Aliyu et al., 1:4
http://dx.doi.org/10.4172/scientificreports.222
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Research Article
Ethanol Suppresses the Effects of Sodium Arsenite in Male Wister Albino
Rats
Muhammad Aliyu*12, Oyeronke A Odunola2, Solomon E Owumi2, Nathan Habila1, Idowu A Aimola1 and Ochuko L Erukainure3
1
Department of Biochemistry, Ahmadu Bello University, Zaria, Nigeria
Department of Biochemistry, University of Ibadan, Ibadan, Nigeria
Food Technology Division, Federal Institute of Industrial Research, Oshodi, Nigeria
2
3
Abstract
Background: Millions of people around the world get exposed to high levels of heavy metals in drinking-water.
Therefore, quality control in drinking-water, food industries and detection of heavy metals is an extremely critical
issue in maintaining the human health. Of such heavy metals is arsenic. Water as one of the major ingredient in both
traditional and modern beer fermentation process may/may not be contaminated with arsenic due to poor quality
control. As a result people are exposed to the end product which constituted arsenic compound. Sodium arsenite
and ethanol has been established to be toxic both in vivo and in vitro.
Objective: This study is primarily designed to investigate the effect of co-administration of sodium arsenite and
ethanol in male Wister albino rats.
Methods: Forty ive (45) albino rats divided into nine (9) groups of ive rats each were administered with distilled
water, 2.5mg and 5mg/kg body weight of sodium arsenite, 3% and 6% (v/v) respectively. Treatment was based on
single and combined administration. Micronucleated polychromatic erythrocytes, acetylcholine esterase, Aspartate
Transaminase (AST), Alkaline Phosphatase (ALP), Alanine Transaminase (ALT) and hematological parameters
were determined by standard procedures (Figure 1).
Results: Combined treatment with sodium arsenite and ethanol signiicantly decreased the number of micro
nucleated polychromatic erythrocytes, AST, ALT and ALP activities as against the single treated groups. However,
there was stabilization of acetylcholine esterase activity in the brain. The hematological parameters level was also
stabilized.
Conclusions: We therefore proposed that the chemical interaction between sodium arsenite and ethanol is
what was responsible for the suppression of sodium arsenite – induced clastogenic, hepatotoxic, anti-acetylcholine
esterase and anemic effects.
Keywords: Sodium arsenite; Ethanol; Micronucleated polychromatic
erythrocyte; Acetylcholine esterase, Hematology
Introduction
Continuous exposure of humans to arsenic through long-term
ingestion of contaminated water and its attendant health problems
has been widely reported. Inorganic arsenic compounds are widely
distributed in nature and a lot of epidemiological evidence exist
associating occupational and environmental exposure to them with
human carcinogenesis [1,2]. For instance, exposure to trivalent and
pentavalent forms of arsenic, which occurs worldwide primarily through
occupational and environmental exposure, causes characteristic skin
alterations (ulceration), including hyperkeratosis and skin cancer
[3]. Epidemiological studies conducted in Taiwan [4], Chile [5] and
Japan [6] indicated a connection between arsenic exposures from
contaminated drinking water among the inhabitants. It is also known
that arsenic interact with other substances, metals inclusive there by
potentiating its efects and/or vice versa [7]. here is growing evidences
that sodium arsenite intoxication can compromise the integrity of
the liver in mouse, rat, ish, and goat [8,9,10]. Recently, some studies
suggest the use of antioxidants and antioxidant rich foods and herbal
medicinal plant for the management of arsenicosis [11]. Induction of
cancer is frequently associated with DNA damage, changes in ploidy
of cells, and non-random chromosome aberrations which can result
from exposure to arsenic [12]. Association between chronic alcohol
abuse and the development of cirrhosis, as well as between cirrhosis
and the development of Hepatocellular Carcinoma (HCC), is well
documented [13,14]. Acute and chronic ethanol treatment has been
shown to increase the production of reactive oxygen species, lower
cellular antioxidant levels, and enhance oxidative stress in many tissues,
especially the liver [15]. Ethanol-induced oxidative stress plays a major
role in the mechanisms by which ethanol produces liver injury [15].
