CEREBELLUM

Vitamin E, a fat-soluble antioxidant, plays a crucial role in protecting cellular membranes from oxidative damage. Its neuroprotective properties have garnered attention in recent studies, particularly concerning neurotoxicity induced by aluminum chloride (AlCl3). Exposure to AlCl3 has been linked to cognitive deficits and neurodegenerative changes in the brain, making it a significant concern in neurobiology. Research has demonstrated that Vitamin E administration can mitigate the adverse effects of AlCl3 by reducing oxidative stress and inflammation in the brain. This research aims to explore the activity of Vitamin E in the cerebellum of Wistar rats treated with aluminum chloride. A total of twenty-eight (28) adult Wistar rats with an average weight of 180g were used for this study. They were randomly assigned into four groups (A, B, C, and D) with each group consisting of Seven rats. Group A served as control, Group B was administered 5mg/kg of Aluminum chloride, Group C was
administered 5mg/kg of Aluminum chloride + Vitamin E and Group E was administered Vitamin E only. Administration lasted for 28 days and was done via oral route. Neurobehavioural activity was assessed after administration on the 28th day. The rats
were ;sacrificed after the neurobehavioural activity was assessed. The key findings of this study suggest that Vitamin E administration mitigated the adverse effects of aluminum chloride exposure on the cerebellum of Wistar rats by reducing oxidative stress, improving antioxidant enzyme activity, and preventing neurodegeneration in the Purkinje cell layer. The findings of
this study indicate that Vitamin E can effectively protect the cerebellum of Wistar rats against the neurotoxic effects of aluminum chloride exposure by modulating oxidative stress and improving antioxidant defense mechanismsUN