作者: Audrey F. Dumax-Vorzet , M. Tate , Richard Walmsley , Rhod H. Elder , Andrew C. Povey
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摘要: Ambient air particulate matter (PM)-associated reactive oxygen species (ROS) have been linked to a variety of altered cellular outcomes. In this study, three different PM samples from diesel exhaust particles (DEPs), urban dust standard reference material SRM1649a and collected in Manchester tested for their ability oxidise DNA cell-free assay, increase intracellular ROS levels induce CYP1A1 gene expression mammalian cells. addition, the cytotoxicity genotoxicity were assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay alkaline comet respectively. All catalysed Fenton reaction but only DEP resulted generation as measured by dichlorodihydrofluorescein diacetate oxidation However, there was no evidence that increased consequence polycyclic aromatic hydrocarbon metabolism via induction dust, not DEP-induced expression. Urban more cytotoxic murine embryonic fibroblasts (MEFs) than other also induced GADD45a GreenScreen Human Cell without S9 activation suggesting presence direct-acting genotoxicant. produced comparable damage, MEFs at higher those PM. conclusion, results genotoxic assays are consistent with production being sole determinant PM-induced toxicity. This suggests organic component can contribute significantly toxicity further work is required better characterise extent which components