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The Role of Antioxidants on Oxidative Stress in

Diabetes Mellitus

Article in The Journal of pharmacy technology: jPT: official publication of the Association of Pharmacy Technicians ·
September 2010
DOI: 10.1177/875512251002600507

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The Role of Antioxidants on Oxidative Stress
in Diabetes Mellitus
LUNAWATI L BENNETT AND TERESA SEEFELDT

Objective: To evaluate the literature on the role of oxidative stress in diabetes mellitus and search sources of
promising antioxidants: pharmaceutical, dietary supplements, or investigational compounds.
Data Sources: A preliminary literature search of PubMed (1966-June 2010) was performed, using the MeSH
database when possible, with the terms antioxidants, oxidative stress, antioxidants and diabetes, insulin
resistance, and antioxidants and diabetic neuropathy. Bibliographies of all articles retrieved were also
reviewed.
Study Selection and Data Extraction: All studies published in English with data describing the role of
antioxidants and oxidative stress in humans or animals were included.
Data Synthesis: Oxidative stress plays a significant role in the pathogenesis of diabetes and insulin resistance.
α-Lipoic acid (ALA) and N-acetylcysteine (NAC) were shown to be potent antioxidants in several clinical
trials, including the SYDNEY trial, SYDNEY 2 trial, and ALADIN III study, in diabetes with albuminuria,
and in women with polycystic ovarian syndrome.
Conclusions: ALA and NAC supplementations, along with a well-balanced diet rich in fruits and vegetables
containing antioxidants, provide a potential approach in the treatment of diabetes associated with oxidative
stress.
J Pharm Technol 2010;26:293-9.

Many patients use dietary supplements, including vita-
mins, minerals, and herbal products, on a daily basis to
improve their health. Pharmacists can educate patients
about the proper use of dietary supplements and the role
of these supplements on their health.
Oxidative stress plays a significant role in the patho-
genesis of numerous disorders including insulin resis-
tance, cardiovascular disease, inflammation, and neu-
rodegenerative diseases.1 Oxidative stress results from
the imbalance between production and removal of reac-
tive oxygen species (ROS) or reactive nitrogen species
(RNS).2 These reactive molecules include superoxide rad-
ical, peroxynitryl radical, hydroxyl radical, and hydrogen
peroxide. ROS and RNS are generated from the mito-
chondrial electron transport chain including cytochrome
P450, the NADP (H) oxidase, and nitric oxide synthase3
and are produced continually in all cells to support nor-
mal cellular function.2 Under normal physiologic condi-
tions, approximately 0.1%-5% of oxygen that enters the
body is reduced to ROS and RNS, and the remaining is
used for metabolic processes.2 ROS and RNS can be
made from endogenous or exogenous sources, but ineffi-
cient removal of ROS and RNS could result in pathologic
conditions.2 ROS and RNS are highly reactive com-
pounds with the potential to damage various cellular
components including DNA, proteins, lipids, carbohy-
drates, and cell membranes.2 This can lead to the forma-
tion of secondary products that can be as damaging as
the initial ROS.4 Furthermore, overproduction of ROS
and RNS can overwhelm the endogenous antioxidant
systems, such as superoxide dismutase, and reduce glu-
tathione.5 Therefore, oxidative stress is the consequence
of the generation of excess ROS, RNS, and other free rad-
icals beyond the capacity of the body to defend against
them, and it represents the imbalance between excess for-
mation and impaired removal of those reactive mole-
cules.2
Endogenous glutathione levels in human tissues nor-
mally range from 0.1 to 10 mM, with the highest amount
in the liver, spleen, kidney, lens, erythrocytes, and leuko-
cytes.5 When glutathione becomes oxidized, glutathione
disulfide is formed.6 Glutathione is an important molecule

LUNAWATI L BENNETT PhD PharmD, Assistant Professor of Pharmaceutical Science, Lloyd Gregory School of Pharmacy, Palm
Beach Atlantic University, West Palm Beach, FL; and TERESA SEEFELDT PhD PharmD, Assistant Professor of Pharmaceutical Sci-
ence, College of Pharmacy, South Dakota State University, Brookings, SD. Correspondence: Dr. Bennett, Lunawati_bennett@pba.edu
Reprints/Online Access: https://www.hwbooks.com/jpt/abstracts/volume26/september-october/order_article.html
Conflict of interest: Authors reported none

