially mediated through indirect antioxi-
dant activities. This chapter will discuss the indirect and
direct antioxidant activities of green tea and its catechins.
Specifically, it will describe their bioavailability and anti-
oxidant activities within the framework of chronic dis-
orders, such as obesity, cardiovascular disease (CVD),
and nonalcoholic fatty liver disease (NAFLD), that are
characterized by a pathogenesis of significant oxidative
stress.
GREEN TEA AND ITS COMPOSITION
Green tea is a minimally processed product that is
produced from freshly harvested leaves of the tea plant
(Camellia sinensis) (Figure 4.2). Unlike other tea products,
such as black and oolong teas, the tea leaves intended
33
34 4. ANTIOXIDANT CAPACITY OF GREEN TEA

FIGURE 4.1 Chemical structures of the

predominant catechins found in green tea.
Green tea catechins include both catechin
and epicatechin forms. Gallated catechins
include epigallocatechin gallate (EGCG),
gallocatechin gallate (GCG), epicatechin
gallate (ECG), and catechin gallate (CG).
The major non-gallated catechins are epi-
catechin (EC), catechin (C), epigallocat-
echin (EGC), and gallocatechin (GC).

PAN-FRYING OR ROLLING AND GREEN

STEAMING DRYING TEA

FRESHLY
WITHERING BRUISE TEA PARTIAL PAN FRYING OOLONG
HARVESTED
LEAF EDGES FERMENTATION OR DRYING TEA
TEA LEAVES

FULL BLACK
ROLLING DRYING
FERMENTATION TEA

FIGURE 4.2 Post-harvest processing of green, black, and oolong teas. Common teas, including green tea, oolong tea, and black tea, are derived
from the same tea plant (Camellia sinensis). Freshly harvested tea leaves are withered, and those directed for the production of green tea are then
immediately fried or steamed, and subsequently rolled and dried. In contrast, oolong and black tea are fermented prior to drying. Steaming or
frying in combination with the lack of fermentation of tea leaves preserves the naturally occurring catechins that are otherwise oxidized during
the production of oolong and black tea.

for green tea are harvested, immediately withered, and
steamed or pan fried to rapidly inactivate polyphenol
oxidase and preserve its fresh character and monomeric
polyphenol profile (Frei and Higdon, 2003). Thus, these
timely post-harvest processes preserve the catechins that
would have been otherwise oxidized. In fact, catechins
account for approximately one-third of the dry weight
of the tea leaves, with the eight major green tea catechins
being epigallocatechin gallate (EGCG), gallocatechin
gallate (GCG), epicatechin gallate (ECG), catechin gal-
late (CG), epigallocatechin (EGC), gallocatechin (GC),
epicatechin (EC) and catechein (C) (Figure 4.1) (Neil-
son and Ferruzzi, 2011). Of these compounds, EGCG,
EGC, ECG, and EC are the most common in tea leaves
and brewed tea products (Graham, 1992). EGCG is the
most abundant representing 50% of the total catechin
content (Figure 4.3) and exhibits the greatest antioxidant
activity. In contrast, partially fermented oolong tea and
fully fermented black tea have high levels of theaflavins
and thearubigins, but a total catechin content that can
be more than 50% lower than that of green tea. Regard-
less of the catechin quantity and distribution, green,
black, and oolong teas have similar caffeine content with
4050mg of caffeine per freshly brewed cup of tea.
BIOAVAILABILITY OF GREEN TEA
CATECHINS
The potential bioactivity of green tea catechins invivo
is contingent upon their bioavailability and rates of bio-
transformation and elimination. Oral administration
of green tea catechins to rats results in their intestinal
absorption and subsequent delivery to the liver via the

