Effects of insulin treatment on endoneurial and systemic oxidative stress in relation to nerve conduction in streptozotocin-diabetic rats |
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Authors: | P. S. VAN DAM,B. BRAVENBOER,B. S. VAN ASBECK,J. F. L. M. VAN OIRSCHOT,J. J. M. MARX,& W. H. GISPEN |
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Affiliation: | Rudolf Magnus Institute for Neurosciences, Utrecht University, Utrecht, The Netherlands,;Department of Internal Medicine, University Hospital, Utrecht, The Netherlands |
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Abstract: | As increased oxidative stress is probably a pathogenetic factor in the development of diabetic complications, we studied nerve function and endogenous antioxidants in plasma, erythrocytes and sciatic nerve of untreated and insulin-treated streptozotocin-diabetic rats. After 18 weeks, the diabetes-induced sciatic nerve conduction velocity deficits were approximately 65% improved by insulin ( P <0.001). Plasma superoxide dismutase was significantly reduced in diabetes ( P <0.01); smaller decreases in plasma catalase and glutathione levels were observed. These changes were corrected by insulin treatment. In erythrocytes, decreased superoxide dismutase ( P <0.05) and increased total glutathione levels ( P <0.05) were found. All effects of diabetes, including a rise in plasma malonyldialdehyde ( P <0.05), were partially reversed by insulin treatment. In nervous tissue, diabetes caused increased catalase activity, uninfluenced by insulin ( P <0.05). Nerve superoxide dismutase and glutathione did not change. The data suggest that, in diabetes, changes in systemic rather than endoneurial oxidative stress lead to nerve dysfunction. |
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Keywords: | Catalase experimental diabetes glutathione nerve conduction oxidative stress superoxide dismutase |
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