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Oxidative damage mechanism in Saccharomyces cerevisiae cells exposed to tetrachlorobisphenol A
Environmental Toxicology and Pharmacology ( IF 4.3 ) Pub Date : 2020-09-29 , DOI: 10.1016/j.etap.2020.103507
Xiaoru Zhang , Yaxian Zhang , Zhihua Ji , Fengbang Wang , Lei Zhang , Maoyong Song , Hao Li

Tetrachlorobisphenol A (TCBPA) can promote intracellular reactive oxygen species (ROS) accumulation. However, limited attention has been given to mechanisms underlying TCBPA exposure-associated ROS accumulation. Here, such mechanisms were explored in the simple eukaryotic model organism Saccharomyces cerevisiae exposed to multiple concentrations of TCBPA. Addition of diphenyleneiodonium, a specific inhibitor of NADPH oxidase, blocked TCBPA treatment-associated intracellular ROS accumulation. NADPH oxidase can be activated by calcineurin, mitogen-activated protein kinase (MAPK), and tyrosine kinase. Therefore, corresponding specific inhibition respectively on these three kinases was performed and results suggested that the Ca2+ signaling pathway, MAPK pathway, and tyrosine kinase pathway all contributed to the TCBPA exposure-associated intracellular ROS accumulation. In addition, TCBPA exposure-associated up-regulation of genes involved in ROS production and down-regulation of catalase promoted ROS accumulation in S. cerevisiae. To sum up, our current results provide insights into the understanding of TCBPA exposure-associated ROS accumulation.



中文翻译:

暴露于四氯双酚A的酿酒酵母细胞中的氧化损伤机制

四氯双酚A(TCBPA)可以促进细胞内活性氧(ROS)的积累。但是,对与TCBPA暴露相关的ROS积累的潜在机制只给予了有限的关注。在此,在暴露于多种浓度TCBPA的简单真核模型生物酿酒酵母中探索了这种机制。加入NADPH氧化酶的特异性抑制剂联苯二碘铵可阻止TCBPA治疗相关的细胞内ROS积累。NADPH氧化酶可以被钙调神经磷酸酶,促分裂原激活的蛋白激酶(MAPK)和酪氨酸激酶激活。因此,分别对这三种激酶进行了特异性抑制,结果表明Ca 2+信号通路,MAPK通路和酪氨酸激酶通路均促成TCBPA暴露相关的细胞内ROS积累。此外,TCBPA暴露相关的参与ROS产生的基因上调和过氧化氢酶的下调促进了酿酒酵母中ROS的积累。综上所述,我们目前的结果为了解TCBPA暴露相关的ROS积累提供了见识。

更新日期:2020-10-02
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