1. COMPOSITION AND CHARACTERIZATION OF ANTIOXIDANTS

 IN VITRO ANTIOXIDANT ACTIVITIES OF CATECHINS
portal vein (Okushio etal., 1996). The pharmacokinetics
of green tea catechins have received considerable study
resulting in the understanding that: (1) catechin concen-
trations in the circulation peak at 15M within 24h
following oral ingestion of tea or purified catechins; (2)
plasma half-lives of catechins are relatively short, rang-
ing from 0.75 to 4.0h following green tea ingestion; (3)
those catechins that are absorbed undergo extensive bio-
transformation through phase II xenobiotic metabolism
resulting in numerous catechin metabolites that are gluc-
uronidated, sulfated, and/or methylated; and (4) efflux
transport proteins such as p-glycoprotein and multidrug
resistance proteins (MRP)-1 and -2 limit enterocyte reten-
tion and/or apical-to-basolateral transport of catechins
(Feng, 2006). For example, biotransformation of EGCG
and EGC by catechol-O-methyltransferase (COMT)
results in the formation of 4-O-methyl-()-EGC and
4-O-methyl-()-EGCG or 4,4-O-dimethyl-()-EGCG
(Lambert etal., 2007). However, the extent to which
methylation is a major route of catechin biotransforma-
tion is unclear since COMT activity in liver cytosolic
fractions from rats is greater than those from humans.
Catechin methylation is also mediated in a concentra-
tion-dependent manner such that dimethylated EGCG is
the major product when EGCG is at low concentrations
whereas monomethylated metabolites of EGCG are more
abundant when EGCG is administered at higher doses.
Unsurprisingly, mice co-administered EGCG with an
inhibitor of glucuronidation had greater bioavailability
of EGCG by increasing its intestinal absorption (Lambert
etal., 2004). Similarly, studies invitro that co-treat cells
with chemical inhibitors of MRP along with EGCG dem-
onstrate greater uptake and retention of EGCG (Hong
etal., 2003). These studies emphasize that phase II and III
xenobiotic metabolism occurring in the small intestines
substantially regulate catechin bioavailability.
Further complicating the bioavailability of catechins
is their susceptibility to auto-oxidation at near-neutral
1. COMPOSITION AND CHARACTERIZATION OF ANTIOXIDANTS
35
FIGURE 4.3 Analysis and distribution of catechins
and caffeine found in green, black, and oolong teas.
HPLC analysis of freshly brewed teas in 250mL of boiled
water shows that green tea is especially high in epigal-
locatechin gallate (EGCG) compared to black and oolong
teas. Green tea also contains appreciably higher levels of
epigallocatechin (EGC), epicatechin gallate (ECG), and
epicatechin (EC). In total, the catechin content of freshly
brewed green tea is more than 3-times higher than that of
black or oolong tea.
pH (Neilson and Ferruzzi, 2011). This implicates not
only low-acid foods/beverages, but also the human
intestines as a potential site of conversion of monomers
to dimerized products. Indeed, simulated gastric and
intestinal digestion of EGCG, EGC, and ECG results
in substantial degradation of these compounds. For
example, degradation of EGCG resulted in the forma-
tion of the auto-oxidation homodimers theasinensins A
and D. Collectively, the oral bioavailability of green tea
catechins is rather low resulting from a combination of
instability during gastrointestinal digestion, relatively
poor absorption, and rapid metabolism and elimination.
This has resulted in controversy over whether green tea
catechins from dietary sources can exert antioxidant
activity invivo similar to the direct reactive oxygen/
nitrogen species scavenging activities observed invitro.
In addition, studies are currently underway that are con-
sidering the health-promoting bioactivities of specific
catechin metabolites that result from phase II xenobiotic
metabolism. It should be noted that the unique acidic
environment of the stomach may provide stabilization
of tea catechins invivo and promote their uptake and/or
bioactivity in the gastric epithelium. Interestingly, epide-
miological evidence also suggests that tea consumption
is correlated with reduced risk of gastric cancer. The sta-
bilization, uptake, and antioxidant/anti-inflammatory
effects of green tea and its catechins during the gastric
phase of digestion are not well understood but are cur-
rently the focus of ongoing research efforts.
IN VITRO ANTIOXIDANT ACTIVITIES
OF CATECHINS
The propensity of green tea catechins to exert anti-
oxidant activity by chemically reducing an oxidative
species (i.e., free radical) is related to their one-electron
reduction potential. Compounds having lower electron
36 4. ANTIOXIDANT CAPACITY OF GREEN TEA

FIGURE 4.4 Detoxification of reactive oxygen species. Aerobic organisms are exposed to oxygen, which becomes oxidized to superoxide in
response an initiating event of oxidative stress. Green tea protects against oxidative stress, in part, by upregulating the activities of superoxide
dismutases (Cu/Zn- and Mn-SOD) that detoxify superoxide to hydrogen peroxide. Subsequently, green tea-mediated increases in the activities of
catalase and glutathione peroxidase (GSH-Px) result in the detoxification of hydrogen peroxide.

