1. No category

Ibrahim et al., J Forensic Toxicol Pharmacol 2015, 4:1
http://dx.doi.org/10.4172/2325-9841.1000135
Journal of Forensic
Toxicology and
Pharmacology
Research Article
A SCITECHNOL JOURNAL
Elucidation of Acrylamide
Genotoxicity and Neurotoxicity
and the Protective Role of Gallic
Acid and Green Tea
Abdelaziz E Ibrahim1*, Rania A El Kareem2 and Marwa A Sheir3
1Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine,
Suez Canal University, Ismailia, Egypt
2Department
of Histology and Histochemistry, Faculty of science, Suez University,
Egypt
3Food
Technology Research Institute, Agricultural Research Center, Giza, Egypt
*Corresponding
author: Abdelaziz E Ibrahim, 1Department of Forensic Medicine
and Toxicology, Faculty of Veterinary Medicine, Suez Canal University, Ismailia,
Egypt, E-mail: abdelazizzeftawy@yahoo.com
Rec date: Feb 27, 2015 Acc date: Mar 11, 2015 Pub date: Mar 13, 2015
Abstract
Objective: Acrylamide is a chemical compound used in many
technological applications and can be formed naturally when
foods, especially those are rich in sugars and low in protein
cooked at high temperatures during (e. g. frying, grilling, baking
or toasting). It has several harmful health effects including
neurotoxicity,
carcinogenicity,
reproductive
toxicity,
genotoxicity, and mutagenicity. Humans have chronic contact
with acrylamide through eating, e. g. fried potato chips and/or
French fries; cereal products, including bread, breakfast
cereals, cakes and biscuits; as well as, roasted coffee and
probably also from smoking. This study was carried out to
investigate the protective effects of gallic acid and green tea on
brain damage induced by acrylamide in rats.
Material and Methods: Biochemical analysis using antioxidant
enzymes as markers of toxicity, molecular study using comet
assay indicating DNA degenerative effect and histopathological
examination of brain tissue.
Results: Acrylamide caused a significant decrease in serum
butyryl cholinesterase, lactate dehydrogenase, glutathione-Stransferase, glutathione peroxidase, superoxide dismutase and
catalase activities while malonaldehyde content was
significantly increased, Comet assay revealed that acrylamide
caused DNA degeneration in brain, while histopathological
studies showed moderate to marked changes in brain tissue by
acrylamide.
Conclusion: All these findings greatly indicating the genotoxic
and neurotoxic effect of acrylamide that improved by treatment
with gallic acid or green tea.
Keywords: Acrylamide; Genotoxicity; Neurotoxicity; Protective role;
Gallic Acid; Green Tea; Rat
Introduction
Acrylamide is chemical compound with formula of CH2=CH–CO–
NH2 and several harmful health effects including neurotoxicity,
reproductive toxicity, carcinogenicity, genotoxicity and mutagenicity
[1].
In daily life, acrylamide can be formed during the cooking and
processing of foods via the decarboxylation of the Schiff base derived
from carbonyl reactants, resulting in human consumption of relatively
high doses of acrylamide [2].
For decades acrylamide has been used for the production of
polyacrylamide, which has various industrial applications in water
treatment, cosmetics, soil conditioning, and biomolecular laboratories
for use in gel electrophoresis [3]. Exposure to acrylamide was
previously thought to occur through industrial activities or through
cigarette smoking, as the compound is also found in tobacco smoke. It
is now known that acrylamide forms in numerous baked or fried
carbohydrate-rich foods, particularly in plant-based products such as
potato chips, crisps, breads, and coffee [4].
Morphological studies indicated that acrylamide-induced
neurotoxic syndrome was associated with nerve damage characterized
by distal axonal swelling with neurofilament accumulation and
retrograde degeneration in both central and peripheral myelinated
axons [5]. However, the mechanisms underlying these processes are
still not well understood. Sickles et al. proposed that acrylamide bound
to and inhibited the motor protein kinesin, leading to the inhibition of
the anterograde and retrograde transport and Inadequate support of
the distal axon or terminals producing the behavioral outcomes [6],
others thought that aberrant cell body processing and deficient axonal
transport induced by acrylamide decreased Na/K-ATPase activity.
