Induction of c-Jun by air particulate matter (PM10) of Mexico city: Participation of polycyclic aromatic hydrocarbons

• Published in: Environmental pollution (1987) Vol. 203; pp. 175 - 182
• Main Authors: Salcido-Neyoy, Martha Estela, Sánchez-Pérez, Yesennia, Osornio-Vargas, Alvaro Román, Gonsebatt, María Eugenia, Meléndez-Zajgla, Jorge, Morales-Bárcenas, Rocío, Petrosyan, Pavel, Molina-Servin, Edith Danny, Vega, Elizabeth, Manzano-León, Natalia, García-Cuellar, Claudia M.
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.08.2015
• Subjects: Air Pollutants - toxicity; Air pollution; aryl hydrocarbon receptor; carcinogenic potential; Carcinogens; Cell Line, Tumor; Cities; cJun; Cytochrome P-450 CYP1B1 - metabolism; DNA Adducts - metabolism; Humans; Interleukin-6 - metabolism; Interleukin-8 - metabolism; Mexico; Particulate emissions; Particulate matter; Particulate Matter - toxicity; Pathways; Pollution abatement; Polycyclic aromatic hydrocarbons; Polycyclic Aromatic Hydrocarbons - metabolism; Polycyclic Aromatic Hydrocarbons - toxicity; Proteins; Proto-Oncogene Proteins c-jun - metabolism; Receptors, Aryl Hydrocarbon - antagonists & inhibitors; Receptors, Aryl Hydrocarbon - metabolism; Resveratrol; Secretions; Stilbenes - pharmacology; Mexico, Distrito Federal, Mexico City; polycyclic aromatic hydrocarbons; carcinogenic potential; Particulate matter; cJun; aryl hydrocarbon receptor
• ISSN: 0269-7491; 1873-6424
• DOI: 10.1016/j.envpol.2015.03.051

The carcinogenic potential of urban particulate matter (PM) has been partly attributed to polycyclic aromatic hydrocarbons (PAHs) content, which activates the aryl hydrocarbon receptor (AhR). Here we report the effect of PM with an aerodynamic size of 10 μm (PM10) on the induction of AhR pathway in A549 cells, evaluating its downstream targets CYP1B1, IL-6, IL-8 and c-Jun. Significant increases in CYP1B1 protein and enzyme activity; IL-6 and IL-8 secretion and c-Jun protein were found in response to PM10. The formation of PAH-DNA adducts was also detected. The involvement of AhR pathway was confirmed with Resveratrol as AhR antagonist, which reversed CYP1B1 and c-Jun induction. Nevertheless, in IL-6 and IL-8 secretion, the Resveratrol was ineffective, suggesting an effect independent of this pathway. Considering the role of c-Jun in oncogenesis, its induction by PM may be contributing to its carcinogenic potential through induction of AhR pathway by PAHs present in PM10. •We analyzed the induction of AhR pathway targets by exposure to PM10 in A549 cells.•We suggest that PAHs content in PM10 are responsible for the induction of c-Jun.•C-Jun induction could represent part of mechanism of carcinogenicity of PM10. We report the role of the aryl hydrocarbon receptor pathway in cJun induction caused by PM10 exposure in human lung cells, which could represent part of its mechanism of carcinogenicity.