reduction potentials are more likely to participate in
hydrogen or electron exchange, thereby resulting in
reduction of the reactive species and simultaneous oxi-
dation of the reducing agent. Green tea catechins (Figure
4.1) have reduction potentials in the range of 430570mV
suggesting that they have antioxidant activities similar
to -tocopherol (480mV), but somewhat less than that of
ascorbic acid (280mV) (Jovanovic etal., 1996, 1998; Frei
and Higdon, 2003).
Studies invitro have provided clear evidence that
green tea catechins protect against reactive oxygen spe-
cies (ROS). Studies invitro taking advantage of a super-
oxide-generating system showed that green tea extract
readily scavenged superoxide at a high rate (Nakagawa
and Yokozawa, 2002). Direct comparison of purified
green tea catechins in this free radical generating sys-
tem indicated that catechins having a galloyl moeity
have higher scavenging activities than those lacking
this structure. This implies that EGC, GC, EGCG and
ECG (Figure 4.1) have greater antioxidant scavenging
against ROS in comparison to the non-gallated forms (C,
EC). Likewise, studies utilizing electron spin resonance
technology demonstrated that green tea catechins also
scavenge peroxyl radicals as well as singlet oxygen (Guo
etal., 1999).
Green tea catechins also effectively scavenge reac-
tive nitrogen species (RNS) (Paquay etal., 2000). Invitro,
catechins were shown to scavenge nitric oxide and per-
oxynitrite (Haenen etal., 1997; Haenen and Bast, 1999).
Moreover, green tea, containing 4.8-times more cat-
echins than black tea, was 5-times more effective than
black tea in scavenging nitric oxide (Paquay etal., 2000).
A separate line of evidence also indicates that green tea
catechins chelate redox-active transition metals, such as
free iron and copper, supporting that these polyphenols
may mitigate metal-catalyzed ROS generation (Frei and
Higdon, 2003; Higdon and Frei, 2003). Taken together,
green tea has the potential to protect against an array of
ROS and RNS, and these effects are mediated, in part,
through its polyphenolic catechins.
Contrasting these antioxidant activities are stud-
ies showing that EGCG exerts pro-oxidant activities at
high doses. Indeed, in studies, mice that were provided
a single high dose of EGCG intragastrically were shown
to exhibit hepatotoxicity characterized by substantially
higher levels of the liver injury marker plasma alanine
aminotransferase, moderate to severe hepatic necrosis,
and a dramatically lower survival rate (Lambert etal.,
2010). Livers from these mice also had higher levels of
lipid peroxidation markers and pro-inflammatory cyto-
kines. Thus, physiologically relevant intakes of green
tea or its catechins are seemingly beneficial to health
outcomes with respect to mitigating oxidative stress.
In contrast, supraphysiological doses that bypass tight
homeostatic controls otherwise limiting catechin bio-
availability at the intestinal level readily trigger oxida-
tive stress and inflammatory responses that increase the
risk of morbidity and mortality.
PHYSIOLOGIC ANTIOXIDANT
ACTIVITIES
Despite catechins having similar reduction potentials
to other dietary antioxidants, and clear invitro evidence
showing their direct scavenging of ROS/RNS, the extent
to which green tea catechins exhibit direct antioxidant
activity invivo remains controversial. This is largely
related to the lack of analytical methods available to
detect and accurately quantify oxidized catechin forms
from biological matrices. Because of these limitations,
studies invivo have primarily focused on indirect antiox-
idant activities of green tea catechins. Studies in animal
models suggest that green tea protects against oxidative
stress-mediated antioxidant depletion, including liver
and erythrocyte glutathione (Skrzydlewska etal., 2002;
Oz etal., 2005) and circulating -tocopherol (Nanjo etal.,
1993). Antioxidant activities of green tea catechins also
recycle -tocopheroxyl radicals back to their reduced
-tocopherol form (Zhou etal., 2005), which is an impor-
tant mechanism for maintaining vitamin E status (Bruno
etal., 2006). Antioxidant activities of green tea catechins
also lower oxidative stress by increasing activities of
enzymatic antioxidants, which lowers the magnitude of
ROS by enhancing their detoxification (Figure 4.4). For
example, green tea increases the activities of copper/
zinc- and manganese superoxide dismutase found in the
cytosol and mitochondria, respectively, which facilitates
the detoxification of superoxide radical to hydrogen per-
oxide (Park etal., 2011). Green tea also increases catalase

