| Autor: |
Gispen, W.H., Dam, P.S. van, Asbeck, B.S. van, Bravenboer, B., Oirschot, J.F.L.M. van, Marx, J.J. |
| Jazyk: |
angličtina |
| Rok vydání: |
1997 |
| Předmět: |
|
| Zdroj: |
Free radical biology & medicine, 24(1), 18. Elsevier |
| ISSN: |
0891-5849 |
| Popis: |
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. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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