Virgin Coconut Oil Resists Arsenic-Induced Cerebral Neurotoxicity and Cholesterol Imbalance via Suppression of Oxidative Stress, Adenosine Deaminase and Acetylcholinesterase Activities in Rats

Abstract

Arsenic (As) is a classic neurotoxicant; its pathogenesis is associated with oxidative stress and oxidative stress-mediated cholinergic deficits. This study explored antioxidant activity of virgin coconut oil (VCO) against sodium arsenite-induced oxidative stress-mediated cerebral neurotoxicity in rats. Eighteen rats were divided into 3 groups- Normal control, As control and VCO + As. The VCO (5 mL/kg) was given once daily by oral gavage from day 1 to day 21, while As (10 mg/kg) was given once daily by oral gavage from day 15 to day 21. Cerebral superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), malondialdehyde (MDA), adenosine deaminase (ADA) and acetylcholinesterase (AchE) activities were analysed. Nitric oxide (NO), lipid profile, phospholipid (PL), and reduced glutathione (GSH) were also evaluated in cerebral homogenate. The cerebrum was sectioned for histological analysis. Administration of As induced significant depressions in antioxidant enzymes, GSH, PL, and HDL-c compared to normal control. Levels of MDA, NO, total cholesterol and activities of ADA, AchE in the cerebrum were markedly increased by As compared to normal rats. Lipid profile indices and PL were prominently altered by As. Histopathological study supported the biochemical findings through extensive cerebral damage. In contrast, oral supplementation of VCO prior to and along with As treatment significantly attenuated the As-induced biochemical alterations and restored near-normal histology. VCO attenuates cerebral neurotoxicity by strengthening endogenous antioxidant defence and cholinergic function via counteracting free-radical-mediated arsenic toxicity.