期刊文献+

环境内分泌干扰物暴露致心肌线粒体损伤的研究进展 被引量:6

The Effects of Environmental Endocrine Disruptors on Myocardial Mitochondrial:A Review
下载PDF
导出
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、Ca^2+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。 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,Ca^2+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.
作者 唐兰 俞捷 许洁 Tang Lan;Yu Jie;Xu Jie(School of Public Health,Zunyi Medical University,Zunyi 563000,China)
出处 《生态毒理学报》 CAS CSCD 北大核心 2020年第4期123-128,共6页 Asian Journal of Ecotoxicology
基金 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)”。
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 environmental endocrine disruptors cardiac toxicity mitochondrial dysfunction PGC-1α oxidative stress
  • 相关文献

参考文献3

二级参考文献36

  • 1Bansal S, Leu A N, Gonzalez F J, et al. 2014. Mitochondrial targeting of cytochrome P450 (CYP) 1B1 and its role in polycyclic aromatic hydrocarbon-induced mitochondrial dysfunction [ J ]. The Journal of Biological Chemistry, 289(14) : 9936-9951.
  • 2Caiment F, Gaj S, Claessen S, et al. 2015. High-throughput data integration of RNA-miRNA-circRNA reveals novel insights into mechanisms of benzo[ a ] pyrene-induced earcinogenicity [ J ]. Nucleic Acids Research, 43(5) : 2525-2534.
  • 3Carugno M, Pesatori A C, Dioni L, et al. 2012. Increased mitochondrial DNA copy number in occupations associated with low-dose benzene exposure [ J]. Environmental Health Perspectives, 120(2) : 210-215.
  • 4Gentner N J, Weber L P. 2011. Intranasal benzo[ a ] pyrene alters circadian blood pressure patterns and causes lung inflammation in rats [ J ]. Archives of Toxicology, 85 (4) : 337-346.
  • 5Green J L, Jones B C, Reed G A. 1994. Effects of sulfite on the uptake and binding of benzo[ a ] pyrene diol epoxide in cultured murine respiratory epithelial cells [ J ]. Environmental Health Perspectives, 102(2) : 216-220.
  • 6Gmva N, Schroeder H, Farinelle S, et al. 2005. Sub-acute administration of benzo[ a ] pyrene ( B [ a ] P) reduces anxiety-related behaviour in adult mice and modulates regional expression of N- methyl-D-aspartate (NMDA) receptors genes in relevant brain regions[ J ]. Chemosphere, 73 ( Suppl. 1 ) : S295-S302.
  • 7Hadler H I, Cook G L. 1979. The mitochondrial activation of sulfate and arsenate and their role in carcinogenesis [ J ]. Journal of Environmental Pathology and Toxicology, 2(3) : 601-612.
  • 8Hou L F, Zhu Z Z, Zhang X, et al. 2010. Airborne particulate matter and mitochondrial damage: a cross-sectional study [ J ]. Environmental Health: A Global Access Science Source, 9:48.
  • 9Jaeobs D R, Adacbi H, Mulder I, et al. 1999. Cigarette smoking and mortality risk : twenty-five-year follow-up of the seven countries study [J]. Archives of Internal Medicine, 159(7) : 733-740.
  • 10Jiang Y, Xia W, Yang J, etal. 2015. BPA-induced DNA hypermethylation of the master mitochondrial gene PGC-1α contributes to cardiomyopatby in male rats [ J ]. Toxicology, 329: 21-31.

共引文献407

同被引文献60

引证文献6

二级引证文献35

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部