In vitro genotoxicity potential investigation of 7 oxy-PAHs.
Adeline ClergéJérémie Le GoffEmilie BrotinEdwige AbeillardIsabelle VaudorneChristophe DenoyelleLudovic Le HégaratRaphaël DelépéePublished in: Environmental and molecular mutagenesis (2023)
Air pollutants include many compounds among them oxygenated polycyclic aromatic hydrocarbons (oxy-PAHs). As they are suspected to generate DNA damage and mutagenicity, an understanding of their mode of action could highlight a carcinogenic potential risk in exposed population. In this paper, a prospective study on seven oxy-PAHs selected in terms of occurrence in the environment was conducted on mutagenicity, genotoxicity, and cytotoxicity potentials using in vitro assays including Ames test on 5 strains, kinetic analysis of cytotoxicity and apoptosis, phosphorylation of histone H2AX, and p53 induction assays on human lung cell line BEAS-2B. Ames test demonstrated that mutagenicity pattern depended on the oxy-PAH tested. Except for BAQ, all oxy-PAHs tested gave mutagenic effect, in the absence and/or in the presence of metabolic activation (S9 fraction). At 24 hours of exposure, the majority of oxy-PAHs induced γ-H2AX in BEAS-2B cells and/or phosphorylation of p53 at serine 15 and cell death at highest tested concentrations. Although 9,10-AQ and B[b]FO were mutagenic in bacteria, they failed to induce any of the other genotoxicity biomarkers. In comparison with the benzo[a]pyrene, all oxy-PAHs were less potent in terms of genotoxic potential at the same concentration. These results highlighted the genotoxic and mutagenic potential of these oxy-PAHs and provide preliminary information concerning their possible mechanism of action for toxicity, contributing to a better evaluation of the real associated health risks for human and environment. This article is protected by copyright. All rights reserved.
Keyphrases
- polycyclic aromatic hydrocarbons
- cell death
- dna damage
- human health
- oxidative stress
- heavy metals
- endothelial cells
- escherichia coli
- protein kinase
- pulmonary embolism
- cell proliferation
- signaling pathway
- health risk assessment
- anti inflammatory
- climate change
- oxide nanoparticles
- health information
- endoplasmic reticulum stress
- drinking water