Accumulation of Na+ and loss of K+ reversed operation of the Na/Caexchanger, resulting in the distal axon degeneration [7].
Acrylamide induces genetic damage through binding of its
metabolite, glycidamide, with DNA [8], and causes disturbances in the
oxidative status and enzyme activities through the release of large
numbers of free radicals in the body [9].
Gallic acid (GA;3,4,5-triphydroxyl-benzoic acid) is a
polyhydroxylphenolic compound which is widely distributed in
various plants, fruits and foods, where it is present either in free form
or, more commonly, as an ingredient of tannins, namely gallotannin
[10]. Gallnuts, sumac, oak bark, grapes, strawberries, pineapples,
bananas, lemons, witch hazel, red and white wines, apple peels, carob,
mangos and coffee are known to be rich in Gallic acid [11]. Tea is also
an important source of Gallic acid and contains up to 4. 5 g/kg of fresh
weight [12]. Gallic acid has biological activities such as anti-allergic,
anti-mutagenic, antioxidant, anti-bacterial, anti-viral, antiinflammatory, antitumor, anti-carcinogenic and neuroprotective [13].
Other beneficial actions of Gallic acid are anti-diabetic and antiangiogenic effects, nuclear factor kappa-light-chain-enhancer of
activated B cells (NF-jB) activity through modulating the levels of
MMP-2/9 and cytoskeletal reorganization signal pathway in gastric
cancer cells [14].
Green tea belongs to the Theacease family and comes from two
main varieties: Camellia sinensis var. sinensis and C. sinensis var.
assamica has been considered a healthy beverage since ancient times
[15]. The traditional Chinese medicine recommends green tea for
All articles published in Journal of Forensic Toxicology and Pharmacology are the property of SciTechnol and is
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Citation:
Ibrahim AE, Kareem RAE, Sheir MA (2015) Elucidation of Acrylamide Genotoxicity and Neurotoxicity and the Protective Role of Gallic Acid and
Green Tea. J Forensic Toxicol Pharmacol 4:1.
doi:http://dx.doi.org/10.4172/2325-9841.1000135
headaches, body aches and pains, digestion, depression and
detoxification and as an energizer and in general, to prolong the life
[16]. Increasing evidence indicates that green tea has multiple health
benefits,
such
as
antitoxoplasmal,
ant
cataract,
antihypocholesterolemic, antitrypanosomal, antinematodial, antihelminthic, anti-stress, anticancer, antioxidants, antifungal,
antibacterial, anti-inflammation, neuroprotection, anti-obesity,
antiviral, anticoccdial and antidiabetic effects [17].
Material and Methods
Chemicals
Acrylamide (99% pure) C3H5ON and gallic acid (C6H2 (OH)
3COOH) were purchased from Sigma company (Deisenhofer,
Germany).
Animals
Male white albino rats were obtained from Research Institute of
Ophthalmology, Medical Analysis Department, and Giza, Egypt. The
males rat (initial body weight (160-180 g) were approximately of the
same age, they were housed in galvanized iron cages measuring 40 ×
24 × 20 cm (6 rats to each cage).
Kits
Kits for butyryl cholinesterase, malondialdahyde (MDA) and
glutathione-S-transferase (GST) were obtained from Biodiagnostic
Company, Egypt. Lactate dehydrogenase (LDH) obtained from
Stanbio, USA. While superoxide dismutase; glutathione peroxidase
and catalase were obtained from Molecular Probes Company, Egypt.
Experiment biological design
All rats (36 rats) were housed in wire cages in a room maintained at
25 + 2°C fed on basal diet [18] for one - week before starting the
experiment for acclimatization. After one week period, the rats were
divided into 6 groups (6 rats each), all groups were fed for 35 days on
experimental diet as follows: Group (1): This group was fed on
standard diet only as a control (healthy rats). Group (2): This group
was fed on standard diet containing 60 mg acrylamide/Kg of diet.
Group (3): This group was fed on standard diet containing 60mg
acrylamide/Kg of diet and 1% gallic acid. Group (4): This group was
fed on standard diet containing 60mg acrylamide/ Kg of diet and 3%
gallic acid. Group (5): This group was fed on standard diet containing
60mg acrylamide/ Kg of diet and 5% green tea. Group (6): This group
was fed on standard diet containing 60mg acrylamide/ Kg of diet and
10% green tea.
