The role of thymoquinone as a potent antioxidant in ameliorating the neurotoxic effect of sodium arsenate in female rat

Abstract

Arsenic is a neurotoxic substance that makes the brain susceptible to free radicals. Thymoquinone (TQ) is a potent antioxidant extracted from Nigella sativa seeds. It scavenges free radicals and prevents the cell damage resulted from oxidative substances. In this study, the ameliorative effect of TQ in arsenic-induced neurotoxicity was investigated. Rats were treated for 21days with: distilled water, 20mg/kg sodium arsenate, 10mg/kg TQ, and arsenate followed by TQ. Cerebral cortex, cerebellum and brain stem were removed for the measurements of different physiological parameters. Cerebelli were prepared for histopathological studies. Arsenate treatment caused a decrease in the levels of norepinephrine (NE), dopamine (DA), acetylcholine esterase (AChE) and Na+-K+-ATPase activities in cerebral cortex, cerebellum, and brain stem of rats. Similarly, the levels of glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT) were declined. In contrast, serotonin (5-HT), lipid peroxidation (MDA), nitrite/nitrate (NO), and tumour necrosis factor (TNF-α) levels were increased after arsenate treatment. The presence of degenerated Purkinje cells in cerebellum was noticed. Results revealed that, post-treatment with TQ suppressed the arsenate-induced neurotoxic effects as it decreased the levels of 5-HT, MAD, NO, TNF-α and increased the levels of NE, DA, GH, GPx, GR, SOD, and CAT, in the cerebral cortex, cerebellum, and brain stem. Likewise, AChE and Na+-K+-ATPase activities were increased after TQ post-treatment. In conclusion, TQ ameliorated the neurotoxic effect of arsenate and suppressed the oxidative stress induced in the nervous system through its antioxidant mechanism.