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Background Urban air particulate matter (PM) relates to adverse health effects including lung cancer. Previous work from our group demonstrated that the PM10 produce DNA damage, although the mechanisms involved are not known. DNA double-strand breaks (DSBs) are the most deleterious DNA lesions. DSBs arise from exogenous agents such as metals and hydrocarbons, or endogenous agents, such as reactive oxygen species (ROS). We explore the cellular response that senses DNA damage after cell exposure to PM10, evaluating markers such as phosphorylation of ATM (ser1981), γH2A.X (ser139) and p53 (ser15), and senescence-like induction, as well as the identification of ROS co-participation in the response.

PM10from Mexico City (MC) induce senescence-like phenotype and ATM, γH2A.X and p53 activation linked to oxidative stress