Methoxychlor Hepatotoxicity and Trials of Camel Milk Restoration
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Asian Research Journal of Current Science
3(1): 24-35, 2021; Article no.ARJOCS.415
Methoxychlor Hepatotoxicity and Trials of Camel
Milk Restoration
Eman E. Elsharkawy1*, Eman M. Shaker2, Neveen A. El-Nisr3
and Nahed, M. Wahba3
1
Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Assuit University,
Egypt.
2
Department of Food Hygiene, Faculty of Veterinary Medicine, Sohag University, Egypt.
3
Animal Health Research Institute, Assuit, Egypt.
Authors’ contributions
This work was carried out in collaboration among all authors. Author EEE designed the study,
performed the statistical analysis, wrote the protocol and wrote the first draft of the manuscript.
Authors EMS and NAEN managed the analyses of the study. Author NAEN managed the literature
searches. All authors read and approved the final manuscript.
Received 01 March 2021
Original Research Article Accepted 07 May 2021
Published 11 May 2021
ABSTRACT
The present study was carried out to investigate the restoration effect of camel's milk against
methoxychlor induced liver toxicity. The unique characters of camel’s milk make it used extensively
in the field of medicine as anti-microbial, anti-diabetic and as a hepatoprotective agent.
Methoxychlor is an environmental contaminant, which is widely used as a pesticide in many
countries, has been shown to induce hepatotoxicity in rat. MXC caused a significant increase in
serum transaminases (AST and ALT), and alkaline phosphatase, while MXC induced a significant
reduction in total protein and albumin levels. MXC significantly inhibited lipid peroxidation and
markedly enhanced glutathione in liver homogenate. Pathological damages as degeneration and
coagulative necrosis of the hepatocytes were established in liver. Newly formed bile ducteules
denotes neoplastic changes in the portal tract with abnormal mitotic pattern were associated with
the long term exposure. The present study concluded that camel milk treatment may play a
protective role against methoxychlor -induced liver damage in rats.
Keywords: Hepatotoxicity; methoxychlor; AST; ALT; oxidative stress; camel milk.
1. INTRODUCTION might represent such a potential candidate. CM
is different from other ruminant milk; it is lower in
Recently, the interest concerned with using of cholesterol, protein and sugar, but higher in
alternative medicines for the treatment of hepatic minerals, vitamins, and insulin [1,2]. It also
disease has been arisen. Camel’s milk (CM) contains a relatively large amount of
_____________________________________________________________________________________________________
*Corresponding author: Email: medicine1971@yahoo.com, eman.elsharkawy@vet.au.edu.eg;
Elsharkawy et al.; ARJOCS, 3(1): 24-35, 2021; Article no.ARJOCS.415
polyunsaturated fatty acids and linoleic acids, oxidative stress reported in our previous studies
which are essential for human nutrition [3]. [17,9]. Discovering the restoration effect of
Additionally, CM exhibits a wide range of camel’s milk against hepatotoxic effect was the
biological activities; antimicrobial, antioxidative, main reason beyond the conduction of the
antithrombotic, antihypertensive, and immuno- current experiment which aimed to investigate
modulatory effect [4,5]. This might be associated the protective effect of camel’s milk against
with the unique composition of camel's milk: methoxychlor induced liver toxicity.
indeed, the content of immunemodulatory
proteins, fatty acids, important minerals and 2. MATERIALS AND METHODS
vitamins allows camel's milk to be potentially
used as an anti-inflammatory, antidiabetic, 2.1 Chemicals
hepato-protective and cardio-protective food
[6,7]. Camel’s milk samples were collected daily early
in the morning from camel farm. Milk was
Methoxychlor is one of the environmental collected from camels by hand milking. The
contaminants which is widely used as a pesticide samples were collected in sterile screw bottles
in many countries that was developed to replace and kept in cool boxes until transported to the
dichloro-diphenyl-trichloroethane (DDT), and its laboratory. The rats were given this fresh milk
chemical name is 1,1,1-trichloro-2,2-bis (p – (100 mL/24 h/cage) as such without any further
methoxy phenyl) ethane. It has been reported treatment.
that methoxychlor undergo hepatic microsomal
mono oxygenase mediated activation and the Methoxychlor (1,1,1-trichloro-2,2-bis
resultant reactive metabolites possibly free [methoxyphenyl] ethane, Approx 95% was
radicals bind covalently to microsomal purchased from Sigma (St. Louis, Mo., USA).