1. COMPOSITION AND CHARACTERIZATION OF ANTIOXIDANTS

 Safety of Green Tea
and glutathione peroxidase, which function to degrade
hydrogen peroxide to water (Agarwal etal., 1993; Park
etal., 2011). These protective effects are thought to occur
by upregulating nuclear factor erythoid 2-related factor
2 (Nrf2) (Shen etal., 2005), a cytoprotective transcrip-
tion factor regulating gene expression for antioxidant
defenses and xenobiotic metabolism.
PROTECTIVE ASPECTS OF GREEN TEA
IN OBESITY AND RELATED DISORDERS
Green tea and its catechins exert anti-obesity activi-
ties that promote weight loss, and also protect against
oxidative and metabolic insults that otherwise con-
tribute to obesity-related disorders. The role of green
tea in weight management stems largely from work in
rodents because of the relative ease of controlling criti-
cal variables in these models in comparison to human
populations. Green tea and its catechins may protect
against obesity by reducing intestinal lipid absorption
(Koo and Noh, 2007). In humans, a beverage containing
green tea catechins, caffeine, and calcium increased 24h
energy expenditure (Rudelle etal., 2007). This is comple-
mented by studies in rodents showing that green tea or
its catechins lower body mass without affecting energy
intake, and that decreases in body mass are attributed
to lower adiposity (Masterjohn and Bruno, 2012). Green
tea or its catechins also decrease body mass by increas-
ing -oxidation via the upregulation of the expression of
genes from this energy-producing pathway and reduc-
tion of the expression of lipogenic genes. These effects of
green tea are likely, at least in part, to reduce oxidative
stress secondary to decreases in obesity.
Epidemiological evidence from Japan suggests that
5 cups per day of green tea lowers the risk of CVD-
related mortality by 26% and that 10 cups each day
may protect against livery injury (Imai and Nakachi,
1995; Kuriyama etal., 2006). Although these health ben-
efits remain unclear, obese mice provided with green
tea extract are protected from liver steatosis by lowering
lipogenic gene expression concurrent with decreases in
hepatic lipid peroxidation and increases in antioxidant
defenses (Park etal., 2011). Green tea supplementation
also reduces 4-hydroxynonenal in livers from obese
mice having NAFLD in association with lowering the
activity of nicotinamide adenine dinucleotide phos-
phate (NADPH) oxidase and expression of inducible
nitric oxide synthase (iNOS) (Chung etal., 2012). Thus,
green tea-dependent reductions in lipid peroxidation,
an early event implicated in both CVD and NAFLD,
are likely mediated through antioxidant activities that
increase ROS detoxification, anti-inflammatory activities
that suppress ROS/RNS generation, and its hypolipid-
emic activities that reduce the availability of oxidizable
1. COMPOSITION AND CHARACTERIZATION OF ANTIOXIDANTS
37
substrate. Similar to these effects in rodents, chronic
ingestion of green tea in humans with metabolic syn-
drome was shown to reduce circulating levels of malo-
ndialdehyde and hydroxynonenal (Basu etal., 2010).
However, future work is needed to determine whether
green tea reduces lipid peroxidation in humans through
direct or indirect antioxidant activities.
Anti-inflammatory activities of green tea have received
considerable attention because of its role in regulating
oxidative stress. Supplementation of green tea to rats
fed a high-fat diet lowered hepatic and adipose nuclear
factor kappa B (NFB) binding activity and expression
of pro-inflammatory cytokines by decreasing the phos-
phorylation of IB (Park etal., 2012). The mechanism
by which green tea inhibits NFB activation is not fully
understood and is likely mediated through overlap-
ping mechanisms that converge at the phosphorylation
of IB. Antioxidant activities of green tea that increase
hepatic glutathione appear to suppress NFB activation
