P53-Dependent Apoptosis Induced in Human Bronchial Epithelial (16-Hbe) Cells by Pm(2.5) Sampled from Air in Guangzhou, China

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  • 作者：Zhou, B., Liang, G., Qin, H., Peng, X., Huang, J., Li, Q., Qing, L., Zhang, L., Chen, L., Ye, L., Niu, P. & Zou, Y.
  • 期刊：Toxicology mechanisms and methods 24, 552-559 (2014)
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Epidemiological studies have shown that air pollution particulate matter (PM) is associated with increased respiratory morbidity and mortality. However, the mechanisms are not fully understood. Oxidative stress-mediated apoptosis plays an important role in the occurrence of respiratory diseases. In this study, human bronchial epithelial (16-HBE) cells were exposed to different concentrations (16-128??g/ml) of PM(2.5) for 24?h to investigate the apoptosis induced by PM(2.5). The results showed that PM(2.5) exposure significantly induced apoptosis, DNA strand breaks, and oxidative damage in a dose-dependent manner in 16-HBE cells. The expression of p53 and p73 increased significantly along with the dose of PM(2.5) in 16-HBE cells, whereas the expression of p21(Cip1/WAF1) decreased; the expression of mdm2 increased and then decreased, but not significantly. Taken together, these observations indicate that PM(2.5) may lead to oxidative damage and induce apoptosis through the p53-dependent pathway in 16-HBE cells. p53-Dependent apoptosis mediated by DNA strand breaks may be an important mechanism of PM(2.5)-induced apoptosis in 16-HBE cells.

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