Journal of Stress Physiology &
Biochemistry, Vol. 9 No. 4
2013, pp. 230-240 ISSN 1997-0838
Original Text Copyright (cc) 2013 by Necib, Bahi, Zerizer,
Abdennour, Boulakoud
ORIGINAL ARTICLE
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QueryDate : 2016-12-24
Cites : 0
Hepatoprotective Role of
Sodium Selenite Against Oxidative Damage Induced by Mercuric Chloride
in Rat Albinos Wistar
Youcef Necib1*,Ahlem Bahi1,
Sakina Zerizer2, Cherif Abdennour3, Mohamed Salah
Boulakoud3
1 Department of
Biochemistry and biological cellular and
molecular, Faculty of sciences, Mentouri
university, BP 25000 Constantine, Algeria 2 Laboratory of microbiological engineering and application,
Faculty of sciences, Mentouri university, BP 25000 Constantine, Algeria 3 Animal Ecophysiology laboratory, Faculty of Sciences,
Badji Mokhtar University, BP12 Sidi Amar, Annaba, Algeria
*E-Mail: youcefnecib@yahoo.fr
Received July 15, 2013
Background:
The present study was undertaken, to evaluate the protective effect of
sodium selenite against mercuric chloride induced oxidative stress in
experimental rats. Female Albinos Wistar rats randomly divided into
four groups, were the first was served as a control, whereas the
remaining groups respectively treated with: sodium selenite (1mg/ kg
b.w; ip), mercuric chloride (1 mg/kg body weight i.p) and combination
of sodium selenite and HgCl2. Change in liver enzyme activities,
thiobarbituric acid reactive substances (TBARS) level, antioxidants and
reduced glutathione (GSH) contents were determined after 10 days
experimental period. Results: Exposure of rats to
mercuric chloride caused a significant increase the lipid peroxidation
level along with corresponding decrease
in the reduced glutathione and
various antioxidant enzymes in liver. And
increase in serum: glucose level,
APL and transaminases activities and
decreased in total protein and
albumin levels. Furthermore, treatment
with mercuric chloride caused a marked elevation of liver
weight and decreased body weight. Supplementation of sodium
selenite resulted in decreased of
lipid peroxidation level and in the
serum: AST, ALT and APL activities were
decreased along with increase in total protein, albumin and liver GSH
levels. The activities of antioxidants enzymes: glutathione peroxidase
(GSH -Px) and glutathione –S-transferase (GST) were also concomitantly
restored to near normal level by sodium selenite supplementation to
mercuric chloride intoxicated rats. Liver histological studies have
confirmed the changes observed in biochemical parameters and proved the
beneficial role of sodium selenite. Conclusion: The
results clearly demonstrate that sodium
selenite treatment augments the antioxidants defense
mechanism in mercuric chloride induced toxicity and provides evidence
that it may have a therapeutic role in free radical mediated diseases.
