ABSTRACT
Metal poisoning, especially with heavy metals like lead, poses a significant threat to human health due to its widespread presence in the environment. Lead exposure is known to have adverse effects on, brain development, cerebellum, antioxidant enzyme activity, and lipid peroxidation. Vitamin E has gained popularity as antioxidant in recent years including preventing lead toxicity effect. This study investigated the potential protective effects of Vitamin E against lead acetate-induced cerebellar toxicity in Wistar rats. In this experiment, twenty-one (21) Wistar rats were divided into three groups (n=7): a control group (Group A), a lead acetate-treated group (Group B), and a group treated with both lead acetate and Vitamin E (Group C). Group A received standard animal feed and water, Group B was administered with 100 mg/kg of lead acetate and Group C was administered with 100 mg/kg of lead acetate and 200 mg/kg of vitamin E. At the end of the administration, the rats were humanely sacrificed using cervical dislocation and the cerebellum was harvested and processed in the laboratory. The brain and body weight changes, antioxidant (SOD, CAT, GSH, GPx) activity, lipid peroxidation activity and histology of the cerebellum was observed to evaluate the activity of vitamin E on lead toxicity. The results revealed significant decreases in final body weight and whole brain weight in rats exposed to lead acetate alone, indicating growth retardation and neurotoxic effects. Lead exposure also led to a significant reduction in the activity of antioxidants including Superoxide Dismutase (SOD), Catalase (CAT), Glutathione Peroxidase (GPx) and Glutathione activities (GSH) as well as an increase in lipid peroxidation activity. However, rats pretreated with Vitamin E showed improvements in these parameters. Vitamin E supplementation appeared to mitigate the adverse effects of lead exposure, leading to increased body weight, brain weight, and weight change. Furthermore, Vitamin E enhanced the activity of antioxidant enzymes and reduced lipid peroxidation in the cerebellum, indicating its potential as a protective agent against lead-induced oxidative stress. Histological examination of cerebellar tissue supported these findings, as rats exposed to lead acetate alone exhibited signs of cerebellar damage, while those supplemented with Vitamin E showed preserved cerebellar tissue integrity. In conclusion, this study provides valuable insights into the protective potential of Vitamin E against lead-induced cerebellar toxicity. The results suggest that Vitamin E may serve as a therapeutic agent to mitigate the adverse effects of heavy metal poisoning, particularly lead exposure. Further research, including human studies, is warranted to confirm these protective effects and determine the optimal dosage and duration of Vitamin E supplementation in the context of heavy metal toxicity
