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Oxidative stress-mediated cytotoxicity of Endosulfan is causally linked to the inhibition of NADH dehydrogenase and Na+, K+-ATPase in Ehrlich ascites tumor cells.
Molecular and Cellular Biochemistry ( IF 3.5 ) Pub Date : 2020-03-16 , DOI: 10.1007/s11010-020-03711-z
Megha Murali 1, 2, 3 , Mary Sweeta Carvalho 1, 2 , T Shivanandappa 1, 2
Affiliation  

Oxidative stress in cells caused by excessive production of reactive oxygen species (ROS) and decreased antioxidant defense is implicated in the cytotoxicity of xenobiotics including drugs and environmental chemicals. Endosulfan, a highly toxic organochlorine insecticide, causes cytotoxic cell death by inducing oxidative stress. We have investigated the biochemical basis of induction of oxidative stress, involving the role of NADH dehydrogenase and the possible role of Na+, K+-ATPase in endosulfan cytotoxicity and, whether the cytotoxicity could be attenuated by targeting ROS induction using the natural flavonoid antioxidant, quercetin, in Ehrlich ascites tumor (EAT) cells. Exposure of cells to endosulfan caused cytotoxic cell death (necrosis) which was associated with induction of ROS, lipid peroxidation as well as a reduction in glutathione levels, concomitant with loss of NADH dehydrogenase and Na+, K+-ATPase activity in a dose-dependent manner, indicating that oxidative stress and perturbation of membrane function are the major causes of endosulfan cytotoxicity. Our results showed that quercetin, protected against endosulfan-induced cytotoxicity and significantly abrogated oxidative stress, and ameliorated the inhibition of NADH dehydrogenase and Na+, K+-ATPase activity in EAT cells. Our study presents evidence that NADH dehydrogenase inhibition plays an important role in oxidative stress-mediated cytotoxicity, and perturbed membrane function as evident from inhibition of sodium-potassium pump is involved in cytotoxic cell death.

中文翻译:

硫丹的氧化应激介导的细胞毒性与抑制Ehrlich腹水肿瘤细胞中的NADH脱氢酶和Na +,K + -ATPase有关。

活性氧(ROS)过量产生和抗氧化剂防御能力下降引起的细胞氧化应激与异源生物(包括药物和环境化学物质)的细胞毒性有关。硫丹是一种剧毒的有机氯杀虫剂,可通过诱导氧化应激而导致细胞毒性细胞死亡。我们已经研究了诱导氧化应激的生化基础,包括NADH脱氢酶的作用以及Na +,K + -ATPase在硫丹细胞毒性中的可能作用,以及是否可以通过使用天然类黄酮抗氧化剂槲皮素靶向ROS诱导来减弱细胞毒性。 ,在Ehrlich腹水肿瘤(EAT)细胞中。细胞暴露于硫丹会导致细胞毒性细胞死亡(坏死),这与诱导ROS有关,脂质过氧化以及谷胱甘肽水平降低,并伴随着剂量依赖性依赖于NADH脱氢酶和Na +,K + -ATPase活性的丧失,表明氧化应激和膜功能紊乱是硫丹细胞毒性的主要原因。我们的研究结果表明,槲皮素可防止硫丹引起的细胞毒性并显着消除氧化应激,并改善了EAT细胞对NADH脱氢酶和Na +,K + -ATPase活性的抑制作用。我们的研究表明,NADH脱氢酶的抑制作用在氧化应激介导的细胞毒性中起着重要作用,而钠钾泵的抑制作用明显表明膜功能紊乱与细胞毒性细胞死亡有关。K + -ATPase活性呈剂量依赖性,表明氧化应激和膜功能紊乱是硫丹细胞毒性的主要原因。我们的研究结果表明,槲皮素可防止硫丹引起的细胞毒性并显着消除氧化应激,并改善了EAT细胞对NADH脱氢酶和Na +,K + -ATPase活性的抑制作用。我们的研究表明,NADH脱氢酶的抑制作用在氧化应激介导的细胞毒性中起着重要作用,而钠钾泵的抑制作用明显表明膜功能紊乱与细胞毒性细胞死亡有关。K + -ATPase活性呈剂量依赖性,表明氧化应激和膜功能紊乱是硫丹细胞毒性的主要原因。我们的研究结果表明,槲皮素可防止硫丹引起的细胞毒性并显着消除氧化应激,并改善了EAT细胞对NADH脱氢酶和Na +,K + -ATPase活性的抑制作用。我们的研究表明,NADH脱氢酶的抑制作用在氧化应激介导的细胞毒性中起着重要作用,而钠钾泵的抑制作用明显表明膜功能紊乱与细胞毒性细胞死亡有关。可以防止硫丹引起的细胞毒性并显着消除氧化应激,并改善了EAT细胞中NADH脱氢酶和Na +,K + -ATPase活性的抑制作用。我们的研究表明,NADH脱氢酶的抑制作用在氧化应激介导的细胞毒性中起着重要作用,而钠钾泵的抑制作用明显表明膜功能紊乱与细胞毒性细胞死亡有关。可以防止硫丹引起的细胞毒性并显着消除氧化应激,并改善了EAT细胞中NADH脱氢酶和Na +,K + -ATPase活性的抑制作用。我们的研究表明,NADH脱氢酶的抑制作用在氧化应激介导的细胞毒性中起着重要作用,而钠钾泵的抑制作用明显表明膜功能紊乱与细胞毒性细胞死亡有关。
更新日期:2020-04-22
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