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首页> 外文期刊>Journal of applied toxicology >Enantiomer-specific profenofos-induced cytotoxicity and DNA damage mediated by oxidative stress in rat adrenal pheochromocytoma (PC12) cells
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Enantiomer-specific profenofos-induced cytotoxicity and DNA damage mediated by oxidative stress in rat adrenal pheochromocytoma (PC12) cells

机译：对映体特异性丙泊酚磷诱导的大鼠肾上腺嗜铬细胞瘤（PC12）细胞氧化应激介导的细胞毒性和DNA损伤

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摘要

Recent studies have shown that chiral pesticides could enantioselectively induce cytotoxicity and genotoxicity. However, investigations on molecular mechanisms of enantioselective toxicity of pesticides are limited. In this study, the role of oxidative stress in enantiomer-specific, profenofos (PFF)-induced cytotoxicity and genotoxicity was investigated using PC12 cells. The results demonstrated that PFF enantioselectively reduced cell viability and induced DNA damage in PC12 cells. A concentration- and time-dependent significant induction of reactive oxygen species (ROS), malondialdehyde and gene expression encoding antioxidant enzyme (Cu-ZnSOD, GST and CAT) and stress protein (HSP 70 and HSP 90) was observed in (-)-PFF, whereas (+)-PFF and rac-PFF exhibited these effects to lesser degrees. Pre-treatment with vitamin E (600μM) caused a significant attenuation in the toxic effect; reversing subsequent PFF-induced elevation of ROS and malondialdehyde (MDA) levels, further strengthening the involvement of oxidative stress in PFF-mediated toxicity. In addition, the results also showed that PFF-dependent ROS accumulation, MDA release and oxidative stress gene expression preceded the loss of cell viability and induction of DNA damage, and already significantly changed at concentrations which are not yet cytotoxic or genotoxic. These results indicate that oxidative stress may contribute to PFF-induced toxicity and that it was not a consequence of it.
机译：最近的研究表明，手性农药可以对映选择性诱导细胞毒性和遗传毒性。但是，对农药对映选择性毒性的分子机理的研究是有限的。在这项研究中，使用PC12细胞研究了氧化应激在对映体特异性，丙溴磷（PFF）诱导的细胞毒性和基因毒性中的作用。结果表明，PFF对映体选择性降低了细胞活力，并诱导了PC12细胞中的DNA损伤。在（-）-中观察到浓度和时间依赖性显着诱导活性氧（ROS），丙二醛和编码抗氧化酶（Cu-ZnSOD，GST和CAT）和应激蛋白（HSP 70和HSP 90）的基因表达。 PFF，而（+）-PFF和rac-PFF在较小程度上表现出这些作用。维生素E（600μM）的预处理显着减弱了毒性作用。逆转了随后PFF引起的ROS和丙二醛（MDA）水平升高，从而进一步增强了氧化应激对PFF介导的毒性的影响。另外，结果还表明，PFF依赖性ROS积累，MDA释放和氧化应激基因表达先于细胞活力丧失和DNA损伤诱导，并且在尚未具有细胞毒性或遗传毒性的浓度下已经发生了显着变化。这些结果表明氧化应激可能有助于PFF诱导的毒性，而不是其后果。

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