Blood sampling
In all experimental groups, blood samples were collected after 12
hrs fasting at the end of each experiment, using the retoorbital method
by means of micro capillary glass heparin zed tubes. Blood samples
were collected into dry clean centrifuge tubes and left to clot in water
both (37°C.) for half an hour. The blood was centrifuged for 10 min at
3000 rpm to separate the serum; serum was carefully aspirated into
clean cuvette tube and stored frozen at -20°C for analysis as described
by [19].
Volume 4 • Issue 1 • 1000135
Brain samples for histopathological examination and comet
assay
Brain from each rat in each group were immediately dissected out
after 24 hours of the last dose then prepared for histopathological
examination and Comet assay.
Biochemical study
Butyryl cholinesterase, lactate dehydrogenase, and Lipid peroxides
(MDA) were determined in serum using readymade kits according to
[20-22] respectively. Glutathione-S-transferase (GST), glutathione
peroxidase, catalase, Superoxide dismutase was determined in serum
spectophotometrically by the methods of [23-26] respectively.
Comet assay (molecular study)
For comet assay, one gram of crushed brain samples was transferred
to 1 ml ice-cold phosphate buffer saline. This suspension was stirred
for 5 min and filtered and used to evaluate the DNA damage
parameters (Tailed%, Untailed%, Taillength, Tail DNA% and Tail
moment) according to [27].
Histopathological examination
For histological examination by the light microscope, specimens of
brain from all experiment's groups were collected and washed by
saline solution, then fixed in 10% formalin for 10h, at least then
washed in tap water for 12h and prepared to histopathological
examination according to [28].
Statistical analysis
The data were analyzed using SPSS (Statistical Package for Social
Sciences) version, 14. 0. The results are presented as Mean ± S.D. One
way analysis of variance (ANOVA) was used to test the difference
between groups. Comparisons between means of groups were
analyzed by L. S. D test with significance level 0.05 [29].
Results
Effects of acrylamide alone or in combination with gallic acid
or green tea on serum oxidative enzymes
Butyryl cholinesterase and lactate dehydrogenase activities declined
significantly in rats received acrylamide alone; however, the values of
butyryl cholinesterase and lactate dehydrogenase showed markedly
increase when rats treated with Gallic acid or green tea in combination
with acrylamide (Table 1).
MDA level significantly increased in the acrylamide treated group
compared with the control group. The MDA level markedly decreased
in rats treated with gallic acid or green tea tea in combination with
acrylamide (Table 1).
There was significant decrease in serum antioxidant enzymes
glutathione -S-transferase, glutathione peroxidase, Superoxide
dismutase, and Catalase in rats treated with acrylamides alone
compared with the control group, On the other side, acrylamide
treated rats with gallic acid or green tea showed significant increase to
all antioxidant enzymes but not reach the level of the control group
(Table 1).
• Page 2 of 6 •
Citation:
Ibrahim AE, Kareem RAE, Sheir MA (2015) Elucidation of Acrylamide Genotoxicity and Neurotoxicity and the Protective Role of Gallic Acid and
Green Tea. J Forensic Toxicol Pharmacol 4:1.
doi:http://dx.doi.org/10.4172/2325-9841.1000135
Group (1)
Group (2)
Group (3)
Group (4)
Group (5)
Group (6)
244.66a ± 5.51
171.33f ± 5.69
198.33e ± 2.08
205.66d ± 5.86
210.66c ± 10.21
227.00b ± 7.00
Lactate dehydrogenase
(U/L)
135.33a ± 2.52
99.43f ± 0.82
115.33e ± 2.08
118.00d ± 2.25
120.56c ± 2.21
126.00b ± 2.08
Malondialdehyde
(µmol)
1.73d ± 0.77
5.33a ± 1.17
3.13b ± 1.07
2.47c ± 0.76
2.11c ± 0.89
1.15d ± 0.15
Glutathione-Stransferase
117.67a ± 1.00
52.26f ± 3.49
83.63d ± 0.63
89.49c ± 1.42
67.88e ± 0.48
97.33b ± 1.01
Glutathione peroxidase
(nmol/min/m)
162.33a ± 1.00
72.67f ± 0.28
144.88c ± 0.69
155.09b ± 1.23
128.26e ± 4.16
140.61d ± 0.27
Superoxide dismutase
0.230a ± 0.10
0.093d ± 0.02
0.17c ± 0.02
0.19b ± 0.02
0.17c ± 0.021
0.19b ± 0.02
143.73a ± 1.11
68.73e ± 0.55
128.53c ± 1.43
129.71c ± 0.84
120.10d ± 1.24
131.67b ± 1.04
Butyryl colinesterase
(U / L)
(U/L)
(IU/ml)
Catalase
(IU/ml)
Table 1: Effects of acrylamide alone or in combination with gallic acid or green tea on serum oxidative enzymes. (Note: Means under the same
column bearing different superscript letters are different significantly (P ≤ 0.05). Group (1) control, Group (2) acrylamide only, Group (3)
Acrylamide + Gallic acid 1%, Group (4) Acrylamide + Gallic acid 3%, Group (5) Acrylamide +Green tea 5%, Group (6) Acrylamide +Green tea
10%).
