Abstract
In recent years, an increasing number of cases of neuropathy have been reported as a result of accidental or occupational exposure to chemicals. Acrylamide (Acr), a widely used industrial chemical, is known to produce peripheral neuropathy that resembles diabetic neuropathy in many ways. However, the interaction between diabetes and Acr has not been studied. The present study was undertaken to examine the effect of streptozotocin (STZ)-induced diabetes on Acr-induced neurotoxicity in rats. Male Sprague–Dawley rats weighing 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 group 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 administering a single IP injection of STZ (50 mg/kg). The animals in group 3 served as diabetic control, whereas the rats in group 4 received Acr in the same dose regimen as in group 2, a week after induction of diabetes. Neurobehavioral responses including foot print length, hind limb function, landing foot splay, and the ability to stay on an inclined plane were assessed 48 h after the last dose of Acr followed by electrophysiological measurements. The animals were then sacrificed, and sciatic nerves were collected for biochemical analysis. The results of this study clearly showed a significant deterioration of neurobehavioral and electrophysiological responses in Acr-treated rats. Although no significant change in these parameters was observed in the diabetic (only) group, Acr-induced functional deficiency was significantly reduced in diabetic animals. However, the difference in electrophysiological response in Acr-treated diabetic and nondiabetic rats was not found to be statistically significant ( p > 0.05). The precise mechanism by which Acr induced neurobehavioral toxicity is reduced in diabetic animals warrants further investigations.
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