Water as one of the major ingredient in both traditional and modern
beer fermentation process may/may not be contaminated with arsenic
due to poor quality control. As a result people are exposed to the end
product which constituted arsenic compound. Sodium arsenite and
ethanol has been established to be toxic both in vivo and in vitro.
herefore, this study was undertaken to investigate the efect of coadministration of sodium arsenite and ethanol on male Wister albino
rats with a view to establish the facts on whether or not their interaction
could be enhance or suppress by one another.
*Corresponding author: Muhammad Aliyu, Department of Biochemistry, Ahmadu
Bello University, Zaria, Nigeria, Tel: +2347038161430; E-mail: amachida31@gmail.com
Received July 07, 2012; Published August 07, 2012
Citation: Aliyu M, Odunola OA, Owumi SE, Habila N, Aimola IA, et al. (2012) Ethanol Suppresses the Effects of Sodium Arsenite in Male Wister Albino Rats. 1: 222.
doi:10.4172/scientiicreports.222
Copyright: © 2012 Aliyu M, et al. This is an open-access article distributed under
the terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author and
source are credited.
Volume 1 • Issue 4 • 2012
Citation: Aliyu M, Odunola OA, Owumi SE, Habila N, Aimola IA, et al. (2012) Ethanol Suppresses the Effects of Sodium Arsenite in Male Wister Albino
Rats. 1: 222. doi:10.4172/scientiicreports.222
Page 2 of 6
Materials and Methods
Chemicals
Sodium Arsenite (NaAsO , Mol.wt 129.91, 98% prod 30110, BDH
chemicals Ltd Poole England)2 and ethanol (C2H5OH, Mol.wt 46.07,
99.7 to 100% v/v pod 10107, BDH chemicals Ltd Poole England) were
dissolved in distilled water to prepare 3%, and 6% ethanol (v/v).
Animals
bottles for hematological analysis and the remaining were centrifuged at
4,000 rpm for 5 minutes to obtain the serum for analyses. he liver and
brain weight were immediately taken and brain was quickly placed on
an inverted Petri dish on ice. he fore brain was dissected, weighed and
homogenized in 10ml of a medium containing 10mM Tris – HCl bufer
(pH 7.2) and 160mM sucrose. he total homogenate was centrifuged at
3500g at - 4°C in a refrigerated centrifuge for 5 minute. he supernatant
was used for Acetylcholine Esterase (AChE) activity. he femurs were
preserved for micronucleus assay.
Forty ive (45) male albino rats weighing 151 – 198 g were used
for the present investigation. hey were reared at the animal house
of the Department of Pharmacy, Faculty of Pharmaceutical Sciences,
Ahmadu Bello University, and Zaria, Nigeria with the approval of
animal rights review committee. hey were acclimatized for 1 week
on normal diet of pelletized mouse chow, with water given ad libitum
at room temperature within a 12-h light and dark cycle before the
commencement of the experiment.
he Alkaline Phosphatase (ALP), Alanine Aminotransferase
(ALT), and Aspartate Aminotransferase (AST) were determined by
using Auto Analyzer Hitachi Roche 7020 (902), Japan Inc. according to
manufacturer’s protocols. Complete blood counts were also determined
using Coulter HmX Hematology Analyzer Beckman Coulter Inc.
according to manufacturer’s protocols.
Experimental design
Determination of acetylcholine esterase activity
he animals were divided into nine diferent groups of ive (5) rats
each according to their body weight proximity and treated once in a
week for a period of four week as shown below:
Group 4: 3% ethanol (v/v)
he activity of AChE in the brain was determined by the method
described by Ellman et al. [18], as modiied by Srikumar et al. [19] he
mixture was prepared by mixing 0.4mL aliquot of the homogenate and
added to 2.6ml phosphate bufer (0.1M, pH8.0) and 100μL of DTNB
(270μM). his was pre-incubated for 2 minute at 30oC and the reaction
was started with the addition of 20μL ATC (30mM). he product of
thiocholine reaction with DTNB was determined at 412nm for a period
of 10 minute at 2 minute intervals. he absorbance per minute was
determined.
Group 5: 6% ethanol (v/v)
Micronucleus assay
Group 6: 2.5mg/kg body weight Sodium arsenite + 3% ethanol (v/v)
Clastogenic efects were evaluated in the rat bone marrow using
the micronucleus assay as described by Heddle and Salmone, [20] and
modiied by Heddle, et al, [21]. Two hours prior to sacriice, the animals
were injected (i.p.) with 0.04 % colchicine (1ml/100g body weight).