Effects of acrylamide alone or in combination with gallic acid
or green tea on genomic DNA of rats brain cells
In acrylamide treated group tailed%, tail length, DNA tail%, and
DNA moment were significantly increased, while untailed%
significantly decreased compared with control Figure 1. These
elevations were significantly decreased while untailed% significantly
increased in other treated groups with acrylamide in combination with
gallic acid or green tea (Table 2).
Histopathological changes of Brain
Figure 2 microscopically brains of acrylamide treated rat’s revealed
congestion of meningeal blood vessels (photo A), Congestion of
cerebral blood vessels and focal cerebral haemorrhage (photo C),
haemorrhage in virchow space (photo B) and necrosis of many
neurons (photos D).
While that of rats treated with Acrylamide and Gallic acid 1%
revealed neuronophagia of pyknoyic neurons (photos E) and necrosis
of neurous (photo F). Whereas, rats treated with Acrylamide and
Gallic acid 3% showed necrosis of neurons (photos H) and focal gliosis
(photos G).
However, treated group with Acrylamide and green tea 5% showed
focal haemorrhage (photo J), and pyknosis of some neurous (photo I).
On the other hand, Some sections from treated group with Acrylamide
and green tea 10% revealed no histopathological changes (photo M),
whereas, other sections showed necrosis of some neurons (photo L).
Figure 1: Comet assay of genomic DNA of rats brain cells for
control and different treated groups: (1) control, (2) acrylamide
only, (3) Acrylamide + Gallic acid 1%, (4) Acrylamide + Gallic acid
3%, (5) Acrylamide +Green tea 5%, (6) Acrylamide +Green tea
10%.
Volume 4 • Issue 1 • 1000135
• Page 3 of 6 •
Citation:
Ibrahim AE, Kareem RAE, Sheir MA (2015) Elucidation of Acrylamide Genotoxicity and Neurotoxicity and the Protective Role of Gallic Acid and
Green Tea. J Forensic Toxicol Pharmacol 4:1.
doi:http://dx.doi.org/10.4172/2325-9841.1000135
Group (1)
Group (2)
Group (3)
Group (4)
Group (5)
Group (6)
Tailed%
6.00c ± 1.00
8.95a ± 0.78
7.08b ± 1.36
6.08c ± 1.51
6.73bc ± 0.73
8.30a ± 1.07
Untailed%
94.00a ± 1.00
91.05c ± 1.02
93.00b ± 1.00
93.92a ±1 .00
93.27ab ±1.00
91.70c ± 1.00
Taillength µm
2.87c ± 0.67
3.87a ± 0.16
3.14b ± 0.04
2.73c ± 0.21
2.89c ± 0.25
3.26b ± 0.15
Tail DNA%
1.85d ± 0.28
3.42a ± 0.28
3.05b ± 0.28
2.64c ± 0 .28
2.66c ± 0.28
2.93b ± 0.26
Tail moment
4.71d ± 1.00
12.27a ± 0.83
9.98b ± 1.20
7.31c ±1.10
7.80c ± 1.19
9.41b ± 0.66
Table 2: Effects of acrylamide alone or in combination with gallic acid or green tea on genomic DNA of rat’s brain cells. (Note: Means under the
same column bearing different superscript letters are different significantly (P ≤ 0.05). Group (1) control, Group (2) acrylamide only, Group (3)
Acrylamide + Gallic acid 1%, Group (4) Acrylamide + Gallic acid 3%, Group (5) Acrylamide +Green tea 5%, Group (6) Acrylamide +Green tea
10%).
