TY - JOUR AU - Necib, Youcef AU - Bahi, Ahlem AU - Zerizer, Sakina AU - Abdennour, Cherif AU - Boulakoud, Mohamed Salah T1 - Hepatoprotective Role of Sodium Selenite Against Oxidative Damage Induced by Mercuric Chloride in Rat Albinos Wistar JO - Journal of Stress Physiology & Biochemistry Y1 - 2013 VL - 9 IS - 4 SP - 230 EP - 240 UR - http://www.jspb.ru/issues/2013/N4/JSPB_2013_4_230-240.pdf KW - Antioxidant enzymes KW - sodium selenite KW - Mercury KW - Oxidative stress KW - female Rat N1 - Owner: Алексей N1 - Added to JabRef: 2013.10.14 N2 - 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. ER -