(Park etal., 2012). Because green tea increases mRNA
expression of glutamate cysteine ligase (GCL) (Park
etal., 2011), a Nrf2-dependent gene, catechins likely pro-
mote Nrf2-dependent antioxidant activities that attenu-
ate ROS, and in turn, lower NFB activation. It is also
likely that the protective effects occur extracellularly by
reducing toll-like receptor-4 (TLR4) signaling that other-
wise increases NFB activation (Byun etal., 2012). That
green tea reduces TLR4-dependent inflammation sug-
gests the possibility that catechins reduce inflammation
by inhibiting bacterial endotoxin translocation from the
small intestine, potentially by preventing intestinal tight
junction barrier dysfunction (Watson etal., 2004).
SAFETY OF GREEN TEA
Several dozen anecdotal and case reports of idiosyn-
cratic hepatotoxicity in humans have questioned the
safety of green tea (Masterjohn and Bruno, 2012). While
studies in mice demonstrated that single administration
of EGCG at the equivalent of 20 cups of green tea in
humans results in hepatotoxicity (Lambert etal., 2010),
the findings of epidemiologic studies suggest that green
tea at 510 cups/day is associated with lower risks of
liver-related morbidity and CVD-related mortality (Imai
and Nakachi, 1995; Kuriyama etal., 2006). Thus, it is pos-
sible that substantial inter-individual differences exist
for catechin metabolism and/or that only supraphysi-
ological doses are hepatotoxic. Moreover, because most
case reports have been linked to dietary supplements,
and dechallenge/rechallenge evidence is only pro-
vided in relatively fewer reports, product contamination
remains a possibility to explain the acute hepatotoxicity
of green tea (Masterjohn and Bruno, 2012). In contrast,
intervention studies in otherwise healthy overweight
38 4. ANTIOXIDANT CAPACITY OF GREEN TEA
men indicated that dietary supplementation of green tea
polyphenols at 714 mg/day for 3 weeks did not affect
numerous clinical chemistries for liver and kidney func-
tion (Frank etal., 2009). In addition, although a systemic
review performed by the United States Pharmacopeia
was unable to identify a tolerable upper limit for safety,
it concluded that green tea and green tea extracts are
safe when used and manufactured appropriately (Sarma
etal., 2008).
CONCLUSIONS
The 2010 Dietary Guidelines for Americans recom-
mend an increase in the consumption of plant-based
foods that are nutrient dense, low in energy, and rich
in bioactive compounds in order to reduce the risk of
chronic disease. Although a beverage, green tea is clearly
a functional food rich in bioactive polyphenolic catechins
that protect against chronic disorders that are character-
ized by high levels of inflammation and oxidative stress.
Although much of the available evidence regarding the
beneficial effects of green tea has been provided by stud-
ies invitro and in experimental model systems, controlled
studies in humans are accumulating. In some cases,
these clinical interventions are providing experimental
evidence that directly support the profound health rela-
tions observed in epidemiological studies. More work
is clearly needed to identify optimal intake levels and
define safe strategies that optimize catechin bioavailabil-
ity and bioefficacy. In addition, further work is warranted
to consider the potential bioactivity of catechin forms that
evade absorptive processes and accumulate in the lower
gastrointestinal tract. The accumulation of catechins,
their metabolites, and products of oxidation in the colon
have the potential to favorably augment colonic health.
This will certainly be an active area of investigation in
the coming years as considerable technological advances
have made it possible to more fully characterize and
profile the microbiome in response to dietary bioactive
components.
Acknowledgments