Acrylamide caused a decrease in the activities of Catalase and
Superoxide dismutase by its oxidative stress effect and the release of
large numbers of free radicals. Superoxide dismutase and Catalase are
the two enzymes that help to scavenge super- oxide ions and hydroxyl
ions, respectively [37]. The decrease in Superoxide dismutase activity
was suggested to be due to accumulation of H2O2 free radicals [38].
Our results were agreed with results of [39] who found that green tea
extract antioxidant activity exhibited attenuation of ethanol-associated
decrease in serum and liver Superoxide dismutase and Catalase
activities.
Figure 2: Histopathological Changes of Brain
Discussion
Cholinesterase levels inhibition are indicator for possible
neurotoxic effect of acrylamide. The neurological defect associated
with acrylamide intoxication is mediated by impaired neurotransmission at central and peripheral synapses [30].
Acrylamide inhibited the action of lactate dehydrogenase in brain
and serum. These changes were accompanied by increased brain
dopamine receptors in a concentration- dependent manner [31].
Nonetheless, acrylamide caused increased in the activities of
malondialdehyde due to the lipid peroxidation process induced by free
radical caused by acrylamide toxicity [32].
Green tea supplementation resulted in a small but significant
amelioration of 10-15% in the activities of glutathione peroxidase S
transferase and glutathione peroxidase [33]. Oral administration of
green tea extract at doses of (125, 625 and 1250 mg/kg) for 8 weeks
significantly increased the activity of glutathione peroxidase in the
liver [34]. Gallic acid (10 and 20 mg/kg) treatment showed
significantly increased glutathione peroxidase in diabetic rats [35].
Also gallic acid significantly increased antioxidant enzymes such as
peroxidase S transferase and glutathione peroxidase which reduced by
treatment with Lindane [36].
Volume 4 • Issue 1 • 1000135
Acrylamide acts as an indirect genotoxic agent and cannot induce
chromosomal damage but it converted to the mutagenic metabolite
glycidamide in the liver cells. Glycidamide is potent genotoxic agent
[33]. Our results are supported by the findings of [40] who indicated
that ACR-induced DNA damage and oxidative changes in rat brain.
These results were in agreement with those obtained by [41] who
indicated that administration of GA to mice prior to whole body
radiation exposure reduced the peroxidation of lipids and the damage
to the cellular DNA indicating in vivo radiation protection of
membranes and DNA by GA. Furthermore consumption of green tea
catechins (GT-catechin), which are potent antioxidants, decreases
oxidative damage to DNA and improves brain function in aged mice
with accelerated senescence (SAMP10 mice) [42].
Histopathological findings were accordance with that of [43] who
found a great damage in brain of rats orally administered acrylamide
(20 mg/Kg of basal diet) daily for 35 days. Also our results were agreed
with those of [44] who found that, the microscopical examination of
brain sections of control and green tea-treated rats showed normal
histopathological structure, while in lead treated rats, brain oedema
was observed in the hippocampus area associated with focal gliosis in
the cerebrum. The cerebellum showed vacuolization, while the
medulla oblongata had neuronal degeneration and gliosis). On the
other side histopathology of brain confirmed the protective effects of
gallic acid by 10 and 20 mg/kg [35].
References
1.
2.
Chen JH, Yang CH, Wang YS, Lee JG, Cheng CH, et al. (2013)
Acrylamide-induced mitochondria collapse and apoptosis in
human astrocytoma cells. Food Chem Toxicol 51: 446-452.
Rydberg P, Eriksson S, Tareke E, Karlsson P, Ehrenberg L, et al.
(2005) Factors that influence the acrylamide content of heated
foods. Adv Exp Med Biol 561: 317-328.
• Page 4 of 6 •
Citation:
Ibrahim AE, Kareem RAE, Sheir MA (2015) Elucidation of Acrylamide Genotoxicity and Neurotoxicity and the Protective Role of Gallic Acid and
Green Tea. J Forensic Toxicol Pharmacol 4:1.
doi:http://dx.doi.org/10.4172/2325-9841.1000135
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
Parzefall W (2008) Minireview on the toxicity of dietary
acrylamide. Food Chem Toxicol 46: 1360-1364.