JPHARMTECHNOL.COM SEPTEMBER/OCTOBER 2010 I VOLUME 26 I J PHARM TECHNOL 293

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and serves as a cofactor for enzymes that require thiol-re-
ducing equivalents.7 The glutathione/glutathione disul-
fide ratio is used as an indicator of the cell’s redox state,
and the proper ratio is crucial for homeostasis, cellular
performance, and survival.6,7
Because of the role of oxidative stress in disease devel-
opment, there has been significant interest in using an-
tioxidants in the prevention and treatment of disorders
that have an oxidative stress component. This review fo-
cuses on the role of the antioxidants α-lipoic acid (ALA)
and N-acetylcysteine (NAC) and natural compounds on
oxidative stress in patients with diabetes mellitus, with
data obtained from a PubMed search from 1966 to June
2010.
Oxidative Stress and Diabetes Mellitus
In patients with diabetes, sustained hyperglycemia can
have micro- and macrovascular complications throughout
the body, including diabetic sensorimotor polyneuropa-
thy (DSPN), retinopathy, and kidney disease. While pa-
tients with type 1 diabetes do not produce insulin, those
with type 2 diabetes produce limited insulin or have in-
sulin resistance. Insulin resistance, defined as the body’s
inadequate response to a given amount of insulin, has
been known to be exacerbated by environmental factors
such as obesity, hyperglycemia, aging, and oxidative
stress.8-10
Four biochemical pathways by which hyperglycemia
could lead to overproduction of ROS and RNS have been
proposed: (1) increased influx of glucose through the
polyol pathway in which glucose is reduced to sorbitol,
which can cause depletion of NADPH and glutathione;
(2) increased formation of advanced glycation end prod-
ucts, which causes an increase in proinflammatory medi-
ators; (3) activation of the protein kinase C pathway,
which causes the expression of proinflammatory genes;
and (4) increased shunting of excess glucose to the hex-
osamine pathway, causing increased transcription of
proinflammatory cytokines.11,12 In the presence of excess
glucose, endothelial cells generate ROS and RNS at the
mitochondrial level13 through several pathways, includ-
ing NADPH oxidase, xanthine oxidase, lipoxygenase
and cyclooxygenase, and microsomal enzymes.14 Under
physiologic conditions, an increase in reactive molecules
and free radicals does not necessarily cause oxidative
stress since it is usually counterbalanced by the endoge-
nous antioxidant network (ie, glutathione , superoxide
dismutase, and catalase).15,16 When the production of re-
active molecules exceeds the capacity for their clearance,
a redox imbalance occurs, causing oxidative stress lead-
ing to cellular damage.16 Other endogenous antioxidant
systems include proteins (ie, thioredoxin, metallo-
thionein), and low-molecular-weight antioxidants (ie,
ALA, ascorbate, α-tocopherol).16
A randomized, double-blind clinical trial involving 20
patients with type 2 diabetes examined the relationship
294 J PHARM TECHNOL I VOLUME 26 I SEPTEMBER/OCTOBER 2010
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between oxidative stress and diabetes mellitus.17 Patients
were 53-56 years old, with body mass index (BMI) of 24-
26 kg/m2, and had been diagnosed with diabetes for 6-8
years. They were given either low- or high-carbohydrate
meals designed to produce different levels of postprandi-
al hyperglycemia to allow researchers to study how
blood glucose level affects plasma oxidative status and
low-density lipoprotein cholesterol (LDL-C) oxidation.
Plasma glucose, insulin, cholesterol, triglycerides, non-es-
terified fatty acids, malondialdehyde (marker of lipid
peroxidation), and TRAP (assay to measure antioxidant
capacity in the plasma) were measured. Patients with
high-carbohydrate meals had a significantly higher level
of glucose and malondialdehyde (p < 0.01) and lower
TRAP value. The lower TRAP value suggests that post-
prandial hyperglycemia may contribute to oxidative
stress in patients with diabetes, providing a possible link
between oxidative stress and pathogenesis of diabetes. A
limitation of the study is the small sample size. Oxidative
damage also has been implicated in the development of
some of the complications of diabetes.18,19
α-Lipoic Acid
Antioxidants are compounds that are able to trap
ROS, RNS, and other free radicals and, therefore, are ca-
pable of reducing oxidative damage.20 Ideal antioxidants
should fulfill several criteria: good absorption, easy con-
version in cells and tissues to a usable form, ability to in-
teract with other antioxidants, and low toxicity.21
ALA, known also as thioctic acid, is an 8-carbon fatty
acid with 2 thiol groups. It is synthesized in plants, ani-
mals, and humans and functions as a cofactor in several
mitochondrial enzyme complexes responsible for oxida-
tive glucose metabolism and cellular energy produc-
tion.20,22 ALA is unique among natural antioxidants in its
ability to fulfill the ideal antioxidant criteria due to its
ability to scavenge ROS; to regenerate endogenous an-
tioxidants including glutathione, ascorbate, and α-toco-
pherol ; and to chelate metal, which in turn results in re-
duction of ROS production.23 ALA has good absorption,
is easy to be converted in cells and tissues into a usable
form, is able to interact with other antioxidants, and has
low toxicity.21
Unlike other antioxidants that are either water soluble
(ascorbate) or lipid soluble (α-tocopherol), ALA has both
hydrophilic and hydrophobic properties that allow its ac-
tion in the cytosol, the plasma membrane, serum, and
lipoproteins.23 ALA supplementation significantly in-
creased scavenging of ROS and RNS in plasma of
healthy volunteers,24 increased glutathione synthesis in
aged animals,25 decreased oxidative damage in vitro,26
and inhibited excess metals accumulation (iron and cop-
per) in animal models.27
In healthy humans, endogenous plasma levels of ALA
are reported to be 1-25 ng/mL, and its reduced form, di-
hydrolipoic acid (DHLA), is 33-145 ng/mL.28 DHLA has
JPHARMTECHNOL.COM

