ABSTRACT
Exposure of human populations to harmful metals can lead to damage to various organs and systems. Aluminium (Al) is one of the most commonly studied toxic metals and has been associated with numerous diseases. Aluminium is reported to directly damage primary human neural cells, leading to genotoxic effects while promoting neurodegeneration in different regions of the brain by increasing the accumulation of iron (Fe) and the production of reactive oxygen species (ROS). The use of exogenous antioxidants to counteract the oxidative damage of aluminium accumulation in the brain has been linked. Ascorbic acid, a water-soluble vitamin is reported to play a crucial role in various biological processes in the body. Ascorbic acid possesses antioxidant properties which are reported to have a synergistic effect in modulating neuroinflammation and mitigating neuronal damage. Accordingly, this study was aimed at investigating the antioxidant and anti-cholinesterase activity of ascorbic acid in the cerebrum of Wistar rats treated with Aluminium Chloride. In this study, forty-eight (48) Wistar rats were randomly divided into six (6) groups of eight (8) rats each. Group A rats served as the control group to be given 1ml of sterile water. Group B rats were given 100 mg/kg body weight of Aluminium Chloride only. Group C rats were administered with 100 mg/Kg body weight of Ascorbic Acid and 100 mg/kg body weight of Aluminium Chloride. Group D rats were administered with 200 mg/Kg body weight of Ascorbic Acid and 100 mg/kg body weight of Aluminium Chloride. Group E rats were administered with 100 mg/Kg body weight of Ascorbic Acid only. Group F rats were administered 200 mg/Kg body weight of Ascorbic Acid only. The administration was done orally for twenty-eight (28) days. At the end of the administration, the neurobehavioral activity was evaluated using the novel object recognition test. The rats were sacrificed and antioxidant enzymes (Catalase, Glutathione Peroxidase, Superoxide Dismutase, Glutathione), lipid peroxidation activity, as well as anticholinesterase were assessed. The cerebrum was weighed and the Relative brain weight was calculated. Also, routine hematoxylin and eosin staining techniques were utilized to evaluate the cytoarchitectural changes in the cerebrum of experimental rats. Results showed that AlCl3 reduced relative brain weight, caused cognitive impairments, altered antioxidant activity, and increased lipid peroxidation, all indicating cerebral dysfunction. Histological analysis showed that aluminium chloride exposure also resulted in severe cerebral cortical damage, characterized by shrunken and pyknotic neuronal cell bodies. However, results showed that ascorbic acid attenuated the effects of AlCl3 which was evident in improved body weight changes, preserved brain weight, enhanced cognitive function, and regulation of anticholinesterase enzyme activity and antioxidant levels. Also, histological results showed that ascorbic acid attenuated the effects of AlCl3 which was evidenced by the protection against cerebral neuronal damage taken together. Ascorbic acid possesses neuroprotective properties against AlCl3-induced cerebral damage, possibly through its potential antioxidant and anticholinesterase activity.
