Comparison of genotoxic effects of major diesel exhaust components in human alveolar basal epithelial cells (A549)
Abstrakt
Internal combustion engines (ICE), including diesel engines, power most of the motorized road vehicles. ICE are a major source of air pollution in metropolitan areas.
Among other compounds they emit polycyclic aromatic hydrocarbons (PAHs) and their nitro-derivatives. Genotoxicity of benzo[a]pyrene (B[a]P), a model PAH, and PAH nitro-derivatives (1-nitropyrene (1-NP) and 3-nitrobenzantrone (3-NBA)), was studied in a model cell line A549.
The cells were treated for 4 and 24 h with different concentrations of tested compounds (B[a]P: 0.1 and 1 μM; 1-NP: 1 and 10 μM; 3-NBA: 0.5 and 5 μM) and several endpoints, including bulky DNA adducts and oxidative stress markers (lipid peroxidation, protein and DNA oxidation) were analyzed. All tested compounds increased bulky DNA adduct levels after both the 4-h and 24-h treatment, although the effect of 1-NP was relatively weak.
A 24-h treatment resulted mostly in higher DNA adduct levels than the 4-h treatment with the exception of 3-NBA. 1-NP induced protein oxidation after both the 4-h and 24-h treatment. Interestingly, lipid peroxidation measured as levels of 15-F2t-isoprostane decreased after the B[a]P treatment, but was elevated after incubation of the cells with 1-NP and 3-NBA. 8-Oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), a marker of oxidative DNA damage, was not affected by either compound and/or treatment period.
Our data highlight differences in genotoxic mechanisms of PAHs and their nitro-derivatives, particularly for oxidative stress markers.