Long-term exposure to copper induces mitochondria-mediated apoptosis in mouse hearts
文献类型：期刊论文
| 作者 | Pan, Ming2,6; Zi-Wei Cheng6; Chen-Guang Huang6; Zhu-Qing Ye6; Li-Jun Sun6; Chen, Hua6; Bei-Bei Fu6; Zhou, Kai6; Zhi-Rui Fang6; Zi-Jian Wang1 |
| 刊名 | ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
 |
| 出版日期 | 2022-04-01 |
| 卷号 | 234 |
| ISSN号 | 0147-6513 |
| 关键词 | Copper Cardiomyocytes Mitochondria Apoptosis |
| 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. |
| WOS关键词 | OXIDATIVE STRESS ; BREAST-CANCER ; CELL-DEATH ; DISEASE ; MORTALITY ; KIDNEY ; REDOX ; ZINC |
| 资助项目 | National Natural Science Foundation of China[81873126] ; Special Professor of Wanjiang Scholars |
| 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 |
| 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, Clin Med Sch Med, Hefei 230031, Peoples R China 2.Nanjing Univ, Jinling Hosp, Sch Med, Dept Pharmaceut, Nanjing 210002, Jiangsu, Peoples R China 3.Anhui Med Univ, Affiliated Hosp 1, Dept Anesthesiol, Hefei 230022, Peoples R China 4.Queen Mary Univ London, Ctr Clin Pharmacol, Barts & London Sch Med & Dent, William Harvey Res Inst, London, England 5.Chinese Acad Sci, Canc Hosp, Hefei 230032, Peoples R China 6.Anhui Med Univ, Basic Med Coll, Dept Pharmacol, Hefei 230032, 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). |
入库方式： OAI收割
来源：合肥物质科学研究院
浏览0
下载0
收藏0
其他版本
除非特别说明，本系统中所有内容都受版权保护，并保留所有权利。