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首页> 外文期刊>Toxicology and Applied Pharmacology >Trichloroethylene metabolite S-(1,2-dichlorovinyl)- l -cysteine induces lipid peroxidation-associated apoptosis via the intrinsic and extrinsic apoptosis pathways in a first-trimester placental cell line
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Trichloroethylene metabolite S-(1,2-dichlorovinyl)- l -cysteine induces lipid peroxidation-associated apoptosis via the intrinsic and extrinsic apoptosis pathways in a first-trimester placental cell line

机译：三氯乙烯代谢物S-（1,2-二氯丙烯基） - L-琥珀酸盐通过胎儿胎盘细胞系中的内在和外在凋亡途径诱导脂质过氧化相关的凋亡

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摘要

Abstract Trichloroethylene (TCE), a prevalent environmental contaminant, is a potent renal and hepatic toxicant through metabolites such as S-(1, 2-dichlorovinyl)- l -cysteine (DCVC). However, effects of TCE on other target organs such as the placenta have been minimally explored. Because elevated apoptosis and lipid peroxidation in placenta have been observed in pregnancy morbidities involving poor placentation, we evaluated the effects of DCVC exposure on apoptosis and lipid peroxidation in a human extravillous trophoblast cell line, HTR-8/SVneo. We exposed the cells in vitro to 10–100μM DCVC for various time points up to 24h. Following exposure, we measured apoptosis using flow cytometry, caspase activity using luminescence assays, gene expression using qRT-PCR, and lipid peroxidation using a malondialdehyde quantification assay. DCVC significantly increased apoptosis in time- and concentration-dependent manners (p Graphical abstract Display Omitted Highlights ? DCVC induced apoptosis in a placental cell line in a concentration-dependent manner. ? DCVC activated both intrinsic and extrinsic apoptotic pathways via tBID cross talk. ? DCVC stimulated differential intrinsic and extrinsic pathway gene expression. ? Cellular lipid peroxidation byproduct malondyaldehyde levels were increased by DCVC. ? Antioxidant (±)-α-tocopherol attenuated DCVC-induced caspase activity.
机译：摘要三氯乙烯（TCE）是一种常见的环境污染物，通过S-（1，2-二氯乙烯基）-l-半胱氨酸（DCVC）等代谢物，是一种有效的肾脏和肝脏毒物。然而，TCE对其他靶器官（如胎盘）的影响研究甚少。由于在涉及胎盘不良的妊娠疾病中观察到胎盘中的细胞凋亡和脂质过氧化升高，我们评估了DCVC暴露对人类绒毛外滋养层细胞系HTR-8/SVneo中的细胞凋亡和脂质过氧化的影响。我们在体外将细胞暴露于10–100μM DCVC中，持续不同时间点，直至24小时。暴露后，我们用流式细胞术检测细胞凋亡，用发光分析检测半胱天冬酶活性，用qRT PCR检测基因表达，用丙二醛定量分析检测脂质过氧化。DCVC以时间和浓度依赖的方式显著增加细胞凋亡（p）图形摘要显示：DCVC以浓度依赖的方式诱导胎盘细胞系凋亡。DCVC通过tBID串扰激活内源性和外源性凋亡途径。DCVC刺激差异内源性和外源性途径基因表达。DCVC增加细胞脂质过氧化副产物丙二醛水平。抗氧化剂ant（±）-α-生育酚减弱DCVC诱导的caspase活性。

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