Tareke E, Rydberg P, Karlsson P, Eriksson S, Törnqvist M (2002)
Analysis of acrylamide, a carcinogen formed in heated foodstuffs.
J Agric Food Chem 50: 4998-5006.
LoPachin RM Jr, Lehning EJ (1994) Acrylamide-induced distal
axon degeneration: a proposed mechanism of action.
Neurotoxicology 15: 247-259.
Sickles DW, Stone JD, Friedman MA (2002) Fast axonal
transport: a site of acrylamide neurotoxicity? Neurotoxicology
23: 223-251.
LoPachin RM, Lehning EJ (1994) Acrylamide-induced distal.
Neurotoxicology 15: 247-59.
Belinda J Nixon, Simone J Stanger, Brett Nixon, Shaun D Roman
(2012) Chronic Exposure to Acrylamide Induces DNA Damage
in Male Germ Cells of Mice. Toxicol Sci 129: 135-145
Yousef MI, El-Demerdash FM (2006) Acrylamide-induced
oxidative stress and biochemical perturbations in rats.
Toxicology 219:133–141.
Ferk F Chakrabortya, Gerb WJ, Kundic M, Bichlera J, Misk M, et
al. (2011) Potent protection of gallic acid against DNA oxidation:
Results of human and animal experiments. Mutation Research
715: 61-71.
You BR, Moon J, Han YH, PaW (2010) Gallic acid inhibits the
growth of HeLa cervical cancer cells via apoptosis and/or
necrosis. Food ChemToxicol 48: 1334-1340.
Tomas-Barberan FA, Clifford MN (2000) Dietary hydroxy
benzoic acid derivatives and their possible role in health
protection. J Sci Food Agric 80: 1024-1032.
Mansouri MT, Farbood Y, Sameri MJ, Sarkaki A, Naghizadeh B,
et al. (2013) Neuroprotective effects of oral gallic acid against
oxidative stress induced by 6-hydroxydopamine in rats. Food
Chem 138: 1028-1033.
Ho HH, Chang CS, Ho WC, Liao SY, Hand Wang, et al. (2010)
Anti-metastasis effects of gallic acid on gastric cancer cells
involves inhibition of NF-kappaB activity and down regulation
of PI3K/AKT/small GTPase signals. Food Chem. Toxicol 48:
2508-2516.
SangS, Cheng X, Stark RE, Rosen R, Yang CS, et al. (2002)
Chemical studies on antioxidant mechanism of tea catechins:
analysis of radical reaction products of catechin and epicatechin
with 2,2- diphenyl-1-picrylhydrazyl. Bioorg Med Chem 10:
2233-7.
Petti S, Scully C (2009) Polyphenols, oral health and disease: A
review. J Dent 37: 413-423.
Hsu YW, Tsai CF, Chen WK, Huang CF, Yen CC (2011) A
subacute toxicity evaluation of green tea (Camellia sinensis)
extract in mice. Food Chem Toxicol 49: 2624-2630.
O Compactum Benth (1993) American Institute of Nutrition
Purified Diet for Laboratory Rodent Final Report. J Nutrition
123: 1939 - 1951
Schermer S (1967) The Blood Morphology of Laboratory
Animal. Longmans. Printed in Great Britain, Green and CoLTd.
Knedel M, Böttger R (1967) [A kinetic method for determination
of the activity of pseudocholinesterase (acylcholine acylhydrolase 3.1.1.8.)]. Klin Wochenschr 45: 325-327.
Friedman RB, Young DS (1997) Effect of Diseases on Clinical
Laboratory Tests. (3rdedn), AACC Press, Washington.
Volume 4 • Issue 1 • 1000135
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
Mihara M, Uchiyama M (1978) Determination of malonaldehyde
precursor in tissues by thiobarbituric acid test. Anal Biochem 86:
271-278.
Habig WH, Pabst MJ, Jakoby WB (1974) Glutathione Stransferases. The first enzymatic step in mercapturic acid
formation. J Biol Chem 249: 7130-7139.
