Diabetes Type-II Exaggerates Renal Ischemia Reperfusion Injury by Elevation of Oxidative Stress and Infl ammatory Response

Objective: The present work was designed to investigate the role of Diabetes Mellitus Type-II (DM-II) on renal ischemia reperfusion (I/R)-associated pathophysiology in renal damage. Materials and Methods: DM-II in rats was induced by the administration of nicotinamide (230 mg /kg, i.p.), 15 min prior to a single dose of streptozotocin (65mg / kg, i.v.). In vivo renal I/R was performed in both DM-II and normal rats. Results and Discussions: Lipid peroxidation, xanthine oxidase activity, and nitric oxide levels were signiÞ cantly increased in renal tissue after I/R in diabetic rats compared to I/R in normal rats. Levels of antioxidant enzymes such as glutathione, superoxide dismutase, catalase, and glutathione peroxidase were signiÞ cantly reduced after I/R in diabetic rats compared to normal rats. Serum TNF-α levels, renal tissue myeloperoxidase activity, and apoptosis were also signiÞ cantly increased after I/R in DM-II rats. Furthermore, DM-II rats that underwent I/R, showed severe tubular cell swelling, interstitial edema, tubular dilatation, hyaline casts, and moderate to severe necrosis. Conclusion: In conclusion, DM-II rats showed exaggerated renal I/R injury. These Þ ndings have a major implication in ischemic injury that is prone to develop in DM-II.