Attenuation of acrylamide-induced neurotoxicity in diabetic rats

In recent years, an increasing number of cases of neuropathy have been repo rted as a result of accidental or occupational exposure to chemicals. Acryl amide (Acr), a widely used industrial chemical, is known to produce periphe ral neuropathy that resembles diabetic neuropathy in many ways. However, th e interaction between diabetes and Acr has not been studied. The present st udy was undertaken to examine the effect of streptozotocin (STZ)-induced di abetes on Acr-induced neurotoxicity in rats. Male Sprague-Dawley rats weigh ing 300 +/- 10 g were divided into four groups of 10 animals each. The rats in group 1 served as control, and received normal saline. The animals in g roup 2 were given Acr dissolved in physiological saline (50 mg/kg IP 3 days /week) for 2 weeks. The rats in group 3 and 4 were made diabetic by adminis tering a single IP injection of STZ (50 mg/kg). The animals in group 3 serv ed as diabetic control, whereas the rats in group 4 received Acr in the sam e dose regimen as in group 2, a week after induction of diabetes. Neurobeha vioral responses including foot print length, hind limb function, landing f oot splay, and the ability to stay on an inclined plane were assessed 48 h after the last dose of Acr followed by electrophysiological measurements. T he animals were then sacrificed, and sciatic nerves were collected for bioc hemical analysis. The results of this study clearly showed a significant de terioration of neurobehavioral and electrophysiological responses in Acr-tr eated rats. Although no significant change in these parameters was observed in the diabetic (only) group, Acr-induced functional deficiency was signif icantly reduced in diabetic animals. However, the difference in electrophys iological response in Acr-treated diabetic and nondiabetic rats was not fou nd to be statistically significant (p > 0.05). The precise mechanism by whi ch Acr induced neurobehavioral toxicity is reduced in diabetic animals warr ants further investigations. (C) 2000 Elsevier Science Inc. All rights rese rved.