Acute Lead (II) Acetate 3-Hydrate Neurotoxicity Alters Neurocognition and Induced Depressive-like Behavior Via 5-Hydroxytryphtamine, Neurohormone Melatonin and (Na+,K+)-ATPase Activity in Female Wistar Rats

Abstract

Aims: Lead (II) acetate 3-hydrate also known as lead acetate is a neurotoxin that accumulates in soft tissues and bones causing damage to the nervous system of the human body. Hence, this study investigated the effect of short-term administration of Lead (II) Acetate 3-hydrate on serotonin, melatonin, (Na+, K+)-ATPase enzyme activity and neurocognition. Methodology: Female Wistar rats (150-200 g b.wgt) were divided into groups (n=14). Control group (n=7) received 0.5 ml of normal saline and the treated group (n=7) were administered lead (II) acetate 3-hydrate at 100mg/kg for seven (7) days intraperitoneally (IP). Serotonin (5-HT), Melatonin and Sodium/Potassium-Adenosine Triphosphate [(Na+, K+)-ATPase] enzyme was investigated in the brain tissue and neurobehavior: Tail suspension test (TST), Forced swimming test (FST) and Novel object recognition test (NORT) were investigated. Body weight of the rats was also taken daily. Results: The result obtained revealed significant (P<0.05) decrease in body weight in the treated group. Neurobehavioral results investigated showed a significant (P<0.05) increase immobility time both in FST and TST and a significant (P<0.05) decrease in retention latency in the NORT. The biochemical analysis reveals a significant (P<0.05) increase level of serotonin (5HT), but melatonin and (Na+, K+)-ATPase enzyme activity decreased significantly (P<0.05) when compared with the control group. Conclusion: This current study shows that lead (II) acetate 3-hydrate affect neurocognition and can possibly initiate depressive-like behavior via melatonin and serotonin imbalance and also tampering with the (Na+, K+)-ATPase mechanism in the brain mitochondria.