Oxidative stress and diabetic neuropathy: pathophysiological mechanisms and treatment perspectives
Article first published online: 29 APR 2002
Copyright © 2002 John Wiley & Sons, Ltd.
Diabetes/Metabolism Research and Reviews
Volume 18, Issue 3, pages 176–184, May/June 2002
How to Cite
Sytze van Dam, P. (2002), Oxidative stress and diabetic neuropathy: pathophysiological mechanisms and treatment perspectives. Diabetes Metab. Res. Rev., 18: 176–184. doi: 10.1002/dmrr.287
- Issue published online: 7 JUN 2002
- Article first published online: 29 APR 2002
- Manuscript Accepted: 18 JAN 2002
- Manuscript Revised: 17 JAN 2002
- Manuscript Received: 24 SEP 2001
- diabetic neuropathy;
- oxidative stress;
- nerve blood flow
Increased oxidative stress is a mechanism that probably plays a major role in the development of diabetic complications, including peripheral neuropathy. This review summarises recent data from in vitro and in vivo studies that have been performed both to understand this aspect of the pathophysiology of diabetic neuropathy and to develop therapeutic modalities for its prevention or treatment. Extensive animal studies have demonstrated that oxidative stress may be a final common pathway in the development of diabetic neuropathy, and that antioxidants can prevent or reverse hyperglycaemia-induced nerve dysfunction. Most probably, the effects of antioxidants are mediated by correction of nutritive blood flow, although direct effects on endoneurial oxidative state are not excluded. In a limited number of clinical studies, antioxidant drugs including α-lipoic acid and vitamin E were found to reduce neuropathic symptoms or to correct nerve conduction velocity. These data are promising, and additional larger studies with α-lipoic acid are currently being performed. Copyright © 2002 John Wiley & Sons, Ltd.