components and induce liver damage [8,9]. MXC was dissolved in corn oil (1:100). Reduced
Antioxidants/free radical scavengers, and glutathione (GSH) antioxidant enzyme and lipid
sulfhydryl containing compounds inhibit covalent peroxide thiobarbituric acid reacting substances
binding of methoxychlor in human liver (TBARS) were measured using commercial test
microsomes, suggesting that the reactive kits supplied Bio-diagnostics (Bio- diagnostics,
intermediate is a free radical [10]. It has also Cairo, Egypt). All other chemicals used in the
been reported that human cytochrome P-450 experiment were of analytical grade.
enzymes responsible for conversion of MXC into
its major metabolites, the mono-o-demethylated 2.2 Animals and Treatment
derivatives and CYP1A2, have been shown to
play predominant role in this reaction [11]. The A total of 100 adult female Sprague Dawley rats,
ability of cytochrome P-450 system to induce 4 to 6 weeks old, weighed about 100–150 gm
reactive oxygen species (ROS) has been were used in all experiments. They were
reported [12]. ROS are formed in both obtained from the Laboratory Animal House,
physiological and pathological conditions in Assiut University, Egypt. The animals were
mammalian tissues, due to their high reactivity housed in plastic cages on wood chips for
they may interact with biomolecules inducing bedding and acclimated for 10 days before
oxidative stress [13]. Free radicals/ROS starting the experiment. All animals were housed
generated in tissues subcellular compartments in standard cages (6 rats/cage), feeding with
are efficiently scavenged by the antioxidant standard laboratory diet and tap water ad libitum.
defense system, which constitutes antioxidant The rats were housed at 24-25 ‘C and humidity
enzyme such as superoxide dismutase, catalase, (65%) and in daily dark/light cycle. The studies
and glutathione reductase and glutathione were conducted in accordance with the principles
peroxidase. Under normal physiological and procedures outlined in the National Institute
conditions free radicals/ROS are generated in of Health of USA (NIH) guide for the Care and
subcellular compartments of liver which are Use of the Laboratory Animals [18].
subsequently scavenged by the antioxidant
defense system of the corresponding cellular 2.3 Experimental Design
compartments [14]. The organs production of
free radicals and dis-function of the antioxidant The experiment is divided to two stages: First
defense system have been reported upon stage for 6 months and the second stage for 12
exposure to toxic chemicals [15,16]. MXC months. In both stages, rats were randomly
induced several organs damage due to the divided into four groups of twenty-five animals
25
Elsharkawy et al.; ARJOCS, 3(1): 24-35, 2021; Article no.ARJOCS.415
each as follows: MXC -treated group received an Na OH, 1.5 ml of 0.8% aqueous solution of
oral dose of MXC 200 mg/ kg b.w, twice/ week, thiobarbituric acid and 0.2 ml liver homogenate
by gavages for 6 or 12 months. This dose was (20% in 1.15% K Cl). The mixture was made up
selected according to Murono et al. [19]. MXC to 4.0 ml with distilled water and kept in boiling
plus camel’s milk - treated group received water bath for 60 min. After cooling with tap
(100 ml/24 h/cage) as their sole source of water, the mixture was centrifuged at 2500g for
drinking for 6 or 12 months. Camel milk -treated 10 min. The supernatant was taken out and the
group was received daily a dose of intensity of pink color was measured at 532 nm
(100 ml/24 h/cage) as their sole source of on a spectrophotometer. TBARS were quantified
drinking, for 6 or12 months. This dose was used using an extinction coefficient of 1.56 - 105 M1
according to the studies of Althnaian et al. [20]. cm1 and expressed as nmol of TBARS per mg
Control group received a daily oral dose of 2 ml protein.
corn oil.
2.5.3 Estimation of reduced glutathione in
2.4 Sample Collections liver
After 6 and 12 months of MXC exposure, female GSH in the liver was assayed by the method
rats were anesthetized with CO, and decapitated. described by Sun et al. [24]. The fresh tissues
Trunk blood was collected after decapitation and were immediately homogenized in ice-cold 0.02
allowed to clot at 4°C. Sera were collected and M EDTA solution. Aliquots of tissue homogenate
stored at -80°C to determine of serum total were treated with a 50% w/v trichloroacetic acid
protein as well as liver function enzyme activities while shaking, kept for 15 min and centrifuged.
