Journal
ENVIRONMENTAL TOXICOLOGY
Volume 30, Issue 9, Pages 1063-1072Publisher
WILEY-BLACKWELL
DOI: 10.1002/tox.21979
Keywords
PCB; quinone; apoptosis; mitochondrial; caspase
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Funding
- National Natural Science Foundation of China [NSFC-21005064, 21035005]
- Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry [2011[508]]
- Fundamental Research Funds for the Central Universities [XDJK2010B008, XDJK2013B009]
- State Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University [2012009]
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Polychlorinated biphenyl (PCB) quinones are known to cause toxic effects, but their mechanisms are quite unclear. In this study, we examined whether 2,3,5-trichloro-6-phenyl-[1,4]benzoquinone, PCB29-pQ, induces cell death via apoptosis pathway. Our result showed PCB29-pQ exposure decreased HepG2 cell viability in a time-dependent manner. Lactate dehydrogenase leakage assay also implied the cytotoxicity of PCB29-pQ. 4,6-Diamidino-2-phenylindole dihydrochloride staining and flow cytometry assays both confirmed PCB29-pQ caused dose-dependent apoptotic cell death in HepG2 cells. Furthermore, we found that PCB29-pQ exposure increased cellular reactive oxygen species (ROS) level, decreased mitochondrial membrane potential and induced the translocation of cytochrome c from mitochondria into cytosol in HepG2 cells. Moreover, PCB29-pQ exposure induced B-cell lymphoma 2 (Bcl-2) downregulation and Bcl-2-associated X (Bax) upregulation, poly(ADP-ribose) polymerase cleavage, accompanied with the increased caspase-3/9 and p53 expressions. Taking together, these results suggested PCB29-pQ induced HepG2 cells apoptosis through a ROS-driven, mitochondrial-mediated and caspase-dependent pathway. (c) 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 1063-1072, 2015.
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