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This Article Full Text Full Text (PDF) All Versions of this Article: 285/3/L671    most recent 00419.2002v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (61) Citing Articles via Google Scholar Google Scholar Articles by Baulig, A. Articles by Baeza-Squiban, A. Search for Related Content PubMed PubMed Citation Articles by Baulig, A. Articles by Baeza-Squiban, A.

Involvement of reactive oxygen species in the metabolic pathways triggered by diesel exhaust particles in human airway epithelial cells

¹Laboratoire de Cytophysiologie et Toxicologie cellulaire, Université Paris 7 - Denis Diderot, 75251 Paris cedex 05; and ²Institut National de la Santé et de la Recherche Médicale U490, Centre universitaire des Saints-Pères, 75006 Paris, France

Submitted 6 December 2002 ; accepted in final form 30 April 2003

Diesel exhaust particles (DEP) induce a proinflammatory 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. Because cellular effects induced by DEP are prevented by antioxidants, they could be mediated by reactive oxygen species (ROS). Using fluorescent probes, we detected ROS production in bronchial and nasal epithelial cells exposed to native DEP, organic extracts of DEP (OE-DEP), or 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 P-450 1A1 (CYP1A1)] and phase II [NADPH quinone oxidoreductase-1 (NQO-1)] xenobiotic metabolization enzymes, suggesting that DEP-adsorbed organic compounds become bioavailable, activate transcription, and are metabolized since the CYP1A1 enzymatic activity is increased. Because 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. In conclusion, we show 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.

cytochrome P-450 1A1; NADPH quinone oxidoreductase-1; antioxidant responsive element

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