ABSTRACT
Exposure to certain chemicals, such as heavy metals, pesticides, and industrial pollutants, is reported to induce neurotoxicity and have detrimental effects on neurological development, cognition, and overall brain health. Mercury chloride, a compound composed of mercury and chlorine, is well-known for its neurotoxic effects. When mercury chloride enters the body, it is absorbed and distributed to various organs, including the brain, where it exerts its neurotoxic actions. The neurotoxicity of mercury chloride stems from its ability to interfere with essential cellular processes to disrupt normal neuronal function through the generation of reactive oxygen species (ROS), disruption of mitochondrial function, glutamate, and calcium ion homeostasis in neurons. Hence, a preventive or treatment approach to enhance the body's antioxidant defense is considered pivotal in preventing mercury chloride toxicity. Folic acid, also known as vitamin B9, is a synthetic version of the B vitamin folate, which naturally occurs in leafy greens, eggs, and citrus fruits, among other foods. Folic acid is an essential nutrient involved in various physiological processes, including DNA synthesis, cell division, and amino acid metabolism. Accordingly, this study investigated the possible neuroprotective activity of Folic acid on Mercury Chlorideinduced neurotoxicity in adult Wistar rats. Thirty-six (36) Wistar rats were randomly divided into six (6) groups of six (6) rats each. Group A rats served as the control group and were given 1 ml of distilled water. Group B rats were administered Mercury Chloride only at a dose of 4 mg/kg body weight. Group C rats were administered 5 mg/kg body weight of Folic acid and 4 mg/kg body weight of Mercury Chloride. Group D rats were administered 10 mg/Kg body weight of Folic acid and 4 mg/kg body weight of Mercury Chloride. Group E rats were administered 5 mg/kg body weight of Folic acid only. Group F rats were administered 10 mg/Kg body weight of Folic Acid only. The administration was done orally for twenty-eight (28) days. At the end of the administration, neurobehavioral activity was evaluated using the novel object, string, and movement initiation tests. The rats were sacrificed by cervical dislocation, and the cerebella were harvested for antioxidants (Catalase, Glutathione Peroxidase, Superoxide Dismutase, Glutathione) and lipid peroxidation evaluation. Concentration levels of Mercury Chloride in the cerebellum were also determined. The results from this study showed that mercury chloride caused a significant decrease (p<0.05) in body weight and impaired motor functions, as demonstrated in the neurobehavioral tests. Also, an increase in the concentration of HgCl2 in the cerebellum and lipid peroxidation activity as well as a reduction in antioxidant enzymes activity was observed in rats treated with HgCl2 alone. However, Folic acid treatment improved body weight, neurobehavioral activity, reduced cerebellar HgCl2 concentration, antioxidants activity, and decreased lipid peroxidation in HgCl2-exposed rats. In conclusion, Folic acid possesses neuroprotective properties against mercury chloride-induced cerebellar damage, mediated possibly through its ability to mitigate accumulation of mercury chloride and its antioxidant properties.