Bone marrow cells from both femurs were used for preparing slides.
he slides were ixed, air-dried and pretreated with May-Grunewald
solution. hey were then stained with 5% Giemsa solution. he
slides were scored for the presence of micronucleated polychromatic
erythrocytes (mPCEs) in 1000 cells according to standard procedure.
Group 1: Distilled water
Group 2: 2.5mg/kg body weight of sodium arsenite
Group 3: 5mg/kg body weight Sodium arsenite
Group 7: 5mg/kg body weight Sodium arsenite + 6% ethanol (v/v)
Group 8: 2.5mg/kg body weight Sodium arsenite using 3% Ethanol
as solvent (v/v)
Group 9: 5mg/kg body weight Sodium arsenite using 6% Ethanol
as solvent (v/v)
Twenty-four (24) hours ater the last administration, animals were
sacriiced by using 60mg/kg body weight of sodium pentothal. Liver,
Brain, Femur and Blood samples were collected, part of the blood
samples were placed in Ethylene Diamine Tetra acetic Acid (EDTA)
Group Treatment
1
Determination of biochemical and hematological parameters
Statistical analysis
he results were expressed as mean ± Standard error. Diferences
IBW
FBW
Distilled Water
198.60 ± 12.67
246.40 ± 15.66 24.13 ± 1.94d,h,i
%WT CHANGE
Liver
Brain
RLW
RBW
7.16 ± 0.54 1.67 ± 0.04 2.99 ± 0.39 0.69 ± 0.04
2
2.5mg/kg Body weight SA
182.44 ± 15.89
225.00 ± 21.86 25.59 ± 4.41d,h
7.17 ± 0.56 1.54 ± 0.07 3.36 ± 0.55 0.71 ± 0.08
3
5mg/kg Body Weight SA
195.00 ± 7.52
235.40 ± 14.74 21.57 ± 3.74g,h,i
6.81 ± 0.15 1.54 ± 0.03 2.95 ± 0.26 0.67 ± 0.04
4
3% Ethanol
184.56 ± 9.23
229.80 ± 7.33
34.69 ± 3.50a,b,e
7.58 ± 0.35 1.63 ± 0.04 3.25 ± 0.25 0.70 ± 0.02
5
6%Ethanol
161.20 ± 7.57
204.60 ± 8.25
27.15 ± 2.20d,f,h,i
6.72 ± 0.29 1.60 ± 0.05 3.29 ± 0.13 0.79 ± 0.05
6
2.5mg/kg Body Weight SA+3% Ethanol
169.00 ± 6.37
219.80 ± 3.82
30.53 ± 3.34
6.74 ± 0.21 1.67 ± 0.05 3.01 ± 0.09 0.76 ± 0.03
7
5mg/kg Body Weight SA+6%Ethanol
151.20 ± 4.68
200.00 ± 2.32
32.74 ± 4.00c,e
6.27 ± 0.19 1.65 ± 0.05 3.14 ± 0.12 0.82 ± 0.03
8
2.5mg/kg body weight Sodium arsenite using 3%
Ethanol as solvent (v/v)
153.40 ± 5.36
212.20 ± 2.90
38.77 ± 3.28a,b,c,e
7.01 ± 0.29 1.55 ± 0.06 3.31 ± 0.15 0.73 ± 0.04
9
5mg/kg body weight Sodium arsenite using 6% 155.00 ± 9.05
Ethanol as solvent (v/v)
207.80 ± 11.20
34.28 ± 2.00a,c,e
5.52 ± 0.17 1.66 ± 0.08 2.67 ± 0.22 0.80 ± 0.03
a= statistically signiicant (p<0.05) when compared with group 1 b= statistically signiicant (p<0.05) when compared with group 2 c= statistically signiicant (p<0.05) when
compared with group 3 d= statistically signiicant (p<0.05) when compared with group 4 e= statistically signiicant (p<0.05) when compared with group 5 f= statistically
signiicant (p<0.05) when compared with group 6 g= statistically signiicant (p<0.05) when compared with group 7 h= statistically signiicant (p<0.05) when compared with
group 8 i= statistically signiicant (p<0.05) when compared with group 9 SA= Sodium Arsenite IBW= Initial Body weight FBW= Final Body weight %WT = % weight RLW
=relative liver weight RBW = relative brain weight
Table 1: Body and Organ weight (g) for n=5, (mean ± SE) of the experimental animals before and after exposure to sodium arsenite and ethanol.
