PFOS-induced apoptosis through mitochondrion-dependent pathway in human-hamster hybrid cells

doi:10.1016/j.mrgentox.2013.04.004

	PFOS-induced apoptosis through mitochondrion-dependent pathway in human-hamster hybrid cells
	Wang, Xiaofei1 ; Zhao, Guoping1 ; Liang, Junting 1; Jiang, Jiang 1; Chen, Ni 2; Yu, Jing 2; Wang, Qisen 1; Xu, An1 ; Chen, Shaopeng1 ; Wu, Lijun1,2
	2013-06-14
发表期刊	MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS
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.
文章类型	Article
关键词	Pfos Apoptosis Mutagenicity Mtdna-depleted (Rho(0)) a(l) Cells Oxidative Stress
WOS标题词	Science & Technology ; Life Sciences & Biomedicine
DOI	10.1016/j.mrgentox.2013.04.004
关键词[WOS]	PERFLUOROOCTANE SULFONATE PFOS ; REACTIVE OXYGEN ; PERFLUORINATED COMPOUNDS ; MAMMALIAN-CELLS ; ZEBRAFISH EMBRYOS ; OXIDATIVE STRESS ; EXPRESSION ; TOXICITY ; PLASMA ; GENOTOXICITY
收录类别	SCI
语种	英语
WOS研究方向	Biotechnology & Applied Microbiology ; Genetics & Heredity ; Toxicology
WOS类目	Biotechnology & Applied Microbiology ; Genetics & Heredity ; Toxicology
WOS记录号	WOS:000320495200007
引用统计	被引频次：27[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	http://ir.hfcas.ac.cn:8080/handle/334002/22206
专题	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.