This work was supported by state and federal funds appropriated to
The Ohio State University Ohio Agricultural Research and Develop-
ment Center (to RSB and JAB), and grants from the USDI-NRI to RSB
(CSREES 2007-02303) and the Food Innovation Center at The Ohio
State University (to RSB and JAB).
References
Agarwal, R., Katiyar, S.K., Khan, S.G., Mukhtar, H., 1993. Protection
against ultraviolet B radiation-induced effects in the skin of SKH-1
hairless mice by a polyphenolic fraction isolated from green tea.
Photochem. Photobiol. 58, 695700.
1. COMPOSITION AND CHARACTERIZATION OF ANTIOXIDANTS
Basu, A., Sanchez, K., Leyva, M.J., Wu, M., Betts, N.M., Aston, C.E.,
Lyons, T.J., 2010. Green tea supplementation affects body weight,
lipids, and lipid peroxidation in obese subjects with metabolic syn-
drome. J. Am. Coll. Nutr. 29, 3140.
Bruno, R.S., Leonard, S.W., Atkinson, J., Montine, T.J., Ramakrishnan,
R., Bray, T.M., Traber, M.G., 2006. Faster plasma vitamin E disap-
pearance in smokers is normalized by vitamin C supplementation.
Free Radic. Biol. Med. 40, 689697.
Byun, E.B., Choi, H.G., Sung, N.Y., Byun, E.H., 2012. Green tea poly-
phenol epigallocatechin-3-gallate inhibits TLR4 signaling through
the 67-kDa laminin receptor on lipopolysaccharide-stimulated den-
dritic cells. Biochem. Biophys. Res. Commun. 426, 480485.
Chung, M.Y., Park, H.J., Manautou, J.E., Koo, S.I., Bruno, R.S., 2012.
Green tea extract protects against nonalcoholic steatohepatitis in
ob/ob mice by decreasing oxidative and nitrative stress responses
induced by proinflammatory enzymes. J. Nutr. Biochem. 23,
361367.
Feng, W.Y., 2006. Metabolism of green tea catechins: an overview. Curr.
Drug. Metab. 7, 755809.
Frank, J., George, T.W., Lodge, J.K., Rodriguez-Mateos, A.M., Spencer,
J.P., Minihane, A.M., Rimbach, G., 2009. Daily consumption of an
aqueous green tea extract supplement does not impair liver func-
tion or alter cardiovascular disease risk biomarkers in healthy men.
J. Nutr. 139, 5862.
Frei, B., Higdon, J.V., 2003. Antioxidant activity of tea polyphenols
invivo: evidence from animal studies. J. Nutr. 133, 3275S3284S.
Graham, H.N., 1992. Green tea composition, consumption, and poly-
phenol chemistry. Prev. Med. 21, 334350.
Guo, Q., Zhao, B., Shen, S., Hou, J., Hu, J., Xin, W., 1999. ESR study on
the structure-antioxidant activity relationship of tea catechins and
their epimers. Biochim. Biophys. Acta. 1427, 1323.
Haenen, G.R., Bast, A., 1999. Nitric oxide radical scavenging of flavo-
noids. Methods Enzymol. 301, 490503.
Haenen, G.R., Paquay, J.B., Korthouwer, R.E., Bast, A., 1997. Peroxyni-
trite scavenging by flavonoids. Biochem. Biophys. Res. Commun.
236, 591593.
Higdon, J.V., Frei, B., 2003. Tea catechins and polyphenols: health
effects, metabolism, and antioxidant functions. Crit. Rev. Food Sci.
Nutr. 43, 89143.
Hong, J., Lambert, J.D., Lee, S.H., Sinko, P.J., Yang, C.S., 2003. Involve-
ment of multidrug resistance-associated proteins in regulating
cellular levels of ()-epigallocatechin-3-gallate and its methyl
metabolites. Biochem. Biophys. Res. Commun. 310, 222227.
Imai, K., Nakachi, K., 1995. Cross sectional study of effects of drink-
ing green tea on cardiovascular and liver diseases. BMJ 310,
693696.
Jovanovic, S.V., Steenken, S., Hara, Y., Simic, M.G., 1996. Reduction
potentials of flavonoid and model phenoxyl radicals. Which ring
in flavonoids is responsible for antioxidant activity? J. Chem. Soc.
Perkin Trans. 2: Phys. Organ. Chem., 24972504.
Jovanovic, S.V., Steenken, S., Simic, M.G., Hara, Y., 1998. Antioxidant
properties of flavonoids: reduction potentials and electron transfer
reactions of flavonoid radicals. Antioxid. Health Dis. 7, 137161.
Koo, S.I., Noh, S.K., 2007. Green tea as inhibitor of the intestinal absorp-
tion of lipids: potential mechanism for its lipid-lowering effect. J.
Nutr. Biochem. 18, 179183.
Kuriyama, S., Shimazu, T., Ohmori, K., Kikuchi, N., Nakaya, N.,
