Abstract

This study aimed to evaluate the efficacy of zinc as a nutritional supplement in preventing chlorpyrifos-induced neurotoxicity in rats. The rats were segregated into 4 groups, which included normal controls and chlorpyrifos-treated, zinc-treated, and chlorpyrifos- and zinc-treated animals. Eight weeks of chlorpyrifos treatment resulted in a significant increase in the levels of lipid peroxidation (LPO) and reactive oxygen species (ROS) in both cerebellum and cerebrum as compared to normal animals. On the contrary, the activities of glutathione-s-transferase (GST), glutathione reductase (GR), superoxide dismutase (SOD), and reduced glutathione (GSH) levels were found to be significantly decreased following chlorpyrifos treatment. Furthermore, chlorpyrifos resulted in anxiety in rats as observed by the elevated plus maze test. In addition, an appreciable decrease was noticed in the muscular as well as locomotor activity of chlorpyrifos-treated animals was noticed by rotarod and actophotometer tests, respectively. However, zinc supplementation to chlorpyrifos-treated animals brought back the already raised levels of LPO and ROS to near normal limits in cerebrum. Moreover, zinc treatment to the chlorpyrifos-treated animals also resulted in a significant improvement in the levels of reduced glutathione, and enzyme activities of GST in both cerebrum as well as cerebellum. Also, improvement was observed in the behavior of chlorpyrifos-treated animals upon zinc supplementation. The present study thus concludes that zinc has potential to act as a neuroprotectant against pesticide-induced neurodegenerative and behavioral disorders but further investigations need to be conducted to understand the exact mechanism of neuroprotection.

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