Role of hepatic and pancreatic oxidative stress in arsenic induced diabetic condition in Wistar rats.

Arsenic, a potent environmental toxicant has been reported to induce diabetes mellitus, but its potential biological mechanism(s) has not been much investigated. The present study was designed to correlate pancreatic and hepatic oxidative stress with arsenic induced diabetes mellitus in experimental animals. Male albino Wistar rats were administered with low (1.5 mg kg(-1) b.wt.) and high (5.0 mg kg(-1) b.wt.) sodium arsenite orally for 4 week. Hyperglycemic condition was observed in arsenic exposed groups as indicated by increased (P < 0.001) fasting plasma glucose, glycosylated hemoglobin (HbA1c) and impaired glucose tolerance (IGT), which were accompanied by an increase in the level of lipid peroxidation (P < 0.001), protein oxidation (P < 0.05 at low dose and P < 0.001 at high dose) and nitric oxide (NO) (P < 0.001) in hepatic and pancreatic tissue compared to control. Furthermore, superoxide dismutase (SOD) (P < 0.001), catalase (CAT) (P < 0.001) and glutathione-S-transferase (GST) (P < 0.05 at low dose and P < 0.001 at high dose) activities were elevated, while glutathione peroxidase (GPx) (P < 0.05 at low dose and P < 0.001 at high dose) and GSH level showed significant (P < 0.001) depletion in both studied tissue of arsenic exposed rats compared to control. Arsenic induced hepatotoxicity was manifested by an increase (P < 0.001) in serum ALT, AST and ALP. Arsenic exposure leads to accumulation of arsenic (P < 0.05) and significant (P < 0.05) depletion of copper and zinc level in hepatic and pancreatic tissue as compared to control. Our data suggests that sub-chronic arsenic exposure induces diabetic condition which may be mediated due to increased oxidative stress in hepatic and pancreatic tissue.