Long-term exposure to copper induces mitochondria-mediated apoptosis in mouse hearts

doi:10.1016/j.ecoenv.2022.113329

	Long-term exposure to copper induces mitochondria-mediated apoptosis in mouse hearts
	Pan, Ming 1,5; Zi-Wei Cheng 1; Chen-Guang Huang 1; Zhu-Qing Ye 1; Li-Jun Sun 1; Chen, Hua 1; Bei-Bei Fu 1; Zhou, Kai 1; Zhi-Rui Fang 1; Zi-Jian Wang 6
刊名	ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
	2022-04-01
卷号	234
关键词	Copper Cardiomyocytes Mitochondria Apoptosis
ISSN号	0147-6513
DOI	10.1016/j.ecoenv.2022.113329
通讯作者	Feng-Qin Zhu(tczfq88@126.com) ; Gao, Shan(gaoshan@ahmu.edu.cn)
英文摘要	Copper is a trace element necessary for the normal functioning of organisms, but excessive copper contents may be toxic to the heart. The goal of this study was to investigate the role of excessive copper accumulation in mitochondrial damage and cell apoptosis inhibition. In vivo, the heart copper concentration and cardiac troponin I (c-TnI) and N-terminal forebrain natriuretic peptide (NT-pro-BNP) levels increased in the copper-laden model group compared to those of the control group. Histopathological and ultrastructural observations revealed that the myocardial collagen volume fraction (CVF), perivascular collagen area (PVCA) and cardiomyocyte crosssectional area (CSA) were markedly elevated in the copper-laden model group compared with the control group. Furthermore, transmission electron microscopy (TEM) showed that the mitochondrial double-layer membrane was incomplete in the copper-laden model groups. Furthermore, cytochrome C (Cyt-C) expression was downregulated in mitochondria but upregulated in the cytoplasm in response to copper accumulation. In addition, Bcl-2 expression decreased, while Bax and cleaved caspase-3 levels increased. These results indicate that copper accumulation in cardiomyocyte mitochondria induces mitochondrial injury, and Cyt-C exposure and induces apoptosis, further resulting in heart damage.
资助项目	National Natural Science Foundation of China[81873126] ; Special Professor of Wanjiang Scholars
WOS关键词	OXIDATIVE STRESS ; BREAST-CANCER ; CELL-DEATH ; DISEASE ; MORTALITY ; KIDNEY ; REDOX ; ZINC
WOS研究方向	Environmental Sciences & Ecology ; Toxicology
语种	英语
出版者	ACADEMIC PRESS INC ELSEVIER SCIENCE
WOS记录号	WOS:000779491300005
资助机构	National Natural Science Foundation of China ; Special Professor of Wanjiang Scholars
内容类型	期刊论文
源URL	[http://ir.hfcas.ac.cn:8080/handle/334002/128505]
专题	中国科学院合肥物质科学研究院
通讯作者	Feng-Qin Zhu; Gao, Shan
作者单位	1.Anhui Med Univ, Basic Med Coll, Dept Pharmacol, Hefei 230032, Peoples R China 2.Chinese Acad Sci, Canc Hosp, Hefei 230032, Peoples R China 3.Queen Mary Univ London, Ctr Clin Pharmacol, Barts & London Sch Med & Dent, William Harvey Res Inst, London, England 4.Anhui Med Univ, Affiliated Hosp 1, Dept Anesthesiol, Hefei 230022, Peoples R China 5.Nanjing Univ, Jinling Hosp, Sch Med, Dept Pharmaceut, Nanjing 210002, Jiangsu, Peoples R China 6.Anhui Med Univ, Clin Med Sch Med, Hefei 230031, Peoples R China
推荐引用方式 GB/T 7714	Pan, Ming,Zi-Wei Cheng,Chen-Guang Huang,et al. Long-term exposure to copper induces mitochondria-mediated apoptosis in mouse hearts[J]. ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY,2022,234.
APA	Pan, Ming.,Zi-Wei Cheng.,Chen-Guang Huang.,Zhu-Qing Ye.,Li-Jun Sun.,...&Gao, Shan.(2022).Long-term exposure to copper induces mitochondria-mediated apoptosis in mouse hearts.ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY,234.
MLA	Pan, Ming,et al."Long-term exposure to copper induces mitochondria-mediated apoptosis in mouse hearts".ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY 234(2022).