(ALT, AST, and ALP). Meanwhile, the abdominal After supernatant fractions were mixed with Tris
cavity was dissected immediately; the livers were buffer (pH 8.9) and DTNB, absorbance at 412
separated for the histopathological examination. nm was measured. Reduced glutathione was
used as an external standard. GSH levels were
2.5 Methodology expressed as l mol/g tissue.
2.5.1 Biochemical assays 2.5.4 Determination of protein
Serum was used to determine total protein and Protein concentrations were measured by the
albumin by colorimetric method according to method of Bradford [25], using bovine serum
Doumas, [21]. The serum samples were assayed albumin as a standard. Protein concentration
for aspartate transaminase (AST), alanine used for the concentration of reduced glutathione
transaminase (ALT), alkaline phosphatase (ALP) and lipid peroxidation TBARS and can be
according to Rec, [22]. expressed as activity per milligram of protein by
dividing the units by milliliter of protein
2.5.1.1 Preparation of liver homogenate concentration.
Liver tissue homogenate was prepared according 2.6 Histopathological Examination
to the instruction of the kits. Briefly, 500 mg of
hepatic tissues was homogenized in 10 mL ice- Liver specimens were fixed with 10%
cold phosphate buffer saline (50 mM, pH 7.4). formaldehyde and processed routinely for
The homogenate mixture was centrifuged at paraffin embedding technique. Embedded
3800 × g (4 °C) for 15 min. The supernatant was tissues were sectioned at 5mµ and stained with
used for measurement of reduced glutathione hematoxylin and eosin (H&E) [26] for routine
dismutase ((TBARS)), thiobarbituric acid histopathological examination. They were then
((TBARS)), examined under the light microscope.
2.5.2 Estimation of lipid peroxidation in liver 2.7 Statistical Analysis
A breakdown product of lipid peroxidation, The data were analyzed using one-way ANOVA
thiobarbituric acid reacting substances (TBARS) for all the experiments. Statistically significant
was measured by the method described by differences were determined using the Dunnett’s
Rungby and Ernst, [23]. In brief, the reaction test for comparing to the vehicle-treated control
mixture consisted 0.2 ml of 8.1% SDS, 1.5 ml of or the Bonferroni test for multiple comparisons.
20% acetic acid solution adjusted to pH 3.5 with Graph Pad Prism graphing and the analysis
26
Elsharkawy et al.; ARJOCS, 3(1): 24-35, 2021; Article no.ARJOCS.415
software (version 4a; Graph Pad Software, Inc., rats. These alterations were obtained in both first
San Diego, CA) was used for all statistical (6 months) and second stages (12 months) of the
analyses. A statistically significant difference was experiment. However, there was not a significant
confirmed at P < 0. 05. difference between the control and camel milk
treated rats.
3. RESULTS
3.3 Histopathology
3.1 Biochemical Assays
At the first stage of the experiment, after 6
A significant reduction in the serum of total months of exposure, the liver of rats treated with
protein and albumin concentration (g\dl) was MXC showed degeneration of the hepatocytes
obtained in both MXC and MXC plus camel milk which changed to coagulative necrosis
treated groups in the comparison with the control associated with cellular infiltration of
at (P< 0.05), after 6 and 12 months of exposure. mononuclear cells type Fig. (5.a). At the end of
On the other hand, a significant elevation in this stage, there was severe fatty degeneration of
serum ALT, AST and ALP levels (U/I) were the hepatocytes with focal area of kupffer cell
recorded in MXC and MXC plus camel milk proliferation Fig. (5.b). In the second stage of the
treated rates compared with the control at (P < experiment, after 12 months of exposure, the
0.05), after 6 and 12 months of exposure. There liver tissue was severely damaged and there are
was a significant difference between MXC - apoptotic changes including condensation,
treated and MXC plus camel milk-treated increase esinophillia of cytoplasm shrinkage of
groups in total protein, albumin, and ALT, AST the nucleus associated with area of cellular
and ALP serum levels in the first and second reaction Fig. (6.a). The hepatic blood vessels
stages of the experiment. The control and camel were firstly congested and surrounded with
milk-treated rats had equivalent serum leukocytic infiltration (lymphocytes and
concentrations of all previous parameters macrophages) and the large blood vessel filled
(Tables 1 and 2). with prteinous material Fig. (6.b). The portal
areas showed some newly formed bile ducteules
3.2 The Oxidative Status of Liver denotes neoplastic changes in the portal tract
Homogenate associated with coagulation to cytoplasm and
cellular infiltration Fig. (7.a). The hepatocytes
As shown in Figs. 1 & 2 liver GSH levels, were disarranged, dissociated, along with some
expressed as (U/mg protein), were significantly mitotic patterns. The blood vessels and bile ducts
lower in the MXC and MXC plus camel milk were dilated and highly infiltrated with
treated groups than in the control group at (P< lymphocytes Fig. (7.b). The liver of rats treated
0.05). On the other hand, the liver TBARS with MXC and milk in the first and second stages
concentration, expressed as (U/mg protein), in showed only mild degenerative changes in the
MXC and MXC plus camel milk treated groups hepatocytes and mild connective tissue
were significantly higher than in the control group proliferation around the blood vessels and bile
at (P < 0.05) Figs. 3 & 4. There is a significant (p ducts Fig. (8.a). The liver of rats treated with milk
< 0.0 5) difference in the activities of GSH and only showed normal hepatocytes, blood vessels
TBARS levels in MXC plus camel milk treated and bile ducts Fig. (8.b).
