P53-Dependent apoptosis induced in human bronchial epithelial (16-HBE) cells by PM2.5 sampled from air in Guangzhou, China. (20th October 2014)

• Record Type: Journal Article
• Authors: Zhou, Bo; Liang, Guiqiang; Qin, Huiyan; Peng, Xiaowu; Huang, Jiongli; Li, Qin; Qing, Li; Zhang, Li'e; Chen, Li; Ye, Li; Niu, Piye; Zou, Yunfeng
• Is Part Of: Toxicology mechanisms and methods. Volume 24:Number 8(2014)
• Page Start: 552
• Page End: 559
• Publication Date: 2014-10-20
• Subjects: Apoptosis -- DNA damage -- oxidative stress -- p53 -- PM2.5; Analytical toxicology -- Periodicals; Toxicology -- Periodicals; Toxicology -- Methodology -- Periodicals; 615.907
• DOI: 10.3109/15376516.2014.951814
• Languages: English
• ISSNs: 1537-6516

Abstract

Abstract: 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 µg/ml) of PM2.5 for 24 h to investigate the apoptosis induced by PM2.5 . The results showed that PM2.5 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 PM2.5 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 PM2.5 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 PM2.5 -induced apoptosis in 16-HBE cells.