Volume 1 • Issue 4 • 2012
Citation: Aliyu M, Odunola OA, Owumi SE, Habila N, Aimola IA, et al. (2012) Ethanol Suppresses the Effects of Sodium Arsenite in Male Wister Albino
Rats. 1: 222. doi:10.4172/scientiicreports.222
Page 3 of 6
Group Treatment
ALP
ALT
AST
1
Distilled Water
4.97 ± 1.35d,e,g
23.00 ± 4.81b,c,d,e,f,g,,i
108.50 ± 8.50f
2
2.5mg/kg Body Weight SA
17.94 ± 1.38d,e,g
37.00 ± 3.99a
110.00 ± 5.00f
3
5mg/kg Body Weight SA
41.40 ± 9.60e,g
43.80 ± 0.80a
115.00 ± 5.77f
4
3% Ethanol
73.02 ± 22.32a,b
46.60 ± 6.50a,h
142.40 ± 18.35
5
6%Ethanol
105.43 ± 23.01a,b,c,f,h,i
49.50 ± 0.50a,h
150.00 ± 5.00
6
2.5mg/kg Body Weight SA + 3% Ethanol
44.28 ± 15.41e
39.00 ± 4.50a
159.50 ± 9.50a,b,c
7
5mg/kg body weight SA + 6%Ethanol
87.40 ± 13.55a,b,c,g,h,i
44.60 ± 4.27a
130.40 ± 8.16
8
2.5mg/kg body weight Sodium arsenite using 3% Ethanol as solvent (v/v)
31.74 ± 1.38e,g
32.33 ± 3.67d,e
130.20 ± 7.11
9
5mg/kg body weight Sodium arsenite using 6% Ethanol as solvent (v/v)
34.04 ± 9.34e
41.60 ± 2.16a
123.67 ± 7.54
a= statistically signiicant (p<0.05) when compared with group 1 b= statistically signiicant (p<0.05) when compared with group 2 c= statistically signiicant (p<0.05) when
compared with group 3 d= statistically signiicant (p<0.05) when compared with group 4 e= statistically signiicant (p<0.05) when compared with group 5 f= statistically
signiicant (p<0.05) when compared with group 6 g= statistically signiicant (p<0.05) when compared with group 7 h= statistically signiicant (p<0.05) when compared with
group 8 i= statistically signiicant (p<0.05) when compared with group 9 SA= Sodium Arsenite ALP=alkaline phosphatase ALT= alanine amino transferase AST= aspartate
amino transferase
Table 2: Serum level mean ± S.E (U/L) for n=5, of aspartate amino transferase, alanine amino transferase and alkaline phosphatase in sera of rats.
Group
Treatment
1
Distilled Water
Micronuclei/1000 PCE
3.67 ± 1.67b,c,g
2
2.5mg/kg Body Weight SA
15.00 ± 2.02a,c,d,e,f,h,i
3
5mg/kg Body Weight SA
22.80 ± 3.50a,b,d,e,f,g,h,i
4
3% Ethanol
6.00 ± 1.05b,c,g
5
6%Ethanol
7.60 ± 1.70b,c
6
2.5mg/kg Body Weight SA + 3% Ethanol
6.20 ± 1.53b,c,g
7
5mg/kg Body Weight SA + 6%Ethanol
11.80 ± 1.62a,c,d,f
8
2.5mg/kg body weight Sodium arsenite using 3% Ethanol as solvent (v/v)
8.20 ± 1.32b,c
9
5mg/kg body weight Sodium arsenite using 6% Ethanol as solvent (v/v)
8.80 ± 1.24b,c
a= statistically signiicant (p<0.05) when compared with group 1 b= statistically signiicant (p<0.05) when compared with group 2 c= statistically signiicant (p<0.05) when
compared with group 3 d= statistically signiicant (p<0.05) when compared with group 4 e= statistically signiicant (p<0.05) when compared with group 5 f= statistically
signiicant (p<0.05) when compared with group 6 g= statistically signiicant (p<0.05) when compared with group 7 h= statistically signiicant (p<0.05) when compared with
group 8 i= statistically signiicant (p<0.05) when compared with group 9 SA= Sodium Arsenite PCE= Polychromatic Erythrocyte
Table 3: Induction of micronucleated polychromatic erythrocytes (mPCEs) in rat bone marrow cells after exposure to sodium arsenite and ethanol mean ± SE for n=5.
