俞捷,
许洁,
遵义医科大学公共卫生学院, 遵义 563000
作者简介: 唐兰(1995-),女,硕士,研究方向为环境与健康,E-mail:1247822009@qq.com.
通讯作者: 许洁,649904039@qq.com
基金项目: 国家自然科学基金资助项目（81760580）；贵州省科技厅基金重点项目（黔科合基础2018-1429，2019-1466）；贵州省高层次创新型"百层次"人才项目（黔科合平台人才[2020]6014）；普通高等学校科技拔尖人才支持计划项目（黔教合KY2018054）；遵义市"15851"人才项目经费（2019-E262）中图分类号: X171.5
The Effects of Environmental Endocrine Disruptors on Myocardial Mitochondrial: A Review
Tang Lan,Yu Jie,
Xu Jie,
School of Public Health, Zunyi Medical University, Zunyi 563000, China
Corresponding author: Xu Jie,649904039@qq.com
CLC number: X171.5
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摘要:心脏疾病（冠心病、心肌炎及心肌梗死等）发病率持续增高，病因不明。线粒体是心脏进行生命活动时所需能量的供给场所，当受损时会引发心脏疾病。研究表明，环境内分泌干扰物（environmental endocrine disruptors，EEDs）暴露可导致心肌线粒体损伤，其机制包括呼吸链受损、呼吸酶活性降低、线粒体膜损害、Ca2+稳态紊乱、氧化应激增加、抗氧化能力降低、线粒体能量代谢调控基因表达改变和线粒体融合与分裂改变等。本文综述了几种有代表性的EEDs （双酚A、壬基酚、邻苯二甲酸二（2-乙基）己酯、磷化铝、马拉硫磷、镉和汞）及EEDs混合物对心肌线粒体的损伤及其机制。以期为线粒体作为治疗心脏疾病的靶点提供理论依据。
关键词: 环境内分泌干扰物/
心脏毒性/
线粒体损伤/
PGC-1α/
氧化应激
Abstract:The incidence of cardiac disease (e.g., coronary heart disease, myocarditis, myocardial infarction, etc.) continues to rise, and its etiology remains to be unknown. Mitochondrion is the energy producing organelle in the myocardial cell. The findings from the recent scientific literature show that exposure to environmental endocrine disruptors (EEDs) could induce myocardial mitochondrial dysfunction, which involved impaired respiratory chain, damaged mitochondrial membrane, decreased respiratory enzyme activity and antioxidant capacity, Ca2+ homeostasis disorder, increased oxidative stress, alterations in the expressions of regulatory genes which is related to mitochondrial energy metabolism, and mitochondrial fusion and division, etc. We reviewed the literature on the effects of EEDs (bisphenol A, nonylphenol, di (2-ethylhexyl) phthalate, aluminum phosphide, malathion, cadmium and mercury) and EEDs mixtures on myocardial mitochondria and its mechanism for the purpose of providing a potential target of cardiac disease treatment.
Key words:environmental endocrine disruptors/
cardiac toxicity/
mitochondrial dysfunction/
PGC-1α/
oxidative stress.
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