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<title lang=en>Regulation of human hepatic drug transporter activity and expression by diesel exhaust particle extract.</title>
<creator>Le Vee, Marc</creator>
<creator>Jouan, Elodie</creator>
<creator>Stieger, Bruno</creator>
<creator>Lecureur, Valérie</creator>
<creator>Fardel, Olivier</creator>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Division of Clinical Pharmacology and Toxicology ; University hospital of Zurich [Zurich]</contributor>
<contributor>Pôle Biologie ; Hôpital Pontchaillou - CHU Pontchaillou [Rennes]</contributor>
<contributor>The authors have no support or funding to report.</contributor>
<description>International audience</description>
<source>ISSN: 1932-6203</source>
<source>PLoS ONE</source>
<publisher>Public Library of Science</publisher>
<identifier>hal-01138535</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01138535</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01138535/document</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01138535/file/Regulation%20of%20human%20hepatic%20drug.pdf</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01138535</source>
<source>PLoS ONE, Public Library of Science, 2015, 10 (3), pp.e0121232. 〈10.1371/journal.pone.0121232〉</source>
<identifier>DOI : 10.1371/journal.pone.0121232</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0121232</relation>
<identifier>PUBMED : 25803276</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/25803276</relation>
<language>en</language>
<subject>[SDV] Life Sciences [q-bio]</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Diesel exhaust particles (DEPs) are common environmental air pollutants primarily affecting the lung. DEPs or chemicals adsorbed on DEPs also exert extra-pulmonary effects, including alteration of hepatic drug detoxifying enzyme expression. The present study was designed to determine whether organic DEP extract (DEPe) may target hepatic drug transporters that contribute in a major way to drug detoxification. Using primary human hepatocytes and transporter-overexpressing cells, DEPe was first shown to strongly inhibit activities of the sinusoidal solute carrier (SLC) uptake transporters organic anion-transporting polypeptides (OATP) 1B1, 1B3 and 2B1 and of the canalicular ATP-binding cassette (ABC) efflux pump multidrug resistance-associated protein 2, with IC50 values ranging from approximately 1 to 20 μg/mL and relevant to environmental exposure situations. By contrast, 25 μg/mL DEPe failed to alter activities of the SLC transporter organic cation transporter (OCT) 1 and of the ABC efflux pumps P-glycoprotein and bile salt export pump (BSEP), whereas it only moderately inhibited those of sodium taurocholate co-transporting polypeptide and of breast cancer resistance protein (BCRP). Treatment by 25 μg/mL DEPe was next demonstrated to induce expression of BCRP at both mRNA and protein level in cultured human hepatic cells, whereas it concomitantly repressed mRNA expression of various transporters, including OATP1B3, OATP2B1, OCT1 and BSEP. Such changes in transporter expression were found to be highly correlated to those caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a reference activator of the aryl hydrocarbon receptor (AhR) pathway. This suggests that DEPe, which is enriched in known ligands of AhR like polycyclic aromatic hydrocarbons, alters drug transporter expression via activation of the AhR cascade. Taken together, these data established human hepatic transporters as targets of organic chemicals containing in DEPs, which may contribute to their systemic effects through impairing hepatic transport of endogenous compound or drug substrates of these transporters.</description>
<rights>http://creativecommons.org/licenses/by/</rights>
<date>2015</date>
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