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1 Laboratoire de Cytophysiologie et Toxicologie cellulaire, Universite Paris 7, Paris, France
2 Laboratoire de toxicologie moleculaire, INSERM U490, Centre Universitaire des Saints-Peres, Paris, France
* To whom correspondence should be addressed. E-mail: baulig{at}paris7.jussieu.fr.
Diesel exhaust particles (DEP) induce a pro-inflammatory response in human bronchial epithelial cells (16HBE) characterized by the release of proinflammatory cytokines after activation of transduction pathways involving MAPK and the transcription factor NF-
B. Since cellular effects induced by DEP are prevented by antioxidants, they could be mediated by reactive oxygen species (ROS). Using fluorescent probes, ROS production was detected in bronchial and nasal epithelial cells exposed either to native DEP, organic extracts of DEP (OE-DEP) or to several polyaromatic hydrocarbons. Carbon black particles mimicking the inorganic part of DEP did not increase ROS production. DEP and OE-DEP also induced the expression of genes for phase I (cytochrome P450 1A1) and phase II (NADPH quinone oxidoreductase-1, NQO-1) xenobiotics metabolisation enzymes, suggesting that DEP-adsorbed organic compounds become bioavailable, activate transcription and are metabolized since the CYP1A1 enzymatic activity is increased. Since NQO-1 gene induction is reduced by antioxidants, it could be related to the ROS generated by DEP, most likely through the activation of the stress sensitive Nrf2 transcription factor. Indeed, DEP induced the translocation of Nrf2 to the nucleus and increased protein nuclear binding to the antioxidant responsive element (ARE).
In conclusion, we showed that DEP-organic compounds generate an oxidative stress, activate the Nrf2 transcription factor and increase the expression of genes for phase I and II metabolization enzymes.
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