Differential susceptibility of chick and mouse islets to streptozotocin and its co-relation with islet antioxidant status.

Species differences in susceptibility of islets to STZ in different mammals have been well documented. Likewise, failure of diabetes induction in birds by streptozotocin has been reported. We hypothesized that the susceptibility of islets to STZ treatment may be related to generation of reactive oxygen species (ROS) and their antioxidant defense mechanisms. To test this hypothesis, we measured the total ROS generated and estimated the damage caused to the chick islets due to STZ treatment, in terms of lipid peroxidation, protein carbonyl formation and DNA strand breaks and compared it with that of mouse islets. We also compared the activities of antioxidant enzymes like catalase, superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione reductase (GR) and amount of antioxidant molecules like reduced glutathione (GSH) and uric acid under control and STZ-treated conditions. These studies coupled with viability, functionality and presence of glucose transporter GLUT2 in chick and mouse islets clearly indicated that STZ treatment neither affects viability nor functionality of chick islets whereas those of mouse islets are affected significantly. Here we demonstrate for the first time a correlation between the generation of ROS on STZ treatment and antioxidant status with insensitivity of chick islets to STZ resulting into failure of diabetes induction in chick.