Treatment
Activity (μmole of substrate hydrolyzed/min/g of tissue)×10-2
1
Distilled Water
6.44 ± 0.78b,c
2
2.5mg/kg Body Weight SA
1.77 ± 0.85a,c,d,g
3
5mg/kg Body Weight SA
0.93 ± 0.38a,c,d,g
Group
4
3% Ethanol
12.63 ± 5.97a,b,c
5
6%Ethanol
6.95 ± 2.88
6
2.5mg/kg Body Weight SA + 3% Ethanol
7.78 ± 4.21
7
5mg/kg Body Weight SA + 6%Ethanol
13.73 ± 4.09a,b,c
8
2.5mg/kg body weight Sodium arsenite using 3% Ethanol as solvent (v/v)
4.96 ± 1.45
9
5mg/kg body weight Sodium arsenite using 6% Ethanol as solvent (v/v)
7.88 ± 2.91
a= statistically signiicant (p<0.05) when compared with group 1 b= statistically signiicant (p<0.05) when compared with group 2 c= statistically signiicant (p<0.05) when
compared with group 3 d= statistically signiicant (p<0.05) when compared with group 4 e= statistically signiicant (p<0.05) when compared with group 5 f= statistically
signiicant (p<0.05) when compared with group 6 g= statistically signiicant (p<0.05) when compared with group 7 h= statistically signiicant (p<0.05) when compared with
group 8 i= statistically signiicant (p<0.05) when compared with group 9 SA= Sodium Arsenite PCE= Polychromatic Erythrocyte
Table 4: Acetylcholine esterase activity mean ± SE for n=5, in the brain of the rats after exposure to sodium arsenite and ethanol.
between the groups were analyzed by one-way analysis of variance
(ANOVA) with the aid of Statistical Package for Social Sciences (SPSS)
sotware, SPSS Inc., Chicago, Standard version 10.0.1. P-values < 0.05
were considered statistically signiicant for diferences in mean using
the Least of Signiicance Diference (Lsd).
Results
he body weight results from table 1, shows a signiicant (p<0.05)
decrease in % weight change in a concentration dependent manner
with concomitant signiicant (p<0.05) increase in the groups treated
with sodium arsenite and ethanol together. From table 1 there are no
signiicant (p>0.05) diference on the organs and relative organs weight.
Based on the activity of the liver enzymes (ALP, ALT and AST) from
table 2, the interaction of ethanol and sodium arsenite signiicantly
(p<0.05) decrease the activity of the liver enzymes as compared with the
groups treated with sodium arsenite, ethanol alone. his might suggest
the fact that ethanol is suppressing the efect of sodium arsenite.
As depicted in table 3, it was observed that administration of
ethanol and sodium arsenite signiicantly (p<0.05) decreased the
number of micronuclei/1000PCE as compared with the groups treated
with sodium arsenite, ethanol respectively, indicating the fact that the
ethanol administration suppressed the clastogenic efect of sodium
arsenite. his might further suggest an interaction between sodium
arsenite and ethanol which led to the observed anticlastogenic activity
as sodium arsenite is a known clastogen.
Volume 1 • Issue 4 • 2012
Citation: Aliyu M, Odunola OA, Owumi SE, Habila N, Aimola IA, et al. (2012) Ethanol Suppresses the Effects of Sodium Arsenite in Male Wister Albino
Rats. 1: 222. doi:10.4172/scientiicreports.222
Page 4 of 6
From table 4, the activity of acetylcholine esterase in the brain was
signiicantly (p<0.05) inhibited by sodium arsenite in a concentration
dependent manner. At low concentration ethanol did not signiicantly
(p>0.05) inhibit the activity of the enzyme but did at a higher
concentration. However, the co-administration of sodium arsenite and
ethanol led to an increased activity of acetylcholine esterase suggesting
that the interaction might have caused the enzyme induction.
