EFFECTS OF INSULIN-TREATMENT ON ENDONEURIAL AND SYSTEMIC OXIDATIVE STRESS IN RELATION TO NERVE-CONDUCTION IN STREPTOZOTOCIN-DIABETIC RATS

As increased oxidative stress is probably a pathogenetic factor in the development of diabetic complications, we studied nerve function and endogenous antioxidants in plasma, erythrocytes and sciatic nerve of u ntreated and insulin-treated streptozotocin-diabetic rats. After 18 we eks, the diabetes-induced sciatic nerve conduction velocity deficits w ere approximately 65% improved by insulin (P < 0.001). Plasma superoxi de dismutase was significantly reduced in diabetes (P < 0.01); smaller decreases in plasma catalase and glutathione levels were observed. Th ese changes were corrected by insulin treatment. In erythrocytes, decr eased superoxide dismutase (P < 0.05) and increased total glutathione levels (P < 0.05) were found. All effects of diabetes, including a ris e in plasma malonyldialdehyde (P < 0.05), were partially reversed by i nsulin treatment. In nervous tissue, diabetes caused increased catalas e activity, uninfluenced by insulin (P < 0.05). Nerve superoxide dismu tase and glutathione did not change. The data suggest that, in diabete s, changes in systemic rather than endoneurial oxidative stress lead t o nerve dysfunction.