van Dam P S, Bravenboer B, van Asbeck B S, Marx J J, Gispen W H
Department of Medical Pharmacology, Rudolf Magnus Institute for Neurosciences, University Medical Center, Utrecht, The Netherlands.
Eur J Pharmacol. 1999 Jul 9;376(3):217-22. doi: 10.1016/s0014-2999(99)00376-3.
Antioxidants can improve nerve dysfunction in hyperglycaemic rats. We evaluated whether the standard supplementation of rat food with vitamin E (normally added for preservation purposes) or high-dose vitamin E treatment improves nerve conduction in maturing streptozotocin-diabetic rats, a model widely used to study diabetic neuropathy. Hyperglycaemic rats received food containing 25 mg/kg (non-supplemented), 70 mg/kg (standard food) or 12 g/kg (high-dose) vitamin E. Non-diabetic controls received non-supplemented food. Sciatic and tibial sensory and motor nerve conduction velocity were decreased in all diabetic animals. In comparison with standard feeding, the non-supplemented diabetic rats showed lower plasma vitamin E levels but no significant change in nerve conduction. High-dose treatment prevented nerve dysfunction by 50%, and led to attenuated endoneurial lipid peroxidation (measured as malondialdehyde). We conclude that high doses of vitamin E, but not standard vitamin E supplementation of rat food partially prevent nerve dysfunction in young adult streptozotocin-diabetic rats.