superior antioxidant activity when compared with
ALA.23 Furthermore, DHLA is superior to glutathione,
ascorbate, α-tocopherol, or coenzyme Q10 as an antioxi-
dant.23 Healthy humans are able to synthesize enough
endogenous ALA in the liver and other tissues to meet
their needs of ALA/DHLA. In patients with diabetes,
however, additional ALA may be needed from exoge-
nous sources such as foods high in ALA or from oral
supplementation of ALA.23 Food sources that are high in
ALA include spinach, broccoli, tomatoes, and, to a lesser
degree, peas, brussels sprouts, and rice bran.23 ALA has
been prescribed in Germany as a pharmacologic antioxi-
dant for more than 30 years for the treatment of dia-
betes-induced neuropathy.28,29 ALA is safe, well tolerat-
ed, and efficacious. In the US, ALA is available over the
counter as a dietary supplement (200-600 mg). ALA is
generally taken on an empty stomach 1 hour before or 2
hours after eating since food intake can reduce its
bioavailability.30
L 181 patients with type 2 diabetes.33 Patients were 46-68
ALA is safe, well tolerated,
and efficacious.
M it differed significantly from the placebo group (all p <
A cross-sectional, randomized, double-blind, placebo-
controlled study was conducted in 107 patients with type
1 or type 2 diabetes who had poor glycemic control with
albuminuria.31 Patients were 25-67 years old, with
hemoglobin A1c (A1C) values from 6.5-10.5%, and had
diabetes for 5-32 years. Patients were divided into 3
groups based on their A1C (<7.5%, 7.5-9.5%, and >9.5%)
and urinary albumin concentrations (<20, 20-200 [mi-
croalbuminuria], and >200 [macroalbuminuria] mg/L)
and were given placebo or oral ALA 600 mg/day for 3
months. Patients who received ALA supplementation
showed lower plasma lipid hydroperoxide (ROOH) lev-
els and lower ROOH (α-tocopherol/cholesterol) ratio (p
< 0.0001). Using Pearson’s correlation test, the plasma
level ROOHs and the ROOH ratio were significantly
lower in the ALA group compared with the controls at
all A1C levels (p < 0.005) and at microalbuminuria and
macroalbuminuria levels (p < 0.005). With use of multi-
ple regression analysis, ALA was found to be the only
factor significantly predicting low ROOH levels and
ROOH ratio. Neither poor glycemic control nor the pres-
ence of micro- or macroalbuminuria prevented the an-
tioxidant effect of ALA.31 This study provides evidence
that supplementation with ALA significantly improves
the imbalance between oxidative stress and depleted an-
tioxidant defense, even in patients with poor glycemic
control and albuminuria.
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ROLE OF ANTIOXIDANTS ON OXIDATIVE STRESS IN DIABETES MELLITUS
A randomized, parallel, double-blind clinical study
known as the SYDNEY (Symptomatic Diabetic Neuropa-
thy) trial was conducted in 120 patients with type 1 or type
2 symptomatic stage 2 DSPN.32 Patients were 45-66 years
old, with a BMI of 24-35 kg/m2, and had diabetes for 12-25
years and DSPN for less than 1 year to 9 years. Half of the
group (n = 60) received intravenous ALA 600 mg 5 days
per week for 14 treatments; the other half received place-
bo. The primary endpoint of the total symptoms score,
which is the summation of the presence, severity, and du-
ration of lancinating pain, burning pain, and prickling,
was analyzed.32 The ALA group showed significant im-
provement of total symptoms score over the placebo
group, from baseline average of 5.7 to 1.8 (p < 0.001). This
study showed that intravenous ALA rapidly and positive-
ly improved neuropathic sensory symptoms in patients
with diabetes. Limitations of the study include the lack of
comparison of intravenous versus oral ALA efficacy and
report of adverse effects of intravenous ALA.
