Altered glucose homeostasis and oxidative impairment in pancreas of rats subjected to dimethoate intoxication.

The primary objective of this study was to investigate the effect of repeated sublethal doses of dimethoate (DM), an organophosphorus insecticide on glucose homeostasis, oxidative stress induction in pancreas and pancreatic damage in adult rats. Daily oral administration of DM (20 and 40 mg/kg b.w.) for 30 days induced a significant increase in blood glucose levels which was associated with impaired glucose tolerance. DM treatment resulted in elevated levels of pancreatic tissue specific markers such as activities of amylase and lipase in serum and pancreatic tissue indicating pancreatic dysfunction. Further, the activities of DT-diaphorase and NADPH-diaphorase in pancreas of DM treated rats were also found to be elevated. Interestingly, these biochemical dysfunctions were accompanied by a marked dose-related enhancement of lipid peroxidation and ROS levels in the pancreatic tissue indicating significant induction of oxidative damage. Additional evidence such as depletion in reduced glutathione levels and significant alterations in enzymic antioxidant defenses in pancreas among DM treated rats suggested induction of oxidative stress. Taken together, these findings provide experimental evidence that dimethoate at subchronic oral doses has the propensity to impair glucose homeostasis, induce significant pancreatic damage and also provide an account of the associated oxidative damage to pancreatic tissue in adult rats.