Table 1. The effect of the MXC and camel milk on the serum biochemical parameters in
exposed groups for 6 months
Groups Tp ALB Globulin AST ALT ALP
g\dl g\dl g\dl U\l U\l U\l
MXC 5.36±0.2*c 3.20±0.3*c 2.21±0.2 * c 301 ± 27.9 *bc 99.7 ±9.7*bc 786 ± 102.5 * bc
Camel milk 5.82±0.3*c 3.49±0.1*c 2.34±0.3 * c 185 ± 19.8 *ac 67.9± 6.8 *ac 582 ± 29.8* ac
MXC+
Camel milk 6.70±0.4ab 3.72±0.2 ab 2.98±0.4 ab 112 ± 16.3 ab 37.8 ± 5.3 ab 386 ± 47.6 ab
Control 7.56±o.1 4.23±0.2 3.33±0.1 127 ± 13.5 43.1 ± 6.1 385 ± 42.5
Data are expressed as means ± S.D. of twenty animals per group. *denotes P < 0.05 as compared to control group,
a. Denotes P < 0.05 as compared to MXC- group. b. Denotes P < 0.05 as compared to MXC+CM -group.
c. Denotes P < 0.05 as compared to CM – group (One- way ANOVA/Duncan)
27
Elsharkawy et al.; ARJOCS, 3(1): 24-35, 2021; Article no.ARJOCS.415
Table 2. The effect of the MXC and camel milk on the serum biochemical parameters in
exposed groups for 12 months
Groups Tp ALB Globulin AST ALT ALP
g\dl g\dl g\dl U\l U\l U\l
MXC 6.47±0.2* bc 3.42±0.44*c 2.24±0.33*bc 136.26±48.7 *bc 80.5± 6.7 *bc 89.12±10*bc
Camel milk 6.81±0.1*a 3.94±0.34*c 2.34±0.23*ac 131.82±20.6 *ac 57.6± 3.8 *ac 78.88±21* ac
MXC +
Camel milk 6.92±0.2a 4.19±0.23ab 2.94±0.32ab 117.02± 22.6 ab 48.4 ± 3.3 ab 56.13±5 ab
Control 7.56 ±0.3 4.23±0.30 3.35±0.43 112.30±24.5 42.0 ± 3.1 55.43±3
Data are expressed as means ± S.D. of twenty animals per group. *denotes P < 0.05 as compared to control group,
a. Denotes P < 0.05 as compared to MXC- group. b. Denotes P < 0.05 as compared to MXC+CM -group.
