Benzo[ghi]perylene activates the AHR pathway to exert biological effects on the NL-20 human bronchial cell line.

Abstract Polycyclic aromatic hydrocarbons (PAH) are produced by incomplete combustion of organic material. In the Mexico City atmosphere, the most abundant PAH is benzo[ ghi ]perylene (B ghi P), a gasoline combustion marker. At present, there are no reports of the effects of B ghi P on human bronchial cells, so the aim of the study was to evaluate the effects in vitro of B ghi P on the NL-20 cell line. Results showed that B ghi P induced the formation of small vesicles throughout the cytoplasm, with absence of nuclear fragmentation. At 48 h exposition, damage in cell membrane increased significantly at 1.24 μg/mL of B ghi P (p  ghi P provokes nuclear translocation of AhR receptor, which indicates that this compound can induce transcription of genes via receptor binding (AhR pathway activation). B ghi P induced a two-fold increase (p  ghi P induced oxidative stress and in presence of the receptor antagonist this increased significantly. In conclusion, B ghi P can activate the overexpression of AhR and CYP4B1, and the effects are abated by the AhR receptor antagonist. This is the first report to prove that B ghi P utilizes the AhR pathway to exert its toxic effects on the NL-20 human bronchial cell line .