Hossain Murad, Suchi Tamanna Tanjim, Samiha Farzana, Islam M M Monirul, Tully Fahima Abdullah, Hasan Javed, Rahman Md Ashrafur, Shill Manik Chandra, Bepari Asim Kumar, Rahman G M Sayedur, Reza Hasan Mahmud
Department of Pharmaceutical Sciences, School of Health & Life Sciences, North South University, Dhaka 1229, Bangladesh.
Department of Pharmaceutical Sciences, Wilkes university, Pennsylvania, USA, 18766.
Heliyon. 2023 Feb 14;9(2):e13727. doi: 10.1016/j.heliyon.2023.e13727. eCollection 2023 Feb.
Carbofuran is a widely used poisonous pesticide around the world that helps to control insects during farming. Upon oral ingestion to humans, it exaggerates oxidative stress in various organs like the liver, brain, kidney, and heart. Several studies reported that oxidative stress in the liver initiates and propagates hepatic cell necrosis, ultimately resulting in hepatotoxicity. It also reported that coenzyme Q10 (CoQ10) can neutralize oxidative stress due to its antioxidant properties. However, the hepatoprotective and nephroprotective role of CoQ10 against carbofuran toxicity has not been investigated. Therefore, the present study aimed to evaluate the hepatoprotective and nephroprotective role of CoQ10 in carbofuran-induced hepatotoxicity and nephrotoxicity in a mouse model for the first time. We determined the blood serum diagnostic markers, oxidative stress parameters, antioxidant system, and histopathological characteristics of liver and kidney tissues. The administration of 100 mg/kg of CoQ10 in carbofuran-treated rats significantly attenuated AST, ALT, ALP, serum creatinine, and BUN levels. Moreover, CoQ10 (100 mg/kg) remarkably altered the level of NO, MDA, AOPP, GSH, SOD, and CAT in both the liver and kidney. The histopathological data also unveiled that CoQ10 treatment prevented inflammatory cell infiltration in carbofuran-exposed rats. Therefore, our findings infer that CoQ10 may effectively protect liver and kidney tissues against carbofuran-induced oxidative hepatotoxicity and nephrotoxicity.
克百威是一种在全球广泛使用的有毒农药,用于农业生产中的害虫防治。人类经口摄入后,它会加剧肝脏、大脑、肾脏和心脏等多个器官的氧化应激。多项研究报告称,肝脏中的氧化应激会引发并加剧肝细胞坏死,最终导致肝毒性。研究还表明,辅酶Q10(CoQ10)因其抗氧化特性可中和氧化应激。然而,CoQ10对克百威毒性的肝脏保护和肾脏保护作用尚未得到研究。因此,本研究旨在首次评估CoQ10在小鼠模型中对克百威诱导的肝毒性和肾毒性的肝脏保护和肾脏保护作用。我们测定了血清诊断标志物、氧化应激参数、抗氧化系统以及肝脏和肾脏组织的组织病理学特征。在经克百威处理的大鼠中给予100mg/kg的CoQ10可显著降低天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、碱性磷酸酶(ALP)、血清肌酐和尿素氮水平。此外,CoQ10(100mg/kg)显著改变了肝脏和肾脏中一氧化氮(NO)、丙二醛(MDA)、晚期氧化蛋白产物(AOPP)、谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的水平。组织病理学数据还显示,CoQ10治疗可防止克百威暴露大鼠的炎症细胞浸润。因此,我们的研究结果表明,CoQ10可能有效保护肝脏和肾脏组织免受克百威诱导的氧化肝毒性和肾毒性。