The SYDNEY trial 2, a multicenter, randomized, dou-
ble-blind, placebo-controlled study, was conducted in
years old, with a BMI of 23-34 kg/m2 and had diabetes
for 4-26 years. The patients were divided into 4 groups:
placebo and 3 treatment groups that received a once-dai-
ly oral dose of ALA 600 mg, 1200 mg, or 1800 mg for 5
weeks. The primary endpoint total symptoms score did
not differ significantly among the ALA groups; however,
0.05 vs placebo). Oral treatment with ALA for 5 weeks
improved DSPN, with dosing of 600 mg once daily pro-
viding optimum result. Higher doses of 1200 mg or 1800
mg can cause nausea, vomiting, and vertigo.33
The ALADIN (α-Lipoic Acid in Diabetic Neuropathy)
III study, a multicenter, randomized, double-blind, place-
bo-controlled trial, was conducted in 509 patients with type
2 diabetes.29 Patients were 49-64 years old, with a BMI of
25-34 kg/m2, had diabetes for 3-19 years, and had DSPN
for fewer than 3 months to 6 years. Patients were divided
into 3 groups: (1) placebo; (2) sequential treatment of intra-
venous ALA 600 mg once daily for 3 weeks followed by
oral ALA 600 mg 3 times daily for 6 months; and (3) intra-
venous ALA 600 mg once daily for 3 weeks followed by
placebo 3 times daily for 6 months. The primary endpoints
were total symptoms score for neuropathic symptoms in
the feet and the neuropathy impairment scores. After 7
months, the treatment groups and placebo group showed
no clinically significant differences in TSS value. The possi-
bility of insignificant result in total symptoms score value
was due to variability in scoring from 71 different centers
that conducted this study. Treatment groups, however,
were associated with a favorable effect on neuropathic
deficits, without significant adverse reactions.29
N-Acetylcysteine
NAC, a thiol-containing antioxidant, is a potent com-
pound with antimutagenic and anticarcinogenic proper-
SEPTEMBER/OCTOBER 2010 I VOLUME 26 I J PHARM TECHNOL 295
ties and has been used as an antidote for acetaminophen
overdose due to depletion in glutathione.9 NAC has also
been used to counteract metal poisoning and other con-
ditions associated with oxidative stress.34 It has potential
benefits as a potent antioxidant in clinical settings for
such things as management of coronary artery disease,
supplementation in cancer prevention, and therapy in
HIV-positive patients.35-37 NAC can elevate intracellular
glutathione levels and increase insulin sensitivity in lean
and obese women who have polycystic ovarian syn-
drome and are insulin resistant and hyperinsulinemic.1
A prospective, randomized, placebo-controlled study
was conducted in 37 women (6 lean, 31 obese) with poly-
cystic ovarian syndrome.38 Lean subjects were given
NAC 1.8 g/day and the massively obese received NAC 3
g/day, for 5-6 weeks. Six of the obese subjects served as
controls. The insulin area under the curve after oral glu-
cose tolerance test was decreased and peripheral insulin
sensitivity was increased after NAC supplementation (p
< 0.005). This study showed that NAC supplementation
has positive effects on insulin secretion, peripheral in-
sulin sensitivity, and changes in the lipid profile.38
L milk, or wheat products should not take NAC.
NAC supplementation has
positive effects on insulin
secretion, peripheral insulin
sensitivity, and changes in the
lipid profile.
M lic compounds found in fruits, vegetables, nuts, seeds, and
A randomized, double-blind, placebo-controlled,
small-scale study in 24 males with type 2 diabetes and
hypertension was conducted over 6 months.39 Half of the
subjects were given NAC 600 mg twice daily plus infu-
sions of L-arginine 1200 mg daily. The researchers admin-
istered L-arginine to improve endothelial function. NAC
