Abstract
Oxidative stress is one of the factors contributing to the development of diabetic neuropathy. Several mechanisms, among which glucose autooxidation, glycation of antioxidant enzymes like superoxide dismutase, catalase and glutathione peroxidase, and increased polyol pathway activity, lead to increased production of reactive oxygen species. Both direct toxicity of oxygen free radicals to the peripheral nerve as well as changes in endothelial function and vascular reactivity, possibly by the quenching of nitric oxide, may lead to nerve dysfunction. Antioxidant drugs like iron chelators, N-acetylcysteine, probucol, α-lipoic acid and vitamin E can prevent nerve dysfunction in experimental diabetes. The present review focuses on the potential mechanisms explaining the association between oxidative stress and diabetic neuropathy, and summarizes the studies in which the effects of antioxidant treatment on the diabetic peripheral nerve have been evaluated. © 1997 John Wiley & Sons, Ltd.
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