Tris(1,3-dichloro-2-propyl) phosphate-induced cytotoxicity and its associated mechanisms in human A549 cells

被引:0
作者
Feng, Yixing [1 ]
Li, Ming [1 ]
Yin, Jie [1 ]
Shi, Jiachen [1 ]
Jiang, Qian [1 ]
Zhang, Jing [1 ]
机构
[1] Beijing Ctr Dis Control & Prevent, Beijing Key Lab Diagnost & Traceabil Technol Food, 16 Hepingli Middle St, Beijing 100013, Peoples R China
基金
北京市自然科学基金;
关键词
Tris(1,3-dichloro-2-propyl) phosphate; A549; cells; cell cycle arrest; cell apoptosis; gene expression; ORGANOPHOSPHATE FLAME RETARDANTS; WASTE-WATER; TDCPP; ZEBRAFISH; APOPTOSIS; TOXICITY; EXPOSURE; TDCIPP;
D O I
10.1177/07482337241255711
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
Tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) is a widely used organophosphorus flame retardant and has been detected in various environmental matrices including indoor dust. Inhalation of indoor dust is one of the most important pathways for human exposure to TDCIPP. However, its adverse effects on human lung cells and potential impacts on respiratory toxicity are largely unknown. In the current study, human non-small cell carcinoma (A549) cells were selected as a cell model, and the effects of TDCIPP on cell viability, cell cycle, cell apoptosis, and underlying molecular mechanisms were investigated. Our data indicated a concentration-dependent decrease in the cell viability of A549 cells after exposure to TDCIPP for 48 h, with half lethal concentration (LC50) being 82.6 mu M. In addition, TDCIPP caused cell cycle arrest mainly in the G0/G1 phase by down-regulating the mRNA expression of cyclin D1, CDK4, and CDK6, while up-regulating the mRNA expression of p21 and p27. In addition, cell apoptosis was induced via altering the expression levels of Bcl-2, BAX, and BAK. Our study implies that TDCIPP may pose potential health risks to the human respiratory system and its toxicity should not be neglected.
引用
收藏
页码:387 / 397
页数:11
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