was given to improve antioxidant defense and to in-
crease intracellular nitrosothiol concentration, which in-
creases nitric oxide availability. A decrease in systolic and
diastolic mean arterial blood pressure, total cholesterol,
oxidized LDL-C, and C-reactive protein was observed in
the treatment group. NAC plus L-arginine seems to be
potentially well-tolerated therapy in patients with type 2
diabetes by improving nitric oxide bioavailability via re-
duction of oxidative stress and increased nitric oxide pro-
duction.39 Limitations of the study include small sample
size and lack of comparison to determine whether the
decrease in oxidative stress was due to NAC alone or in
combination with L-arginine.
296 J PHARM TECHNOL I VOLUME 26 I SEPTEMBER/OCTOBER 2010
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A randomized, double-blind, placebo-controlled,
crossover study was conducted in 28 healthy males aged
18-32 years, with a BMI of 69-98 kg.40 The subjects were
divided into 3 groups: placebo, NAC 1200 mg supple-
mentation, or ALA 600 mg. Two daily doses of NAC or
ALA were given for 8 days. NAC and ALA groups had
significantly higher plasma total antioxidant status (TAS)
(p < 0.05) and lower levels of oxidative damage (p < 0.001)
compared with placebo, with a TAS increase 4-fold higher
in the NAC group than in the ALA group. NAC, but not
ALA, significantly elevated glutathione, hemoglobin,
hematocrit, and erythropoietin levels (p < 0.01). This study
showed that NAC and ALA have antioxidant action,
with NAC additionally improving parameters related to
red blood cell production in healthy subjects.40 This study
confirmed the result from another study that correlated
plasma TAS and hematologic response. ROS generation
can suppress erythropoietin synthesis, whereas antioxi-
dants can stimulate erythropoietin synthesis.41
NAC is available over the counter as a dietary supple-
ment (500-600 mg). It is safe at doses as high as 2800 mg
daily for 12 weeks in patients with cystic fibrosis.42 It can
be taken with or without food, with minor adverse ef-
fects such as headache. People with allergies to eggs,
Natural Compounds
Diets rich in fruits and vegetables with antioxidant
properties can reduce or delay the onset of many chronic
diseases including cardiovascular and metabolic diseases.43
Several compounds have been identified as having antioxi-
dant properties including flavonoids, polyphenolic com-
pounds, lycopene, and sulfur-containing compounds.
The flavonoids are low-molecular-weight polypheno-
other foods.44 More than 4000 flavonoids have been classi-
fied, including flavonols, stilbenes, cathechins, flavones, fla-
vanones, anthocyanidins, and isoflavonoids. These com-
pounds are an integral part of the human diet.44 Flavonols
are found mostly in plants, with the highest amount in
grapes and cocoa.45 Flavonols have antioxidant properties
and nitric oxide activity that is useful in producing vasodi-
lation and lowering blood pressure.45,46
Resveratrol, a stilbene polyphenolic compound, is
found in the skin of grapes, red wine, peanuts, and mul-
berries.47-49 Resveratrol has been shown to be a potent
scavenger of hydroxyl radicals, superoxide, and metal-in-
duced oxidative stress47 and can be useful in preventing
cardiovascular disease and inflammation.50-52 Cathechins,
the major polyphenolics found in green tea, exert multiple
mechanisms as antioxidative, antihypertensive, and antiin-
flammatory molecules.53 Green tea catechins can exert both
direct and indirect antioxidant activity through scavenging
ROS, chelating redox-active transition of metal ions, in-
hibiting redox-sensitive transcription factors, inhibiting
pro-oxidant enzymes, and inducing antioxidant en-
JPHARMTECHNOL.COM