c. Denotes P < 0.05 as compared to CM – group (One- way ANOVA/Duncan)
40
35
28.6
GSH levels (U/mg protein)
30 27.3
ab
25
19.2
20
*ac
15 12.5
*bc
10
5
0
1
Expermintal treated groups
MXC MXC+CM CM Control
Fig. 1. The effect of long exposure to MXC for 6 months on GSH levels and the restoration
effect of Camel milk
Data are expressed as means ± S.D. of twenty animals per group. *denotes P < 0.05 as compared to control group, a denotes
P < 0.05 as compared to MXC- group. b denotes P < 0.05 as compared to MXC+CM -group. C denotes P < 0.05 as compared
to CM – group (One- way ANOVA/Duncan)
4. DISCUSSION camel milk could bring a significant decrease in
activities of these enzymes when compared to
In the present study, the chronic exposure of rats MXC exposed groups. The increased serum
to MXC was associated with significant reduction levels of hepatic markers have been attributed to
in the levels of serum total protein and albumin. the liver injury, because these enzymes are
Moreover, the activities of serum marker place in cytoplasmic area of the cell and are
enzymes (AST, ALT and ALP) were found released into circulation in case of cellular
elevated markedly in rats treated with MXC. damage [20]. At this point, our study supports
These changes were not observed in control rat that liver damage is induced by MXC
samples. The present study revealed that administration. As a matter of fact, the elevation
treatment with camel milk alone did not increase in transaminases are encountered in conditions
the activities of serum AST, ALT and ALP levels. causing hepatocellular damage, loss of functional
In addition, the simultaneous treatment with integrity of cell membrane, and necrosis such as
28Elsharkawy et al.; ARJOCS, 3(1): 24-35, 2021; Article no.ARJOCS.415
in chemically induced liver injury and elevation in documented that the beneficial effects of
enzymes [27]. The rise in serum AST and ALT is fermented camel milk against cardiotoxicity
more specific and predominant in the liver injury. induced by carbon tetrachloride in mice.
The modulations in transaminases are also
influenced by the degree of hepatic These studies declared that the protective effect
decomposition related to cell necrosis [28]. A of camel milk against these toxicants induced
significant increase in ALP could occur in oxidative stress is due to its antioxidant
parenchymal liver disorders such as hepatitis properties. Camel milk was found to contain high
and cirrhosis, and striking elevation is concentrations of vitamins A, B2, C and E and is
encountered with extrahepatic biliary tract very rich in magnesium and other trace
(mechanical) obstruction or with intrahepatic elements, these vitamins act as antioxidants and
(functional cholestasis) [29]. Our have been found to be useful in preventing
histopathological findings confirmed toxicant-induced tissue injury [1,34,35]. Camel
hepatocellular damage where, on microscopic milk decreased (p < 0.05) MXC induced elevated
examination the livers in MXC-treated groups enzyme levels in tested groups, indicating the
revealed severe pathological damages such as: protection of structural integrity of hepatocytes
sinusoidal dilatation, congestion of central vein, cell membrane or regeneration of damaged liver
leukocytes and lymphocytes infiltration. Several cells [36]. The increase of albumin concentration
studies have provided a considerable support for after treatment with camel milk may be attributed
evidencing the protective effects of camel milk on to the decrease in lipid peroxidation processes
liver damage [30,31]. The anticytoxic and and increase in the activities of plasma protein
antigenotoxic effects of CM constituents against thiols as a result of treatment with camel
the genotoxic effects of chemicals as cisplatin milk in both animal and human [37,
anti-tumor agent are being investigated by 38,31]. Moreover, the results obtained from
Salwa and Lina [32]. Also, Hamed et al. [33] the liver histopathological analysis were in
35
30.6
30
27.3
ab
25
GSH levels (U/mg protein)
20
15.2
15
*ac
9.12
10
5
0
1
Expermintal treated groups
MXC MXC+CM CM Control
Fig. 2. The effect of long exposure to MXC for 12 months on GSH levels and the restoration
effect of Camel milk
Data are expressed as means ± S.D. of twenty animals per group. *denotes P < 0.05 as compared to control group, a denotes
P < 0.05 as compared to MXC- group. b denotes P < 0.05 as compared to MXC+CM -group. C denotes P < 0.05 as compared
to CM – group (One- way ANOVA/Duncan).
