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Environ Pollut ; 203: 175-182, 2015 Aug.
Article in English | MEDLINE | ID: mdl-25909326

ABSTRACT

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.


Subject(s)
Air Pollutants/toxicity , Particulate Matter/toxicity , Polycyclic Aromatic Hydrocarbons/toxicity , Proto-Oncogene Proteins c-jun/metabolism , Cell Line, Tumor , Cities , Cytochrome P-450 CYP1B1/metabolism , DNA Adducts/metabolism , Humans , Interleukin-6/metabolism , Interleukin-8/metabolism , Mexico , Polycyclic Aromatic Hydrocarbons/metabolism , Receptors, Aryl Hydrocarbon/antagonists & inhibitors , Receptors, Aryl Hydrocarbon/metabolism , Resveratrol , Stilbenes/pharmacology
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