zymes.54-56 There is also a growing interest in the develop-
ment of food crops with enhanced levels of flavonoids. En-
hancing flavonoid biosynthesis in chosen crops such as
tomatoes may provide new raw materials that have the po-
tential to be used in foods designed as antioxidants.57,58
Plasma and intracellular flavonoid concentrations are likely
to be 100- to 1000-times lower than concentrations of other
endogenous antioxidants such as vitamin C or gluta-
thione.59,60 These conflicting studies suggest that several
clinical trials are needed to prove or disprove the antioxi-
dant potency of flavonoids.
Lycopene, a carotenoid with no vitamin A activity, is
found in carrots, watermelons, papayas, and tomatoes.
Tomatoes contain lycopene and flavonoids, and have been
shown to decrease biomarkers of oxidative stress and car-
cinogenesis in healthy individuals and in those with type 2
diabetes.61,62 Further clinical trials are needed to prove the
efficacy and potency of lycopene as an antioxidant.
Sulfur-containing compounds, including glucosino-
lates, isothiocyanates, and sulforaphane, also posses an-
tioxidant activities.63,64 Glucosinolates are found in a wide
variety of plants including broccoli, cabbage, cauliflower,
brussels sprouts, salad rocket, garden cress, and mus-
tard.63,64 Most of the glucosinolates are rapidly converted
to isothiocyanates, sulforaphane, and other metabolites,
and these compounds have antioxidant activity.64 As a po-
tent antioxidant, sulforaphane is able to modify glu-
tathione and has chemoprotectant properties.64
Investigational Antioxidants
Investigational antioxidants that act as superoxide dis-
mutase or catalase mimetics65 or L-propionyl carnitine66,67
have a promising future. Low-molecular-weight com-
pounds that act as superoxide dismutase or catalase
mimetics theoretically have the advantage of scavenging
ROS and RNS continuously. They act as catalysts, with ef-
ficiencies similar to those of endogenous antioxidants such
as glutathione, superoxide dismutase, and catalase.64,68,69 L-
Propionyl carnitine has been shown to act as an intracellu-
lar superoxide scavenger, improving mitochondrial func-
tion and reducing DNA damage.66,67 This compound has
been shown to improve heart and peripheral nerve func-
tion and vascular blood flow in diabetic rat heart and ex-
perimental diabetes.66-71 Recent data suggest that antioxi-
dants should be used to scavenge free radicals as well as to
improve the antioxidant defense mechanism.68,69
Summary
The balance between damaging free radicals, ROS and
RNS, and antioxidant systems is important in maintain-
ing health. Excess free radicals induce oxidative stress,
which is usually balanced by the body’s endogenous an-
tioxidant system. If the generation of free radicals ex-
ceeds the protective effects of antioxidants, oxidative
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ROLE OF ANTIOXIDANTS ON OXIDATIVE STRESS IN DIABETES MELLITUS
damage occurs. Oxidative stress plays an important role
in insulin resistance and disease complications of dia-
betes. Diabetes is a complicated disease, and treatments
are directed to inhibit the metabolic abnormalities. Use of
a single drug may not be effective, and antioxidants may
be an integral part of the treatment regimen. ALA and
NAC have been shown to be beneficial for decreasing ox-
idative stress. It is important to encourage patients with
diabetes to consume a well-balanced diet rich in fruits
and vegetables and to talk to their physicians or pharma-
cists about using dietary supplements.
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AN INVITATION TO JOIN
Pharmacy Technician Educators Council
PTEC was founded by, and for, pharmacy technician educators. The changing healthcare sys-
tem places new demands on the pharmacy profession and, as a result, pharmacy technicians re-
quire better training to assume the new, more responsible roles. As pharmacy technician educa-
tors, we realize our profession will become increasingly important to the future of pharmacy
practice.
PTEC members instruct and administer a variety of technician training programs with a
membership that includes pharmacists, pharmacy technicians, allied health educators, nurses
and consultants. This diversity gives PTEC members access to a network of practicing educators
across the United States and Canada.
PTEC MEMBERSHIP BENEFITS INCLUDE:
• Professional Networking: Peer interaction to exchange ideas, make contacts, and share infor-
mation
• Leadership: The opportunity to determine the future direction of pharmacy technician educa-
tion, and expand your professional horizons
• Annual Meeting: Meet together to learn and contribute to future trends in technician educa-
tion. Twelve continuing education credit hours available for pharmacists.
• Journal and Newsletter: Members receive a newsletter and journal containing information
dedicated to pharmacy technician practice, training, and technology.

For more information or to obtain a membership application, please visit our

Web site at rxptec.org

Gail B. Askew PharmD

Executive Director
Pharmacy Technician Educators Council
PO Box 10118
Santa Ana, CA 92711-0118
gailaskewrx@gmail.com

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