Activation of different pathways of apoptosis by air pollution particulate matter (PM2.5) in human epithelial lung cells (L132) in culture

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• 作者：Zeina Dagher ; Guillaume Garç ; on ; Sylvain Billet ; Pierre Gosset ; Fré ; dé ; ric Ledoux ; Dominique Courcot ; Antoine Aboukais and Pirouz Shirali
• 关键词：Human lung epithelial cells (L132) ; Particulate matter ; Physical and chemical characteristics ; Apoptosis
• 刊名：Toxicology
• 出版年：2006
• 期刊代码：47_0300483x
• 类别：pha
• 出版时间：1 August 2006
• 卷：225
• 期：1
• 页码：12-24
• 文件大小：335 K

摘要

Epidemiological studies have associated the increase of respiratory and cardiovascular mortality and morbidity with high levels of air pollution particulate matter (PM). However, the underlying mechanisms of actions by which PM induce adverse health effects are still unclear. We have recently undertaken an extensive investigation of the adverse health effects of air pollution PM_2.5, and shown that in vitro short-term exposure to PM_2.5 induced oxidative stress and inflammation in human lung epithelial cells (L132). Hence, it was convenient to complete the physical and chemical characterization of PM and to investigate whether in vitro short-term exposure to PM could be imply in the activation of apoptosis. Accordingly, we found that 92.15%of PM were equal or smaller than 2.5 μm and their specific surface area was 1 m²/g. Inorganic (i.e. Fe, Al, Ca, Na, K, Mg, Pb, etc.) and organic (i.e. polycyclic aromatic hydrocarbons) chemicals were found in PM, suggesting that much of them derived from wind-borne dust from the industrial complex and the heavy motor vehicle traffic. In other respects, we showed that PM exposure induced apoptosis by activating not only the tumor necrosis factor-alpha (TNF-α)-induced pathway (i.e. TNF-α secretion, caspase-8 and -3 activation), but also the mitochondrial pathway (i.e. 8-hydroxy-2′-desoxyguanosine formation, cytochrome c release from mitochondria, caspase-9 and -3 activation). Moreover, changes in the transcription rates of p53, bcl-2, and bax genes, on the one hand, and DNA fragmentation, on the other hand, were reported in PM-exposed proliferating L132 cells, revealing the occurrence of apoptotic events. Taken together, these findings suggested that in vitro short-term exposure to PM_2.5 induced apoptosis in L132 cells.