Cytotoxicity, mitochondrial impairment, DNA damage and associated mechanisms induced by tris(1,3-dichloro-2-propyl) phosphate and tris (2-butoxyethyl) phosphate in A549 cells
文献类型：期刊论文
| 作者 | Yuan, Shengwu; Ma, Mei; Zhu, Xiaoshan; Han, Yingnan; Rao, Kaifeng; Wang, Zijian |
| 刊名 | SCIENCE OF THE TOTAL ENVIRONMENT
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| 出版日期 | 2021-09-15 |
| 卷号 | 787页码:- |
| ISSN号 | 0048-9697 |
| 关键词 | Phosphorus-containing flame retardants Cellular damage Cell cycle arrest Oxidative stress p53 |
| 英文摘要 | Tris(1,3-dichloro-2-propyl) phosphate (TDCPP) and tris(2-butoxyethyl) phosphate (TBOEP), two of the most widely applied phosphorus-containing flame retardants (PFRs), have been shown to have adverse effects in differ-ent organisms, but their underlying toxicity mechanism remains to be elucidated. In the present study, the toxico-logical effects of TDCPP and TBOEP on human lung carcinoma (A549) cells and their associated mechanisms were investigated at the cellular, organelle and transcriptional levels. Cell Counting Kit-8 assay results showed that TDCPP and TBOEP reduced cell viability in a concentration-dependent manner. High-content screening assays showed that both PFRs caused mitochondrial impairment at the organelle level, decreasing the mitochondrial mem-brane potential and increasing the mitochondrial mass, and leading to increased cell cycle arrest-associated DNA damage that decreased the ratio of cells in S phase and increased the DNA content. In addition, oxidative stress was identified as a possible initial mechanistic process underlying PFR-induced cytotoxicity and mitochondrial im-pairment, as evidenced by intracellular reactive oxygen species and mitochondrial superoxide overproduction from environmentally relevant concentrations. Furthermore, p53 activation was shown to be involved in regulating DNA damage after A549 cell exposure to TDCPP and TBOEP. Quantitative PCR analyses showed that TDCPP and TBOEP triggered p53/p21-mediated cell cycle arrest pathways, indicating that these PFRs can activate p53, and promote as-sociated functional repair. However, the p53/bax-mediated apoptosis pathway was not activated following exposure to PFRs at specific concentrations. Our results showed that TDCPP and TBOEP can cause cytotoxicity, mitochondrial impairment and cell cycle arrest-associated DNA damage in A549 cells, suggesting that oxidative stress is the initial molecular event by which these adverse outcomes are induced. (c) 2021 Elsevier B.V. All rights reserved. |
| WOS研究方向 | Environmental Sciences |
| 源URL | [http://ir.rcees.ac.cn/handle/311016/46187]  |
| 专题 | 生态环境研究中心_中国科学院饮用水科学与技术重点实验室 |
| 作者单位 | 1.Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Aquat Chem, Beijing 100085, Peoples R China 2.Univ Chinese Acad Sci, Coll Resources & Environm, Beijing 100049, Peoples R China 3.Chinese Acad Sci, Res Ctr Ecoenvironm Sci, Key Lab Drinking Water Sci & Technol, Beijing 100085, Peoples R China 4.Tsinghua Univ, Shenzhen Int Grad Sch, Shenzhen 518055, Peoples R China |
| 推荐引用方式 GB/T 7714 | Yuan, Shengwu,Ma, Mei,Zhu, Xiaoshan,et al. Cytotoxicity, mitochondrial impairment, DNA damage and associated mechanisms induced by tris(1,3-dichloro-2-propyl) phosphate and tris (2-butoxyethyl) phosphate in A549 cells[J]. SCIENCE OF THE TOTAL ENVIRONMENT,2021,787:-. |
| APA | Yuan, Shengwu,Ma, Mei,Zhu, Xiaoshan,Han, Yingnan,Rao, Kaifeng,&Wang, Zijian.(2021).Cytotoxicity, mitochondrial impairment, DNA damage and associated mechanisms induced by tris(1,3-dichloro-2-propyl) phosphate and tris (2-butoxyethyl) phosphate in A549 cells.SCIENCE OF THE TOTAL ENVIRONMENT,787,-. |
| MLA | Yuan, Shengwu,et al."Cytotoxicity, mitochondrial impairment, DNA damage and associated mechanisms induced by tris(1,3-dichloro-2-propyl) phosphate and tris (2-butoxyethyl) phosphate in A549 cells".SCIENCE OF THE TOTAL ENVIRONMENT 787(2021):-. |
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来源：生态环境研究中心
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