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Virgin Coconut Oil Resists Arsenic-Induced Cerebral Neurotoxicity and Cholesterol Imbalance via Suppression of Oxidative Stress, Adenosine Deaminase and Acetylcholinesterase Activities in Rats
Natural Product Communications ( IF 1.8 ) Pub Date : 2021-06-30 , DOI: 10.1177/1934578x211016962
Sharon O. Azubuike-Osu 1 , Ademola C. Famurewa 2 , Japheth C. David 1 , Innocent Abi 3 , Patience N. Ogbu 2 , Chiedozie K. Oparaji 1 , Konyefom G. Nwaeze 1 , Godson G. Akunna 4
Affiliation  

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.



中文翻译:

初榨椰子油通过抑制大鼠氧化应激、腺苷脱氨酶和乙酰胆碱酯酶活性来抵抗砷诱导的脑神经毒性和胆固醇失衡

砷 (As) 是一种经典的神经毒物;其发病机制与氧化应激和氧化应激介导的胆碱能缺陷有关。本研究探讨了初榨椰子油 (VCO) 对亚砷酸钠诱导的氧化应激介导的大鼠脑神经毒性的抗氧化活性。十八只大鼠被分成3组-正常对照、As对照和VCO+As。VCO (5 mL/kg) 从第 1 天到第 21 天每天一次通过口服管饲给药,而 As (10 mg/kg) 从第 15 天到第 21 天通过口服管饲给药每天一次。 脑超氧化物歧化酶 (SOD) 、过氧化氢酶 (CAT)、谷胱甘肽过氧化物酶 (GPx)、丙二醛 (MDA)、腺苷脱氨酶 (ADA) 和乙酰胆碱酯酶 (AchE) 活性进行了分析。还在脑匀浆中评估了一氧化氮 (NO)、脂质谱、磷脂 (PL) 和还原型谷胱甘肽 (GSH)。将大脑切片用于组织学分析。与正常对照相比,As 的施用导致抗氧化酶、GSH、PL 和 HDL-c 显着降低。与正常大鼠相比,As 显着增加大脑中 MDA、NO、总胆固醇和 ADA、AchE 的活性。As 显着改变了脂质分布指数和 PL。组织病理学研究通过广泛的脑损伤支持了生化发现。相比之下,在砷治疗之前和同时口服补充 VCO 显着减弱了砷诱导的生化改变并恢复了接近正常的组织学。VCO 通过抵消自由基介导的砷毒性,增强内源性抗氧化防御和胆碱能功能,从而减轻脑神经毒性。

更新日期:2021-06-30
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