NERVE FUNCTION AND OXIDATIVE STRESS IN DIABETIC AND VITAMIN-E-DEFICIENT RATS

Nerve dysfunction in diabetes is associated with increased oxidative s tress. Vitamin E depletion also leads to enhanced presence of reactive oxygen species (ROS). We compared systemic and endoneurial ROS activi ty and nerve conduction in vitamin E-depleted control and streptozotoc in-diabetic rats (CE-and DE-), and in normally fed control and diabeti c animals (CE+ and DE+). Nerve conduction was reduced in both diabetic groups. Vitamin E depletion caused a small further nerve conduction d eficit in the diabetic, but not in the control animals. The combinatio n of vitamin E deficiency and streptozotocin-diabetes (group DE-) appe ared to be lethal. In the remaining groups, an important rise in sciat ic nerve malondialdehyde (MDA) was observed in the vitamin E-depleted control rats. In contrast, plasma MDA levels were elevated in group DE + only, whereas hydrogen peroxide levels were increased in group CE-. Endoneurial total and oxidized glutathione and catalase were predomina ntly elevated in group DE+. These data show that nerve lipid peroxidat ion induced by vitamin E depletion does not lead to reduced nerve cond uction or changes in antioxidant concentrations as observed in STZ-dia betes. The marked systemic changes in MDA and antioxidants suggest tha t nerve dysfunction in experimental hyperglycemia is rather a conseque nce of systemic than direct nerve damage. (C) 1997 Elsevier Science In c.