The first two authors contributed equally to this work.
Perfluorooctane sulfonate induces apoptosis in lung cancer A549 cells through reactive oxygen species-mediated mitochondrion-dependent pathway
Version of Record online: 13 SEP 2012
Copyright © 2012 John Wiley & Sons, Ltd.
Journal of Applied Toxicology
Volume 33, Issue 11, pages 1268–1276, November 2013
How to Cite
Mao, Z., Xia, W., Wang, J., Chen, T., Zeng, Q., Xu, B., Li, W., Chen, X. and Xu, S. (2013), Perfluorooctane sulfonate induces apoptosis in lung cancer A549 cells through reactive oxygen species-mediated mitochondrion-dependent pathway. J. Appl. Toxicol., 33: 1268–1276. doi: 10.1002/jat.2785
- Issue online: 20 SEP 2013
- Version of Record online: 13 SEP 2012
- Manuscript Revised: 16 MAY 2012
- Manuscript Accepted: 16 MAY 2012
- Manuscript Received: 12 MAR 2012
- A549 cells
Perfluorooctane sulfonate (PFOS) is a widespread environmental contaminant that is detected in the lung of mammals. The mechanisms underlying PFOS-induced lung cytotoxicity remain unclear. The main purpose of this study was to evaluate the cytotoxic effects of PFOS on human lung cancer A549 cells and its possible molecular mechanism. A549 cells were treated with PFOS (0, 25, 50, 100 and 200 μm) and the cellular apoptosis, mitochondrial membrane potential as well as intracellular reactive oxygen species were determined. In this study, PFOS induced a dose-dependent increase in A549 cell toxicity via an apoptosis pathway as characterized by increased percentage of sub-G1, activation of caspase-3 and −9, and increased ratio of Bax/bcl-2 mRNA expression. In addition, there was obvious oxidative stress, represented by decreased glutathione level, increased malondialdehyde level and superoxide dismutase activity. N-Acetylcysteine, as an antioxidant that is a direct reactive oxygen species scavenger, can effectively block PFOS-induced reactive oxygen species generation, mitochondrial membrane potential loss and cell apoptosis. These data indicate that PFOS induces apoptosis in A549 cells through a reactive oxygen species-mediated mitochondrial dysfunction pathway mechanism. Copyright © 2012 John Wiley & Sons, Ltd.