环境内分泌干扰物暴露致心肌线粒体损伤的研究进展
The Effects of Environmental Endocrine Disruptors on Myocardial Mitochondrial: A Review
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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。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.
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马丽媛, 吴亚哲, 王文, 等. 《中国心血管病报告2017》要点解读[J]. 中国心血管杂志, 2018, 23(1):3-6 Ma L Y, Wu Y Z, Wang W, et al. Key points of China Cardiovascular Disease Report 2017[J]. Chinese Journal of Cardiovascular Sciences, 2018, 23(1):3-6(in Chinese)
Kabir E R, Rahman M S, Rahman I. A review on endocrine disruptors and their possible impacts on human health[J]. Environmental Toxicology and Pharmacology, 2015, 40(1):241-258 Amara I, Timoumi R, Annabi E, et al. Di (2-ethylhexyl) phthalate induces cardiac disorders in BALB/c mice[J]. Environmental Science and Pollution Research, 2019, 26(8):7540-7549 Su T, Hwang U, Sun C, et al. Urinary phthalate metabolites, coronary heart disease, and atherothrombotic markers[J]. Ecotoxicology and Environmental Safety, 2019, 173:37-44 Genchi G, Sinicropi M, Carocci A, et al. Mercury exposure and heart diseases[J]. International Journal of Environmental Research and Public Health, 2017, 14(1):74 Dominic A, Ramezani A, Anker S, et al. Mitochondrial cytopathies and cardiovascular disease[J]. Heart, 2014, 100(8):611-618 Mohsin A, Chen Q, Quan N H, et al. Mitochondrial complex I inhibition by metformin limits reperfusion injury[J]. Journal of Pharmacology and Experimental Therapeutics, 2019, 369(2):282-290 Boengler K, Lochnit G, Schulz R. Mitochondria "THE" target of myocardial conditioning[J]. American Journal of Physiology-Heart and Circulatory Physiology, 2018, 315(5):H1215-H1231 Brown D A, Perry J B, Allen M E, et al. Expert consensus document:Mitochondrial function as a therapeutic target in heart failure[J]. Nature Reviews Cardiology, 2017, 14(4):238-250 Posnack N G, Jaimes R, Asfour H, et al. Bisphenol A exposure and cardiac electrical conduction in excised rat hearts[J]. Environmental Health Perspectives, 2014, 122(4):384-390 姜颖. 双酚A暴露对大鼠的心脏毒性及其表观遗传学机制的研究[D]. 武汉:华中科技大学, 2015:84-89 Jiang Y. Cardiac effects of bisphenol A exposure in rats and its epigenetic mechanism[D]. Wuhan:Huazhong University of Science and Technology, 2015:84 -89(in Chinese)
Patel B B, Kasneci A, Bolt A M, et al. Chronic exposure to bisphenol A reduces successful cardiac remodeling after an experimental myocardial infarction in male C57bl/6n mice[J]. Toxicological Sciences, 2015, 146(1):101-115 Garcia M, Guéant-Rodriguez R, Pooya S, et al. Methyl donor deficiency induces cardiomyopathy through altered methylation/acetylation of PGC-1α by PRMT1 and SIRT1[J]. The Journal of Pathology, 2011, 225(3):324-335 Jiang Y, Xia W, Yang J, et al. BPA-induced DNA hypermethylation of the master mitochondrial gene PGC-1α contributes to cardiomyopathy in male rats[J]. Toxicology, 2015, 329:21-31 Patel B, Raad M, Sebag I A, et al. Lifelong exposure to bisphenol A alters cardiac structure/function, protein expression, and DNA methylation in adult mice[J]. Toxicological Sciences, 2013, 133(1):174-185 Yue R C, Xia X W, Jiang J H, et al. Mitochondrial DNA oxidative damage contributes to cardiomyocyte ischemia/reperfusion-injury in rats:Cardioprotective role of lycopene[J]. Journal of Cellular Physiology, 2015, 230(9):2128-2141 Aboul Ezz H S, Khadrawy Y A, Mourad I M. The effect of bisphenol A on some oxidative stress parameters and acetylcholinesterase activity in the heart of male albino rats[J]. Cytotechnology, 2015, 67(1):145-155 Bround M J, Wambolt R, Luciani D S, et al. Cardiomyocyte ATP production, metabolic flexibility, and survival require calcium flux through cardiac ryanodine receptors in vivo[J]. Journal of Biological Chemistry, 2013, 288(26):18975-18986 Pace C, Dagda R, Angermann J. Antioxidants protect against arsenic induced mitochondrial cardio-toxicity[J]. Toxics, 2017, 5(4):38-41 Ramadan M, Sherman M, Jaimes R, et al. Disruption of neonatal cardiomyocyte physiology following exposure to bisphenol-A[J]. Scientific Reports, 2018, 8(1):7356 Gao X Q, Liang Q, Chen Y M, et al. Molecular mechanisms underlying the rapid arrhythmogenic action of bisphenol A in female rat hearts[J]. Endocrinology, 2013, 154(12):4607-4617 Yan S J, Chen Y M, Dong M, et al. Bisphenol A and 17β-estradiol promote arrhythmia in the female heart via alteration of calcium handling[J]. PLOS ONE, 2011, 6(9):e25455 Cook S J, Stuart K, Gilley R, et al. Control of cell death and mitochondrial fission by ERK1/2 MAP kinase signalling[J]. FEBS Journal, 2017, 