Nishino, Y., Tsubono, Y., Tsuji, I., 2006. Green tea consumption and
mortality due to cardiovascular disease, cancer, and all causes in
Japan: the Ohsaki study. JAMA 296, 12551265.
Lambert, J.D., Hong, J., Kim, D.H., Mishin, V.M., Yang, C.S., 2004. Pip-
erine enhances the bioavailability of the tea polyphenol ()-epigal-
locatechin-3-gallate in mice. J. Nutr. 134, 19481952.
Lambert, J.D., Kennett, M.J., Sang, S., Reuhl, K.R., Ju, J., Yang, C.S.,
2010. Hepatotoxicity of high oral dose ()-epigallocatechin-3-gal-
late in mice. Food Chem. Toxicol. 48, 409416.
 References
Lambert, J.D., Sang, S., Yang, C.S., 2007. Biotransformation of green tea
polyphenols and the biological activities of those metabolites. Mol.
Pharm. 4, 819825.
Masterjohn, C., Bruno, R.S., 2012. Therapeutic potential of green tea in
nonalcoholic fatty liver disease. Nutr. Rev. 70, 4156.
Nakagawa, T., Yokozawa, T., 2002. Direct scavenging of nitric oxide
and superoxide by green tea. Food Chem. Toxicol. 40, 17451750.
Nanjo, F., Honda, M., Okushio, K., Matsumoto, N., Ishigaki, F., Ishigami,
T., Hara, Y., 1993. Effects of dietary tea catechins on alpha-tocopherol
levels, lipid peroxidation, and erythrocyte deformability in rats fed
on high palm oil and perilla oil diets. Biol. Pharm. Bull. 16, 11561159.
Neilson, A.P., Ferruzzi, M.G., 2011. Influence of formulation and pro-
cessing on absorption and metabolism of flavan-3-ols from tea and
cocoa. Annu. Rev. Food Sci. Technol. 2, 125151.
Okushio, K., Matsumoto, N., Kohri, T., Suzuki, M., Nanjo, F., Hara, Y.,
1996. Absorption of tea catechins into rat portal vein. Biol. Pharm.
Bull. 19, 326329.
Oz, H.S., Chen, T.S., McClain, C.J., de Villiers, W.J., 2005. Antioxidants
as novel therapy in a murine model of colitis. J. Nutr. Biochem. 16,
297304.
Paquay, J.B., Haenen, G.R., Stender, G., Wiseman, S.A., Tijburg, L.B.,
Bast, A., 2000. Protection against nitric oxide toxicity by tea.
J. Agric. Food Chem. 48, 57685772.
Park, H.J., DiNatale, D.A., Chung, M.Y., Park, Y.K., Lee, J.Y., Koo, S.I.,
OConnor, M., Manautou, J.E., Bruno, R.S., 2011. Green tea extract
attenuates hepatic steatosis by decreasing adipose lipogenesis and
enhancing hepatic antioxidant defenses in ob/ob mice. J. Nutr. Bio-
chem. 22, 393400.
1. COMPOSITION AND CHARACTERIZATION OF ANTIOXIDANTS
39
Park, H.J., Lee, J.Y., Chung, M.Y., Park, Y.K., Bower, A.M., Koo, S.I.,
Giardina, C., Bruno, R.S., 2012. Green tea extract suppresses NFkap-
paB activation and inflammatory responses in diet-induced obese
rats with nonalcoholic steatohepatitis. J. Nutr. 142, 5763.
Rudelle, S., Ferruzzi, M.G., Cristiani, I., Moulin, J., Mace, K., Ache-
son, K.J., Tappy, L., 2007. Effect of a thermogenic beverage on
24-hour energy metabolism in humans. Obes. (Silver Spring) 15,
349355.
Sarma, D.N., Barrett, M.L., Chavez, M.L., Gardiner, P., Ko, R., Mahady,
G.B., Marles, R.J., Pellicore, L.S., Giancaspro, G.I., Low Dog, T.,
2008. Safety of green tea extracts: a systematic review by the US
Pharmacopeia. Drug Saf. 31, 469484.
Shen, G., Xu, C., Hu, R., Jain, M.R., Nair, S., Lin, W., Yang, C.S., Chan,
J.Y., Kong, A.N., 2005. Comparison of ()-epigallocatechin-3-gallate
elicited liver and small intestine gene expression profiles between
C57BL/6J mice and C57BL/6J/Nrf2 (/) mice. Pharm. Res. 22,
18051820.
Skrzydlewska, E., Ostrowska, J., Stankiewicz, A., Farbiszewski, R.,
2002. Green tea as a potent antioxidant in alcohol intoxication.
Addict. Biol. 7, 307314.
Watson, J.L., Ansari, S., Cameron, H., Wang, A., Akhtar, M., McKay,
D.M., 2004. Green tea polyphenol ()-epigallocatechin gallate
blocks epithelial barrier dysfunction provoked by IFN-gamma
but not by IL-4. Am. J. Physiol. Gastrointest Liver Physiol. 287,
G954961.
Zhou, B., Wu, L.M., Yang, L., Liu, Z.L., 2005. Evidence for alpha-
tocopherol regeneration reaction of green tea polyphenols in SDS
micelles. Free Radic. Biol. Med. 38, 7884.