| Article ID | Journal | Published Year | Pages | File Type | 
|---|---|---|---|---|
| 2114427 | Cancer Letters | 2009 | 9 Pages | 
Abstract
												We describe the events triggered by a sub-lethal concentration of airborne particulate matter (PM10) in A549 cells, which include the formation DNA double-strand breaks, γH2A.X generation, and 53BP1 recruitment. To protect the genome, cells activated ATM/ATR/Chk1/Chk2/p53 pathway but, after 48 h, cells turned into a senescence-like state. Trolox, an antioxidant, was able to prevent most of the alterations observed after particulate matter exposure, demonstrating the important role of ROS as mediator of PM10-induced genotoxicity and suggesting that DNA damage could be the mechanisms by which particulate matter augment the risk of lung cancer.
Keywords
												
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											Authors
												Yesennia Sánchez-Pérez, Yolanda I. Chirino, Álvaro R. Osornio-Vargas, Rocío Morales-Bárcenas, Concepción Gutiérrez-Ruíz, Inés Vázquez-López, Claudia M. García-Cuellar, 
											