Hans ). Tritschler
AST A Meclica AWD GmbH, Frankfurt, Germany
James D. Schmelzer, Yutaka Kishi, Yoshiyuki Mitsui, Masaaki Nagamatsu, Kim K. Nickander, Paula J. Zollman, and Phillip A. Low
Mayo Foundation, Rochester, Minnesota
There is ample evidence of oxidative stress in both experimental (EDN) and human diabetic neuropathy. Most studies have been done on plasma, with limited study on neural tissues. We briefly review and update our studies.
I. MECHANISMS OF OXIDATIVE STRESS A. Endoneurial Ischemia/Hypoxia
There is a perfusion deficit of approximately 50% that affects peripheral nerve endoneurium (1) and the parent cell bodies in relevant dorsal root and sympathetic ganglia (2). The onset of ischemia occurs within the first week (3) and is due to a reduction in nutritive rather than arteriovenous flow. There is attendant hypoxia, seen in both experimental (4) and human diabetes (5).
Glucose, by a process of autooxidation in the presence of decompartmenta-lized trace transitional metals, can cause lipid peroxidation (6). We have evaluated the role of hyperglycemia in lipid peroxidation in vitro, using an in vitro lipid peroxidation model, with an ascorbate-iron-EDTA system. The addition of 20 raM glucose to the incubation medium increased lipid peroxidation fourfold, confirming rapid and marked glucose-mediated autooxidative lipid peroxidation (7). Glucose autooxidation results in the production of protein reactive ketoaldehydes, hydrogen peroxide highly reactive oxidants, and the fragmentation of proteins (free radical mechanisms). Glycation and oxidation are simultaneous and inextricably linked (8).
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