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氧化应激在三氯乙烯所致毒性效应中的作用 被引量:1

Role of oxidative stress in trichloroethylene-induced toxicity
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摘要 三氯乙烯(TCE)是常见的工业有机溶剂和环境污染物,可通过职业接触和环境污染等途径进入人体,对人类健康产生严重危害。大量研究表明氧化应激在TCE导致的多靶器官的毒效应中发挥了重要作用,但相关信号通路的研究仍有待深入。本文归纳了TCE所致肝脏毒性、肾脏毒性、心脏发育毒性、胎盘发育毒性、神经发育毒性和自身免疫反应相关的流行病学、动物实验和细胞实验研究,总结了TCE通过氧化应激发挥毒效应的分子机制,包括DNA损伤、线粒体功能障碍、细胞凋亡和免疫系统异常活化等。通过文献梳理,提出核因子E2相关因子2在介导TCE所致靶器官毒性中可能发挥重要作用,为TCE造成的健康损害的防治提供理论依据。 Trichloroethylene(TCE)is a common industrial organic solvent and environmental contaminant.People are exposed to TCE through occupational contact or environmental pollution,which leads to serious human health hazards.A large number of studies have shown that oxidative stress plays an important role in the TCE-induced multi-target organ toxicity.However,the research of related signaling pathways remains to be deepened.In this review,we summarized the epidemiological,animal,and cellular studies correlated to liver toxicity,kidney toxicity,cardiac developmental toxicity,placental developmental toxicity,neurodevelopmental toxicity,and autoimmune response induced by TCE.In addition,the possible molecular mechanisms of oxidative stress in TCE-induced toxicity were concluded,including DNA damage,mitochondrial dysfunction,cell apoptosis,and abnormal activation of the immune system.Through literature review,we proposed that nuclear factor E2 related factor 2 may play an important role in mediating TCE-induced target organ toxicity,providing a theoretical basis for the prevention and treatment of adverse health effects caused by TCE.
作者 赵金枫 颜士玉 王瑞 韩雨晴 盘瑶 ZHAO Jinfeng;YAN Shiyu;WANG Rui;HAN Yuqing;PAN Yao(Department of Cosmetics,School of Chemistry and Material Engineering/Beijing Key Laboratory of Plant Research and Development,Beijing Technology and Business University,Beijing 100048,China)
机构地区 北京工商大学
出处 《环境与职业医学》 CAS CSCD 北大核心 2022年第12期1423-1429,共7页 Journal of Environmental and Occupational Medicine
基金 国家自然科学基金项目(81903361)。
关键词 三氯乙烯 氧化应激 靶器官毒性 核因子E2相关因子2 分子机制 trichloroethylene oxidative stress target organ toxicity nuclear factor E2 related factor 2 molecular mechanism
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