However, from table 5, most of the haematological parameters
PCV, Hb and RBC were signiicantly (p<0.05) decreased with increased
sodium arsenite and ethanol concentration but these were observed
to start increasing from group 6 to 9. Furthermore, in terms of WBC
it was only group 8 that showed a signiicant (p<0.05) decrease while
others showed no remarkable increase in WBC. his signiies that
the simultaneous administration of the toxicants in question has a
counteracting efect, thus suggesting that the interaction is possibly
having anti-anaemic efect.
Discussion
Exposure to arsenite has been linked to diverse defects in both
experimental animals and in humans [22-26]. he liver is an important
target organ for arsenic toxicity [27]. Arsenic has been claimed to be
of clinical utility in the treatment of syphilis, amoebiasis, and certain
other tropical diseases [24] and also has been used in Fowler solution
in the treatment of arthritis [24], but recently arsenic intoxication
in experimental animals has been associated with hepatic tumours
[25], the inhibition of testicular steroid genic function [28], and
spermatogenesis [26], as well as with severe metabolic disorders such as
diabetes in humans [22,23]. It is known that (SA) can act as comutagen
due to its ability to inhibit the activities of thiol containing enzymes
[27], such as DNA ligase [28] resulting in defective DNA replication,
Sodium Arsenite-Ethanol Interaction
Acetylcholinesterase acivity
(+)
Liver enzymes acivity (-)
repair, recombination and joining of single- and double-stranded DNA
breaks [29].
Ethanol-induced oxidative stress is as a result of the combined
impairment of antioxidant defences and the production of reactive
oxygen species by the mitochondrial electron transport chain,
the alcohol-inducible Cytochrome P450 (CYP) 2E1 and activated
phagocytes [15]. Furthermore, Hydroxyethyl Radicals (HERs) are
also generated during ethanol metabolism by CYP2E1. he available
evidence indicates that, by favouring mitochondrial permeability
transition, oxidative stress promotes hepatocyte necrosis and/or
apoptosis and is implicated in the alcohol-induced sensitization of
hepatocytes to the pro-apoptotic action of TNF-a. Moreover, oxidative
mechanisms can contribute to liver ibrosis, by triggering the release of
pro-ibrotic cytokines and collagen gene expression in hepatic stellate
cells [30].
his study examines the efect of co-exposure to sodium arsenite
and ethanol on male Wister albino rats. he interaction between
sodium arsenite and ethanol seem to reverse the efect of decreased
body weight. his might be attributed to the fact that ethanol induces
fatty liver with enhanced lipogenesis that ultimately lead to an increase
in weight [31]. he results of the present study clearly demonstrate
that administration of sodium arsenite and ethanol respectively,
signiicantly (P < 0.05) induced the formation of micronuclei in the
Polychromatic Erythrocytes (PCEs) of the rat bone marrow cells.
However, the reversal of that happened when both toxicants were coadministration. his is may be due to the fact that arsenite generates
free radicals that can attack DNA leading to chromosomal breakage.
In addition, acetaldehyde the end product of ethanol metabolism
can form DNA adducts which might also explain why groups treated
with sodium arsenite and ethanol respectively were able to induced
clastogenicity. he results obtained from the assessment of the serum
activities of ALP, ALT and AST shows that their activities increased in
a concentration dependent manner. Interestingly, the activities were
decreased in the groups of co-administration providing a clue that the
chemical interaction between sodium arsenite and ethanol is having a
reversal efect. Exposure to sodium arsenite had been shown to induce
ALP, AST and ALT activity [32], which is clearly an indication of
induction of hepatotoxicity and oxidative stress in the hepatocytes.
Micronucleated polychromaic erythrocytes (-)
+ = increase
- = decrease
Acetylcholine (ACh) is a neurotransmitter that functions in
conveying nerve impulses across synaptic clets within the CNS [33].
