PFOS-induced apoptosis through mitochondrion-dependent pathway in human-hamster hybrid cells
文献类型：期刊论文
| 作者 | Wang, Xiaofei1 ; Zhao, Guoping1; Liang, Junting1; Jiang, Jiang1; Chen, Ni2; Yu, Jing2; Wang, Qisen1; Xu, An1; Chen, Shaopeng1; Wu, Lijun1,2
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| 刊名 | MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS
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| 出版日期 | 2013-06-14 |
| 卷号 | 754期号:1-2页码:51-57 |
| 关键词 | Pfos Apoptosis Mutagenicity Mtdna-depleted (Rho(0)) a(l) Cells Oxidative Stress |
| DOI | 10.1016/j.mrgentox.2013.04.004 |
| 文献子类 | Article |
| 英文摘要 | Perfluorooctane sulfonate (PFOS) was listed as one of the persistent organic pollutants (POPs) in Stockholm Convention in 2009. Recent evidence showed that PFOS could induce apoptosis both in vivo and in vitro. However, the apoptotic mechanisms induced by PFOS as well as the possible relationship between apoptosis and other PFOS-induced endpoints, remain unclear. In the present study, normal human-hamster hybrid (A(L)) cells and mtDNA-depleted (rho(0) A(L)) cells were exposed to PFOS, and assayed for cytotoxicity, mutagenicity, and apoptosis (caspase-3/7, caspase-9 activities). Our results showed that PFOS decreased cell viability in a time- and concentration-dependent manner in A(L) cells, but not in rho(0) A(L) cells. However, long-term exposure to PFOS failed to induce the mutagenic effects at the CD59 locus in A(L) cells. Exposure to 200 mu M PFOS significantly increased the activities of caspase-3/7 and caspase-9 in A(L) cells, but the activities of these caspases were not affected in rho(0) A(L) cells. In addition, PFOS increased the levels of reactive oxygen species (ROS), superoxide anion (O-2(center dot-)), as well as nitric oxide (NO), and decreased mitochondrial membrane potential (MMP) at the concentrations of 100 and 200 mu M in A(L) cells. On the other hand, exposure to PFOS had no effect on intracellular ROS, O-2(center dot-), and NO production in rho(0) A(L) cells. Caspase-3/7 activity, which was increased by 200 mu M PFOS, could be suppressed by ROS/O-2(center dot-) scavengers and nitric oxide synthases (NOSs) inhibitors in A(L) cells. These results implicate that PFOS-induced apoptosis and oxidative stress is mediated by a mitochondrion-dependent pathway and that the induction of apoptosis might be a protective function against mutagenesis in A(L) cells exposed to PFOS. (C) 2013 Elsevier B.V. All rights reserved. |
| WOS关键词 | PERFLUOROOCTANE SULFONATE PFOS ; REACTIVE OXYGEN ; PERFLUORINATED COMPOUNDS ; MAMMALIAN-CELLS ; ZEBRAFISH EMBRYOS ; OXIDATIVE STRESS ; EXPRESSION ; TOXICITY ; PLASMA ; GENOTOXICITY |
| WOS研究方向 | Biotechnology & Applied Microbiology ; Genetics & Heredity ; Toxicology |
| 语种 | 英语 |
| WOS记录号 | WOS:000320495200007 |
| 源URL | [http://ir.hfcas.ac.cn:8080/handle/334002/22206]  |
| 专题 | 合肥物质科学研究院_技术生物与农业工程研究所 |
| 作者单位 | 1.Chinese Acad Sci, Hefei Inst Phys Sci, Key Lab Ion Beam Bioengn, Hefei, Anhui, Peoples R China 2.Univ Sci & Technol China, Sch Nucl Sci & Technol, Hefei 230026, Anhui, Peoples R China |
| 推荐引用方式 GB/T 7714 | Wang, Xiaofei,Zhao, Guoping,Liang, Junting,et al. PFOS-induced apoptosis through mitochondrion-dependent pathway in human-hamster hybrid cells[J]. MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS,2013,754(1-2):51-57. |
| APA | Wang, Xiaofei.,Zhao, Guoping.,Liang, Junting.,Jiang, Jiang.,Chen, Ni.,...&Wu, Lijun.(2013).PFOS-induced apoptosis through mitochondrion-dependent pathway in human-hamster hybrid cells.MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS,754(1-2),51-57. |
| MLA | Wang, Xiaofei,et al."PFOS-induced apoptosis through mitochondrion-dependent pathway in human-hamster hybrid cells".MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS 754.1-2(2013):51-57. |
入库方式： OAI收割
来源：合肥物质科学研究院
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