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Tris(1,3-dichloro-2-propyl) phosphate-induced cytotoxicity and its associated mechanisms in human A549 cells.
Feng, Yixing; Li, Ming; Yin, Jie; Shi, Jiachen; Jiang, Qian; Zhang, Jing.
Affiliation
  • Feng Y; Beijing Key Laboratory of Diagnostic and Traceability Technologies for Food Poisoning, Beijing Center for Disease Control and Prevention, Beijing, China.
  • Li M; Beijing Key Laboratory of Diagnostic and Traceability Technologies for Food Poisoning, Beijing Center for Disease Control and Prevention, Beijing, China.
  • Yin J; Beijing Key Laboratory of Diagnostic and Traceability Technologies for Food Poisoning, Beijing Center for Disease Control and Prevention, Beijing, China.
  • Shi J; Beijing Key Laboratory of Diagnostic and Traceability Technologies for Food Poisoning, Beijing Center for Disease Control and Prevention, Beijing, China.
  • Jiang Q; Beijing Key Laboratory of Diagnostic and Traceability Technologies for Food Poisoning, Beijing Center for Disease Control and Prevention, Beijing, China.
  • Zhang J; Beijing Key Laboratory of Diagnostic and Traceability Technologies for Food Poisoning, Beijing Center for Disease Control and Prevention, Beijing, China.
Toxicol Ind Health ; 40(7): 387-397, 2024 Jul.
Article in En | MEDLINE | ID: mdl-38729922
ABSTRACT
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 µM. 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.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Organophosphorus Compounds / Cell Survival / Apoptosis / Flame Retardants Limits: Humans Language: En Journal: Toxicol Ind Health Journal subject: MEDICINA OCUPACIONAL / TOXICOLOGIA Year: 2024 Document type: Article Affiliation country: China

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Organophosphorus Compounds / Cell Survival / Apoptosis / Flame Retardants Limits: Humans Language: En Journal: Toxicol Ind Health Journal subject: MEDICINA OCUPACIONAL / TOXICOLOGIA Year: 2024 Document type: Article Affiliation country: China
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