Nerve function and regeneration in diabetic and galactosaemic rats: antioxidant and metal chelator effects

Immature rats were made diabetic with streptozotocin or were fed a 40% galactose diet to stimulate the polyol pathway. Separate diabetic and galactosaemic groups were treated with butylated hydroxytoluene or trientine. After 4 weeks the sciatic nerve was freeze-lesioned. Two weeks later, the degree of myelinated fibre regeneration was assessed electrophysiologically and nerve conduction velocity was measured in the contralateral leg. Similar sciatic motor and saphenous sensory nerve conduction velocity deficits of approximately 18% and 19%, respectively, compared to age-matched control rats were found in both models. They were partially prevented by treatment (approximately 68% for butylated hydroxytoluene and 63% for trientine). There were 12% and 10% deficits in nerve regeneration distance with diabetes and galactosaemia respectively, which were markedly attenuated (approximately 80%) by both treatments. The data emphasise the importance of elevated, free radical activity for the aetiology of neural/neurovascular deficits in experimental diabetes and galactosaemia.