Effect of Acrylamide on Stomach,

Cerebellum and Testis of the Albino Rat

THESIS
Submitted for the Partial Fulfillment of the
M.D. Degree in Anatomy
Presented by

Hesham Noaman Abdel Raheem Mustafa

M.B., B.Ch. & M.Sc. of Anatomy
Assistant lecturer of the Anatomy
Supervised by

Professor Dr. Kariman Mohammed El-Gohari

Professor of Anatomy
Head of Anatomy and Embryology Department, Faculty of
Medicine, Ain Shams University

Professor Dr. Ezz El-Deen Helmy Helaeil

Professor of Anatomy
Anatomy and Embryology Department, Faculty of
Medicine, Ain Shams University

Dr. Hassan Mostafa Serry

Assistant Professor of Anatomy
Anatomy and Embryology Department, Faculty of
Medicine, Ain Shams University

Dr. Shahira Samir Zaki

Assistant Professor of Anatomy
Anatomy and Embryology Department, Faculty of
Medicine, Ain Shams University
Faculty of Medicine
Ain Shams University
2005

Introduction
Acrylamide is a white, odorless chemical substance
(C3H5NO) with MW (71.08), used in Mining industry and in
Water treatment (Murray and Seger, 1994).
Recently, it has been reported that acrylamide monomer
may form in certain foods cooked at high temperatures, the
highest concentrations of acrylamide have been identified in
potato chips, French fries and grain-based foods that are cooked at
very high temperatures during frying, grilling or baking (Tareke
et al. 2002). In that respect, the German Federal Institute for Risk
Assessment stated in a December 10, 2002, press release that the
acrylamide content rises suddenly in French fries, from
approximately 300 micrograms per kilogram at 175 degrees
Celsius (347 degrees Fahrenheit) to 1,100 micrograms per
kilogram at 180 degrees Celsius (356 degrees Fahrenheit).
Acrylamide is thought to form in food principally from the
interaction of the amino acid asparagines with glucose or other
carbohydrates (Bachmann et al. 1992).
Acrylamide is thought to produce cancer in animals and
its presence in some foods may harm peoples health. Moreover,
at low levels, acrylamide is a potent neurotoxin affecting both
central and peripheral nervous systems (DeRojas and Goldstein,
1987). Chronic oral exposure to acrylamide in humans has
resulted in nerve damage accompanied by weakness and

numbness in the extremities. Moreover, the acute inhalation of

acrylamide may cause central and peripheral nervous system
damage resulting in symptoms ranging from drowsiness to
hallucinations. In addition, the chronic dermal exposure to
acrylamide may cause a rash (U.S. EPA, 1994). In addition,
acrylamide affects the reproductive function in rats, as it appears
to cause testicular atrophy and produces both a decreased sperm
count and an increase in abnormal sperm morphology (Sakamoto,
J. and Hashimoto, K. 1986). Moreover, hepatoxicity is reported
following acute ingestion of acrylamide (Donovan and Pearson,
1987; Shelly, 1996). In addition, transient impairment in renal
function has been reported following acute ingestion (Shelly,
1996).
Using chronic dosing schedules, it has been observed that
cumulative oral doses of 500-600 mg/kg using daily doses of 2550 mg/kg/day are required to produce ataxia in rats, dogs and
baboons (McCollister et al., 1964; Hopkins, 1970; Thomann et
al., 1974). Smaller daily doses do not produce a clinical effect
until a larger cumulative dose is attained; Fullerton and Barnes
(1966) observed that administration of acrylamide at daily doses
of 6 to 9 mg/kg did not produce evidence of neurotoxicity in rats
until a cumulative dose of 1200 to 1800 mg/kg was attained.

Aim of the Study:

The present study aims at exploring the harmful effects of
acrylamide on the structure of the stomach, cerebellum and testis
in the albino rat, in an attempt to clarify its potential risk on the
human health.

Material and Methods:

Thirty adult male albino rats will be divided into two
main groups. Group I will receive parentral acrylamide while
Group II will receive oral acrylamide in the drinking water. Each
group will be subdivided into three subgroups, 5 animals each, as
follows:
A- The parental Group I:
Subgroup 1, the controls, will be injected with intraperitoneal
saline.
Subgroup 2, will receive intraperitoneal injections of
acrylamide in a dose of 5 mg/kg.
Subgroup 3 will receive intraperitoneal injections of
acrylamide in a dose of 1000 mg/kg.
All animals will be injected once daily for 10 successive days.
B- The oral Group II:
Subgroup 1, the controls, will receive fresh water.
Subgroup 2, will receive 5 mg/kg body weight orally.
Subgroup 3, will receive 1000 mg/kg body weight orally.
All animals will be subjected to this regimen for 10 successive
days.
The animals will be sacrificed at the end of the treatment
period and specimens of stomach, cerebellum and testis will be
processed for histological study.
The procedure will be held at the Anatomy Department Faculty
of Medicine Ain Shams University.

References:
1)

Bachmann, M., Myers, J. and Bezuidenhout, B. (1992):

"Acrylamide monomer and peripheral neuropathy in
chemical workers." Am. J. Ind. Med 21(2): 217-222.

2)

Donovan, J.W. and Pearson, T. (1987): Ingestion of

acrylamide with severe encephalopathy, neurotoxicity and
hepatotoxcity. Vet Hum Toxicol, 29: 462.

3)

DeRojas, T.C. and Goldstein, B.D. (1987): "Primary

afferent terminal function following acrylamide: alterations
in the dorsal root potential and reflex." Tox Appl Pharmacol
88: 175-182.

4)

Fullerton, P.M. and Barnes, J.M. (1966): Peripheral

neuropathy in rats produced by acrylamide. Brit J Industr
Med, 23: 210-221.

5)

Hopkins, A.P. (1970): The effect of acrylamide on the

peripheral nervous system of the baboon.

J Neurol

Neurosurg Psychiatr, 33:805-816.

6)

McCollister, D., Oyen, F. and Rowe, V. (1964):

"Toxicology of acrylamide." Toxicol. Appl. Pharmacol 6:
172-181.

7)

Murray, L.M. and Seger, D.L. (1994): Acrylamide

neurotoxicity following occupation inhalation exposure. XVI
International Congress of the European Association of
Poison Centres and Clinical Toxicologists, Vienna, Austria.

8)

Sakamoto, J., Hashimoto, K. (1986): Reproductive toxicity

of acrylamide and related compounds in mice-effects on
fertility and sperm morphology. Arch Toxicol; 59(4):201-5.

9)

Shelly, (1996): Regina vs. Calder. In: Transcript records of

New Zealand High Court, Christchurch, New Zealand,
March 1996.

10) Tareke, E., Rydberg, P., Karlsson, P., Eriksson, S. and

Tornqvist, M. (2002): Analysis of acrylamide, a carcinogen
formed in heated foodstuffs. J. Agric. Food Chem. 50:49985006.
11) Thomann, P., Koella, W.P., Krinke, G., Peterman, H.,
Zak, G. and Hess, R. (1974): The assessment of peripheral
neurotoxicity in dogs: Comparative studies with acrylamide
and clioquinol. Agent Actions, 4:47-53.
12) U.S. Environmental Protection Agency (1994): Drinking
Water Regulations and Health Advisories.

Office of

Drinking Water, U.S. Environmental Protection Agency,

Washington, D.C.



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