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ABSTRACT
Nickel chloride is known for its neurotoxicity and its exposure poses significant threat to the hippocampus, an essential brain region for learning and memory. This study investigated the neuroprotective effects of selenium (Se) on hippocampal integrity in nickel chloride exposed Wistar rats. After acclimatization for 14days, thirty-six rats were weighed and divided to six groups of (n = 6). Group A (control) was administered 1ml of distilled water. Group B (NiCl2) was administered 5mg/kg body weight (BW) of Nickel chloride only. Group C (NiCl2+ Se1) was administered 0.25mg/kg BW of Selenium and 5mg/kg BW of Nickel chloride. Group D (NiCl2 + Se2) was administered 0.5mg/kg BW of Selenium and 5mg/kg BW of Nickel chloride. Group E (Se1) was administered 0.25mg/kg BW of Selenium only. Group F (Se2) was administered 0.5mg/kg BW of Selenium only. Rats were intraperitoneally administered nickel chloride and orally administered selenium for 28 days, with Selenium pretreatment an hour before nickel chloride administration. Neurobehavioral, (Y-maze and NORT), antioxidant enzymes, lipid peroxidation, gene expression (NRF-2 and Caspase-3) and histological alterations were evaluated at the end of the experiment. Results showed that the treatment with nickel chloride effectuated (p<0.05) anxiety and depression-like behavior in the rats, decreased (p<0.05) the activities of antioxidant enzymes, increased (p<0.05) lipid peroxidation , downregulated (p<0.05) NRF-2 expression, indicating oxidative stress and upregulated (p<0.05) Caspase-3 expression, indicating apoptosis in the hippocampus. Pretreatment of nickel chloride rats with selenium attenuated (p<0.05) the neurobehavioral alterations, enhanced (p<0.05) the activity of antioxidant enzymes, mitigated (p<0.05) oxidative stress and inhibited apoptosis. Histological assessment provided evidence that selenium protected against nickel chloride induced neurodegeneration in the hippocampus. These findings indicate that selenium may have a neuroprotective effect against nickel chloride induced toxicity.
