Asian Journal of Ecotoxicology

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2020 Volume 15 Issue 4

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Tang Lan, Yu Jie, Xu Jie. The Effects of Environmental Endocrine Disruptors on Myocardial Mitochondrial: A Review[J]. Asian Journal of Ecotoxicology, 2020, 15(4): 123-128. doi: 10.7524/AJE.1673-5897.20190903002

Citation:

Tang Lan, Yu Jie, Xu Jie. The Effects of Environmental Endocrine Disruptors on Myocardial Mitochondrial: A Review[J]. Asian Journal of Ecotoxicology, 2020, 15(4): 123-128. doi: 10.7524/AJE.1673-5897.20190903002

The Effects of Environmental Endocrine Disruptors on Myocardial Mitochondrial: A Review

School of Public Health, Zunyi Medical University, Zunyi 563000, China

Corresponding author: Xu Jie, 649904039@qq.com
Received Date: 03/09/2019

Fund Project:

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.
- environmental endocrine disruptors,
- cardiac toxicity,
- mitochondrial dysfunction,
- PGC-1α,
- oxidative stress

References

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)

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

Dominic A, Ramezani A, Anker S, et al. Mitochondrial cytopathies and cardiovascular disease[J]. Heart, 2014, 100(8):611-618

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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)

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

Pace C, Dagda R, Angermann J. Antioxidants protect against arsenic induced mitochondrial cardio-toxicity[J]. Toxics, 2017, 5(4):38-41

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

Houston M C. Role of mercury toxicity in hypertension, cardiovascular disease, and stroke[J]. Journal of Clinical Hypertension, 2011, 13(8):621-627

Google Scholar Pub Med

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

Google Scholar Pub Med

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

Google Scholar Pub Med

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)

Google Scholar Pub Med

李振青. 关于PM_2.5监测与烟花爆竹燃放的研究[J]. 中国化工贸易, 2013, 5(5):268

Google Scholar Pub Med

寇晓晶. PM_2.5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 PM_2.5 on mitochondrial damage in hearts of rats and their molecular mechanisms[D]. Taiyuan:Shanxi University, 2015:20-26(in Chinese)

Google Scholar Pub Med

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The Effects of Environmental Endocrine Disruptors on Myocardial Mitochondrial: A Review

Corresponding author: Xu Jie, 649904039@qq.com

Received Date: 03/09/2019

Fund Project:

Key words:

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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