Ursini F, Maiorino M, Gregolin C (1985) The selenoenzyme
phospholipid hydroperoxide glutathione peroxidase. Biochim
Biophys Acta 839: 62-70.
Aebi H (1984) Catalase in vitro. Methods Enzymol 105: 121-126.
Maier CM, Chan PH (2002) Role of superoxide dismutases in
oxidative
damage
and
neurodegenerative
disorders.
Neuroscientist 8: 323-334.
Singh NP, McCoy M T, Tice RR, Schneider EL (1988) A simple
technique for quantitation of low levels of DNA damage in
individual cells. Exp Cell Res 175: 184-191.
Banchroft JDS, Stevens A, Turner DR (1996) Theory and practice
of histological techniques. (4thedn), Churchil Livingstone, New
York.
SPSS (2000) Statistical package for the social sciences. Chicago
Barber DS, LoPachin RM (2004) Proteomic analysis of
acrylamide-protein adduct formation in rat brain synaptosomes.
Toxicol Appl Pharmacol 201: 120-136.
Friedman M (2003) Chemistry, biochemistry, and safety of
acrylamide. A review. J Agric Food Chem 51: 4504-4526.
Catalgol B, Ozhan G, Alpertunga B (2009) Acrylamide-induced
oxidative stress in human erythrocytes. Hum Exp Toxicol 28:
611-617.
Khan SM, Kour G (2007) Subacute oral toxicity of chlorpyriphos
and protective effect of green tea extract. Pesticide Biochemistry
and Physiology 89: 118-13.
Tsai CF, Hsu YW, Ting HC, Huang CF, Yen CC (2013) The in
vivo antioxidant and antifibrotic properties of green tea
(Camellia sinensis, Theaceae). Food Chem 136: 1337-1344.
Punithavathi VR, Prince PS, Kumar R, Selvakumari J (2011)
Antihyperglycaemic, antilipid peroxidative and antioxidant
effects of gallic acid on streptozotocin induced diabetic Wistar
rats. Eur J Pharmacol 650: 465-471.
Vijaya Padma V, Sowmya P, Arun Felix T, Baskaran R,
Poornima P (2011) Protective effect of gallic acid against lindane
induced toxicity in experimental rats. Food Chem Toxicol 49:
991-998.
Sankar P, Telang AG, Manimaran A (2012) Protective effect of
curcumin on cypermethrin-induced oxidative stress in Wistar
rats. Exp Toxicol Pathol 64: 487-493.
Diplocke AT (1994) Antioxidant and free radical scavengers. In
Catherine Rice-Evans "Free Radical Damage and its Control".
Elsevier, New York.
Frei B, Higdon JV (2003) Antioxidant activity of tea polyphenols
in vivo: evidence from animal studies. J Nutr 133: 3275S-84S.
Alturfan AA, Tozan-Beceren A, Sehirli AO, Demiralp E, Sener G,
et al. (2012) Resveratrol ameliorates oxidative DNA damage and
protects against acrylamide-induced oxidative stress in rats. Mol
Biol Rep 39: 4589-4596.
Gandhi NM, Nair CK (2005) Protection of DNA and membrane
from gamma radiation induced damage by gallic acid. Mol Cell
Biochem 278: 111-117.
• Page 5 of 6 •
Citation:
Ibrahim AE, Kareem RAE, Sheir MA (2015) Elucidation of Acrylamide Genotoxicity and Neurotoxicity and the Protective Role of Gallic Acid and
Green Tea. J Forensic Toxicol Pharmacol 4:1.
doi:http://dx.doi.org/10.4172/2325-9841.1000135
42.
43.
Kishido T, Unno K, Yoshida H, Choba D, Fukutomi R, et al.
(2007) Decline in glutathione peroxidase activity is a reason for
brain senescence: consumption of green tea catechin prevents the
decline in its activity and protein oxidative damage in ageing
mouse brain. Biogerontology 8: 423-430.
Nail (2010) Biochemical Studies on Acrylamide in Egyptian
Food. American Journal of Biochemistry and Biotechnology 9:
90-101
Volume 4 • Issue 1 • 1000135
44.
Khalaf AA, Moselhy WA, Abdel-Hamed MI (2012) The
protective effect of green tea extract on lead induced oxidative
and DNA damage on rat brain. Neurotoxicology 33: 280-289.
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