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

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. - Highlights: • 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