ATTENUATION OF MERCURY CHLORIDE-INDUCED HIPPOCAMPAL TOXICITY IN WISTAR RATS FOLLOWING PRETREATMENT WITH FOLIC ACID

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ABSTRACT

Mercury chloride (HgCl2) is a well-known neurotoxicant with detrimental effects on the central nervous system, particularly the hippocampus, a region crucial for learning and memory processes. The toxicity of mercury chloride is through its ability to interfere with essential cellular processes to disrupt normal neuronal functions. Folic acid is a synthetic form of folate, which is a B-vitamin (vitamin B9). It plays a crucial role in various bodily functions, including the production of DNA and RNA, cell division, and the formation of red blood cells. Accordingly, this study aimed to investigate the possible neuroprotective activity of folic acid on mercury chloride-induced hippocampal toxicity in Wistar rats. A total number of 48 Wistar rats were purchased, acclimatized, and randomly divided into six (6) groups of six (8) rats each. Group A (control) served as a control was given 1ml of sterile water, Group B (HgCl2) was administered 4mg/kg body weight of mercury chloride only , Group C (HgCl2 +FA1) was administered 5mg/kg body weight of folic acid one hour before the administration of  4mg/kg of mercury Chloride, GroupD (HgCl2 +FA2) was administered 10mg/kg body weight of folic acid one hour before  the administration of 4mg/kg body weight of mercury chloride, Group E (FA1) was administered 5mg/kg body weight of folic acid only, Group F (FA2) was  administered 10mg/kg body weight of folic acid only .The administration, via an orogastric tube, lasted for 28 days and rats were fed with standard rat chow and had free access to water throughout the entire study period. At the end of the experiment, neurobehavioral activity (Novel object recognition test) was evaluated, recorded, and the rats were then sacrificed by cervical dislocation for sample collection. Following appropriate harvesting of the hippocampus, the antioxidants (Superoxide dismutase, Catalase, Gluthathione and Gluthathione peroxidase) and lipid peroxidation activity were evaluated as well as the HgCl2 concentration levels. Results showed a significant decrease (p<0.05) in final body weight of rats in the HgCl2 group in contrast to the control and FA groups which showed an increased final body weight. Comparison of neurobehavioral activity showed that rats in the HgCl2 group had significantly reduced (p<0.05) neurobehavioral function and an increase in the mercury chloride concentration levels when compared to those in the Control and FA groups. Assessment of antioxidant activity showed low antioxidant activity and increased lipid peroxidation in the HgCl2 groups whereas in the control and FA groups had significantly higher(p<0.05) antioxidant activity and reduced lipid peroxidation. Histological findings revealed morphological alterations (atrophy and vacuolated pyramidal cells and Astrocytes) in the HgCl2 group while the groups treated with FA showed similar morphology to the control group. This study underscores the potential therapeutic utility of folic acid in mitigating the harmful effects of mercury exposure on hippocampal function. The neuroprotective actions of folic acid may offer insights into novel strategies for preventing or ameliorating neurotoxicity associated with mercury exposure.

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