284(24):4177-4195 Hu Y Y, Zhang L, Wu X X, et al. Bisphenol A, an environmental estrogen-like toxic chemical, induces cardiac fibrosis by activating the ERK1/2 pathway[J]. Toxicology Letters, 2016, 250:1-9 Wang Y, Hu H Y, Zhao M M, et al. Nonylphenol disrupts the cardio-protective effects of 17β-estradiol on ischemia/reperfusion injury in isolated hearts of guinea pig[J]. Journal of Toxicological Sciences, 2013, 38(5):731-740 Gao Q H, Liu S Y, Guo F, et al. Nonylphenol affects myocardial contractility and L-type Ca2+ channel currents in a non-monotonic manner via G protein-coupled receptor 30[J]. Toxicology, 2015, 334:122-129 Li X J, Zhou L T, Ni Y P, et al. Nonylphenol induces pancreatic damage in rats through mitochondrial dysfunction and oxidative stress[J]. Toxicology Research, 2017, 6(3):353-360 Perrotta I, Tripepi S. Ultrastructural alterations in the ventricular myocardium of the adult Italian newt (Lissotriton italicus) following exposure to nonylphenol ethoxylate[J]. Micron, 2012, 43(2):183-191 Posnack N G, Swift L M, Kay M W, et al. Phthalate exposure changes the metabolic profile of cardiac muscle cells[J]. Environmental Health Perspectives, 2012, 120(9):1243-1251 Posnack N G, Lee N H, Brown R, et al. Gene expression profiling of DEHP-treated cardiomyocytes reveals potential causes of phthalate arrhythmogenicity[J]. Toxicology, 2011, 279(1):54-64 Asghari M H, Moloudizargari M, Baeeri M, et al. On the mechanisms of melatonin in protection of aluminum phosphide cardiotoxicity[J]. Archives of Toxicology, 2017, 91(9):3109-3120 Aminjan H H, Abtahi S R, Hazrati E, et al. Targeting of oxidative stress and inflammation through ROS/NF-kappaB pathway in phosphine-induced hepatotoxicity mitigation[J]. Life Sciences, 2019, 232:116607 Akbel E, Arslan-Acaroz D, Demirel H H, et al. The subchronic exposure to malathion, an organophosphate pesticide, causes lipid peroxidation, oxidative stress, and tissue damage in rats:The protective role of resveratrol[J]. Toxicology Research, 2018, 7(3):503-512 Turkmen R, Birdane Y O, Demirel H H, et al. Protective effects of resveratrol on biomarkers of oxidative stress, biochemical and histopathological changes induced by sub-chronic oral glyphosate-based herbicide in rats[J]. Toxicology Research, 2019, 8(2):238-245 Mohammadi H, Karimi G, Rezayat S M, et al. Benefit of nanocarrier of magnetic magnesium in rat malathion-induced toxicity and cardiac failure using non-invasive monitoring of electrocardiogram and blood pressure[J]. Toxicology and Industrial Health, 2011, 27(5):417-429 Shemarova I V, Korotkov S M, Nesterov V P. Influence of oxidative processes in mitochondria on contractility of the frog Rana temporaria heart muscle. Effects of cadmium[J]. Journal of Evolutionary Biochemistry and Physiology, 2011, 47(4):306-310 Oyinloye B E, Ajiboye B O, Adeleke Ojo O, et al. Cardioprotective and antioxidant influence of aqueous extracts from sesamum indicum seeds on oxidative stress induced by cadmium in Wistar rats[J]. Pharmacognosy Magazine, 2016, 12(46):170-174 Lei W W, Wang L, Liu D M, et al. Histopathological and biochemical alternations of the heart induced by acute cadmium exposure in the freshwater crab Sinopotamon yangtsekiense[J]. Chemosphere, 2011, 84(5):689-694 Huang Q Y, Fang C W, Huang H Q. Alteration of heart tissue protein profiles in acute cadmium-treated scallops Patinopecten yessoensis[J]. Archives of Environmental Contamination and Toxicology, 2011, 60(1):90-98 Houston M C. Role of mercury toxicity in hypertension, cardiovascular disease, and stroke[J]. Journal of Clinical Hypertension, 2011, 13(8):621-627 Azevedo B F, Furieri L B, Peçanha F M, et al. Toxic effects of mercury on the cardiovascular and central nervous systems[J]. BioMed Research International, 2012, 2012:949048 Baiyun R Q, Li S Y, Liu B Y, et al. Luteolin-mediated PI3K/AKT/Nrf2 signaling pathway ameliorates inorganic mercury-induced cardiac injury[J]. Ecotoxicology and Environmental Safety, 2018, 161:655-661 秦国华, 武美琼, 桑楠. SO2和BaP复合暴露诱导小鼠心脏线粒体损伤的分子机制初探[J]. 环境科学学报, 2015, 35(8):2620-2625 Qin G H, Wu M Q, Sang N. Molecular mechanism of co-exposure of sulfur dioxide and benzo(a) pyrene on mouse myocardial cell mitochondria damage[J]. Acta Scientiae Circumstantiae, 2015, 35(8):2620-2625(in Chinese)
李振青. 关于PM2.5监测与烟花爆竹燃放的研究[J]. 中国化工贸易, 2013, 5(5):268 寇晓晶. PM2.5暴露对大鼠心脏线粒体损伤效应及分子机制研究[D]. 太原:山西大学, 2015:20-26 Kou X J. Effects of PM2.5
on mitochondrial damage in hearts of rats and their molecular mechanisms[D]. Taiyuan:Shanxi University, 2015:20-26(in Chinese) -
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