Following the transmission of an impulse across the synapse by the
release of Ach, AChE is released into the synaptic clet [34]. his
Clastogenicity (-)
Figure 1:
Group
Treatment
PCV (%)
Hb(g/dL)
RBC(million/μL)
WBC ×109 /L
1
Distilled Water
37.50 ± 2.50
12.50 ± 0.80
7.34 ± 0.27b
2.56 ± 0.31
2
2.5mg/kg Body Weight SA
36.20 ± 2.13
11.35 ± 0.35
5.62 ± 0.29a,c
3.00 ± 0.35
3
5mg/kg Body Weight SA
35.00 ± 1.64
11.00 ± 0.70
6.72 ± 0.31b
3.20 ± 0.54
4
3% Ethanol
31.40 ± 2.42
10.05 ± 1.95
5.64 ± 0.24a,c
2.50 ± 0.35
5
6%Ethanol
28.00 ± 1.73b
9.23 ± 0.52a
5.62 ± 0.33a,c
2.90 ± 0.58
6
2.5mg/kg Body Weight SA+3% Ethanol
34.50 ± 1.50
11.00 ± 1.00
6 ± 0.34a
2.30 ± 0.25
7
5mg/kg Body Weight SA+6%Ethanol
39.00 ± 3.39
14.05 ± 0.95c
6.46 ± 0.2a,b
2.75 ± 0.25
8
2.5mg/kg body weight Sodium arsenite using 3% Ethanol as solvent
(v/v)
34.50 ± 2.50
13.85 ± 0.85
6.96 ± 0.31b
1.30 ± 0.25a,b,c
9
5mg/kg body weight Sodium arsenite using 6% Ethanol as solvent (v/v) 28.20 ± 2.35a,b,c
7.80 ± 0.70a,b,c
5.2 ± 0.51a,c
2.25 ± 0.25
a= statistically signiicant (p<0.05) when compared with group 1 b= statistically signiicant (p<0.05) when compared with group 2 c= statistically signiicant (p<0.05) when
compared with group 3 d= statistically signiicant (p<0.05) when compared with group 4 e= statistically signiicant (p<0.05) when compared with group 5 f= statistically
signiicant (p<0.05) when compared with group 6 g= statistically signiicant (p<0.05) when compared with group 7 h= statistically signiicant (p<0.05) when compared with
group 8 i= statistically signiicant (p<0.05) when compared with group 9 SA= Sodium Arsenite WBC= White Blood Count PCV= Packed cell volume Hb= Haemoglobin
RBC=Red blood cells
Table 5: Results of Heamatological parameters mean ± SE for n=5, of rats after exposure to sodium arsenite and ethanol.
Volume 1 • Issue 4 • 2012
Citation: Aliyu M, Odunola OA, Owumi SE, Habila N, Aimola IA, et al. (2012) Ethanol Suppresses the Effects of Sodium Arsenite in Male Wister Albino
Rats. 1: 222. doi:10.4172/scientiicreports.222
Page 5 of 6
enzyme hydrolyzes ACh to choline and acetate and transmission of
the nerve impulse is terminated [35]. he same scenario surfaced on
acetylcholine esterase activity being suppressed as concentration of
the toxicants increased and elevated in the co-administered groups;
probably the interaction might have initiated an enzyme induction as
the activity of AChE is vital to neurological functions. Similarly, based
on the hematological parameters single and co-administered groups
were depicting an antagonistic efect. his suggests the possibility of an
interaction between sodium arsenite and ethanol to have a stabilizing
efect on the levels of hematological parameters as the toxic compounds
like CCl4, arsenic and ethanol has been found to negatively afect
the levels of these parameters [36]. It is against this background we
proposed that the reaction between sodium arsenite and ethanol in
the presence of water generates dimethyl hydroxyl arsenous acid which
ultimately make it more polar and as such easily excreted without
necessarily causing harm to the system.
Conclusion
We therefore conclude that the chemical interaction between
sodium arsenite and ethanol is what is responsible for the suppression of
sodium arsenite – induced clastogenic, hepatotoxic, anti-acetylcholine
esterase and anemic efects by ethanol. his might be reason why most
people that are addicted to alcoholics don’t easily come down with
arsenic poisoning even though they are exposed to contaminated
drinking water. We recommend further molecular studies in this regard.
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Potential Conlicts of Interest
here are no conlicts of interest.
Acknowledgments
We graciously appreciate the consistent laboratory effort of Azuibuke Okafor,
edet imaikop, Fauziyya Abdullahi, Hope Ataboh, Victory E. and Malam Aliyu
(laboratory technologist) all from the Department of Biochemistry, Ahmadu Bello
University, Zaria, Nigeria.
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Volume 1 • Issue 4 • 2012
Citation: Aliyu M, Odunola OA, Owumi SE, Habila N, Aimola IA, et al. (2012) Ethanol Suppresses the Effects of Sodium Arsenite in Male Wister Albino
Rats. 1: 222. doi:10.4172/scientiicreports.222
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