29Elsharkawy et al.; ARJOCS, 3(1): 24-35, 2021; Article no.ARJOCS.415
70
TBARS levels (nmol/g protein)
60 56.2
50 46.6
*bc
40 *ac 33.2 32.8
30
ab
20
10
0
1
Expermintal treated groups
MXC MXC+CM CM Control
Fig. 3. The effect of long exposure to MXC for 6 months on TBARS levels and the restoration
effect of Camel milk
Data are expressed as means ± S.D. of twenty animals per group. *denotes P < 0.05 as compared to control group, a denotes
P < 0.05 as compared to MXC- group. b denotes P < 0.05 as compared to MXC+CM -group. C denotes P < 0.05 as compared
to CM – group (One- way ANOVA/Duncan)
100
90
TBARS levels (nmol/g protein)
80 76.2
70
*bc
60
48.6
50
40 *ac 32.8
30.2
30
bc
20
10
0
1
Expermintal treated groups
MXC MXC+CM CM Control
Fig. 4. The effect of long exposure to MXC for 12 months on TBARS levels and the restoration
effect of Camel milk
Data are expressed as means ± S.D. of twenty animals per group. *denotes P < 0.05 as compared to control group, a denotes
P < 0.05 as compared to MXC- group. b denotes P < 0.05 as compared to MXC+CM -group. C denotes P < 0.05 as compared
to CM – group (One- way ANOVA/Duncan)
30Elsharkawy et al.; ARJOCS, 3(1): 24-35, 2021;; Article no.ARJOCS.415
no.ARJOCS
Fig. 5. a. Liver of rat treated with MXC for 6 months showed localized area of necrosis with
some apoptic changes in the hepatocytes, congestion, cellular infiltration of mononuclear
cells type. H & E; x25. b. Liver of rat treated with MXC for 6 months showed severe fatty
degeneration of the hepatocytes
patocytes with focal area of kupffer cell proliferation. H & E; x25
Fig. 6. a.. Liver hepatocytes of rat treated with MXC for 12 months’ showed apoptotic changes
including condensation, increase esinophillia of cytoplasm shrinkage of the nucleus
associated with area of cellular reaction. H & E; x25. b. Liver of rat treated with MXC for 12
months’ showed blood vessel filled with porteinous material and R.B.Cs. H & E; x25
31Elsharkawy et al.; ARJOCS, 3(1): 24-35, 2021; Article no.ARJOCS.415
Fig. 7. a. Liver of rat treated with MXC for 12 months showed newly formed bile ducteules
denotes neoplastic changes in the portal tract associated with cytoplasm coagulation. H & E;
x25. b. Liver of rat treated with MXC for 12 months showed large area of cellular infiltration in
the portal tract (lymphocyte type) associated with dissociation, disorganization of hepatocytes
along with some mitotic reactions. H & E; x25
Fig. 8. a. Liver of rat treated with mythoxychlor and camel milk showed nearly normal hepatic
cells and slightly congested central vein. H and E X 10. b. The liver of rats treated with camel
milk only showed normal hepatocytes, blood vessels and bile ducts.
consistence with the biochemical findings, protective role of CM. Furthermore, our findings
indicating that the decreased degeneration of indicated that MXC caused increased ROS
some hepatocytes and normal architecture of production, oxidative damage, and decreased
others. These effects demonstrated the hepato- antioxidant defense in the rat liver, which might
32Elsharkawy et al.; ARJOCS, 3(1): 24-35, 2021; Article no.ARJOCS.415
result in an oxidized state in the cells. It has been Taken together these nutrients enhance the
known that increased TBARS level and production of detoxifying molecules, absorption
decreased GSH concentration indicates an of antioxidant vitamins and activation of
increased generation of ROS, which cause lipid antioxidant enzymes which in turn activate the
peroxidation in the liver [39]. The mechanism of detoxification system and reduce the exerted
methoxychlor mediated oxidative stress is not oxidative stress.
very clear but it has been shown to be mediated
by the activation of microsomal monooxygenase, 5. CONCLUSION
which is involved in the conversion of
methoxychlor into its reactive metabolites [40]. In conclusion, camel milk may have a restoration
During this reaction the reactive metabolites, effect against MXC -induced liver damage and
possibly free radicals, bind covalently to may improve hepatic function parameters. Also,
microsomal components [8]. It has been shown camel milk has several antioxidant properties
that human cytochrome P-450 enzymes, could be efficient in the protection against the
responsible for the conversion of methoxychlor liver injury induced by MXC exposure in rats.
into its major metabolites and CYP1A2, have Therefore, camel milk may be recommended to
been shown to play a predominant role in this use against the hepatotoxic effects of MXC and
reaction [11]. It has been reported that ROS such further studies are needed toward other chemical
as H2O2 appears to be a key agent in the agents.
cytotoxic effects of the methoxychlor [41,42]. Our
results revealed that administration of camel milk COMPETING INTERESTS
in association with MXC slightly reduce TBARS
levels and elevate the level of GSH-Px, these Authors have declared that no competing
result were progressed in group treated with interests exist.
camel milk alone. That is due to the role of camel
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