Nerve Function and Oxidative Stress in Diabetic and Vitamin E-Deficient Rats

• Published in: Free radical biology & medicine 1998, Vol.24 (1), p.18-26
• Main Authors: van Dam, P.Sytze, van Asbeck, B.Sweder, Bravenboer, Bert, van Oirschot, Johannes F.L.M., Gispen, Willem Hendrik, Marx, Joannes J.M.
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants - metabolism; Diabetes Mellitus, Experimental - complications; Diabetes Mellitus, Experimental - physiopathology; Diabetic Neuropathies - physiopathology; Free radicals; Hydrogen Peroxide - blood; Male; Malondialdehyde - blood; Microcirculation; Neural Conduction - physiology; Neuropathy; Oxidative stress; Oxidative Stress - physiology; Peripheral Nerves - blood supply; Rats; Rats, Wistar; Reactive Oxygen Species - metabolism; Sciatic Nerve - metabolism; Vitamin E deficiency; Vitamin E Deficiency - physiopathology
• ISSN: 0891-5849; 1873-4596
• DOI: 10.1016/S0891-5849(97)00122-6

Nerve dysfunction in diabetes is associated with increased oxidative stress. Vitamin E depletion also leads to enhanced presence of reactive oxygen species (ROS). We compared systemic and endoneurial ROS activity and nerve conduction in vitamin E-depleted control and streptozotocin-diabetic rats (CE− and DE−), and in normally fed control and diabetic animals (CE+ and DE+). Nerve conduction was reduced in both diabetic groups. Vitamin E depletion caused a small further nerve conduction deficit in the diabetic, but not in the control animals. The combination of vitamin E deficiency and streptozotocin-diabetes (group DE−) appeared to be lethal. In the remaining groups, an important rise in sciatic 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 predominantly elevated in group DE+. These data show that nerve lipid peroxidation induced by vitamin E depletion does not lead to reduced nerve conduction or changes in antioxidant concentrations as observed in STZ-diabetes. The marked systemic changes in MDA and antioxidants suggest that nerve dysfunction in experimental hyperglycemia is rather a consequence of systemic than direct nerve damage.