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OPFRs and BFRs induced A549 cell apoptosis by caspase-dependent mitochondrial pathway.

Abstract
Organophosphate flame retardants (OPFRs) and brominated flame retardants (BFRs) are frequently detected in indoor environment at high levels, posing health risks to humans. However, the potential cytotoxicity mediated by OPFRs and BFRs in relevant human cell models is limited. In current study, non-small cell lung cancer A549 cell was employed to investigate toxicity mechanisms of typical OPFRs (i.e., tris (2-chloroethyl) phosphate (TCEP), tris-(2-chloropropyl) phosphate (TCPP), tricresy phosphate (TCP), triphenyl phosphate (TPHP) and BFRs (i.e., 2,2',4,4'-tetrabromodiphenyl ether (BDE-47), 3,3', 5,5'-tetrabromobisphenol A (TBBPA)). It was found that BDE-47 exhibited the strongest cytotoxicity, followed by TBBPA, TPHP, TCP, TCPP and TCEP. OPFRs and BFRs could cause the reduction of cell viability of A549 cell in both dose- and time-dependent manner after exposure for 24 and 48 h. Simultaneously, excessive generation of reactive oxygen species (ROS), mitochondrial membrane potential (MMP) dysfunction, cell apoptosis and overload of intracellular free Ca2+ demonstrated that cytotoxicity induced by OPFRs and BFRs were mediated by oxidative stress. Of note, the survival rate of cell significantly increased when pretreated with Ac-DEVD-CHO, suggesting that caspase-3 dependent mitochondrial pathway may have played a primary role in the process of A549 cell apoptosis.
AuthorsXiaolong Yu, Hua Yin, Hui Peng, Guining Lu, Zehua Liu, Zhi Dang
JournalChemosphere (Chemosphere) Vol. 221 Pg. 693-702 (Apr 2019) ISSN: 1879-1298 [Electronic] England
PMID30669111 (Publication Type: Journal Article)
CopyrightCopyright © 2019 Elsevier Ltd. All rights reserved.
Chemical References
  • Flame Retardants
  • Halogenated Diphenyl Ethers
  • Organophosphates
  • 2,2',4,4'-tetrabromodiphenyl ether
  • Caspases
Topics
  • A549 Cells
  • Apoptosis
  • Caspases (metabolism)
  • Flame Retardants (metabolism, toxicity)
  • Halogenated Diphenyl Ethers (toxicity)
  • Halogenation
  • Humans
  • Mitochondria (metabolism)
  • Organophosphates (metabolism, toxicity)
  • Oxidative Stress

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