PMID: 9436610Jan 22, 1998Paper

Nerve function and oxidative stress in diabetic and vitamin E-deficient rats

Free Radical Biology & Medicine
P Sytze van DamJ J Marx

Abstract

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 antioxidan...Continue Reading

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Citations

Jul 12, 2002·Diabetes/metabolism Research and Reviews·P Sytze van Dam
Aug 17, 1999·European Journal of Pharmacology·P S van DamW H Gispen
Jan 13, 2006·Plastic and Reconstructive Surgery·Haruki HigashimoriThomas P Whetzel
Nov 26, 2009·BMC Gastroenterology·Luciana P RoldiMaria R M Natali
Jan 19, 2013·Arquivos De Gastroenterologia·Eleandro Aparecido TronchiniJacqueline Nelisis Zanoni
Apr 12, 2007·European Journal of Clinical Nutrition·B Manuel-Y-KeenoyC van Campenhout
Jan 1, 1998·Nutritional Neuroscience·M J Fryer

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