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

Olusegun G. Adebayo *

Department of Physiology, Neurophysiology Unit, PAMO University of Medical Sciences, Port Harcourt, Nigeria and Department of Physiology, Neurosciences and Oral Physiology Unit, University of Ibadan, Ibadan, Nigeria.

Iheanyichukwu Wopara

Department of Biochemistry, PAMO University of Medical Sciences, Port Harcourt, Nigeria.

Benneth Ben-Azu

Department of Pharmacology, Neuropharmacology Unit, PAMO University of Medical Sciences, Port Harcourt, Nigeria.

W. Aduema

Department of Physiology, Neurophysiology Unit, PAMO University of Medical Sciences, Port Harcourt, Nigeria.

Oluwakemi R. Adebayo

Department of Human Nutrition and Dietetics, University of Ibadan, Ibadan, Nigeria.

Omeje U. Nicodemus

Department of Physiology, Neurosciences and Oral Physiology Unit, University of Ibadan, Ibadan, Nigeria.

*Author to whom correspondence should be addressed.


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.

Keywords: Lead, serotonin (5HT), melatonin, Adenosine Triphosphate (ATP), neurocognition and neuerotoxin.


How to Cite

Adebayo, Olusegun G., Iheanyichukwu Wopara, Benneth Ben-Azu, W. Aduema, Oluwakemi R. Adebayo, and Omeje U. Nicodemus. 2020. “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”. Asian Journal of Biotechnology and Genetic Engineering 3 (1):31-40. https://www.journalajbge.com/index.php/AJBGE/article/view/29.

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