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<publisher>HAL CCSD</publisher>
<title lang=en>Benzo[a]pyrene-induced nitric oxide production acts as a survival signal targeting mitochondrial membrane potential</title>
<creator>Hardonnière, Kevin</creator>
<creator>Huc, Laurence</creator>
<creator>Podechard, Normand</creator>
<creator>Fernier, Morgane</creator>
<creator>Tekpli, Xavier</creator>
<creator>Gallais, Isabelle</creator>
<creator>Sergent, Odile</creator>
<creator>Lagadic-Gossmann, Dominique</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>Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>ToxAlim (ToxAlim) ; Institut National Polytechnique [Toulouse] (INP) - Institut National de la Recherche Agronomique (INRA) - Université Paul Sabatier - Toulouse 3 (UPS) - Ecole Nationale Vétérinaire de Toulouse</contributor>
<contributor>University of Oslo (UiO)</contributor>
<contributor>We wish to thank Drs. Aubin Penna and Kenji Shoji for their scientific advice on fluorescence imaging, and Dr. Doris Cassio for karyotyping experiments. KH was a recipient of a fellowship from French Ministry for Education and Research. We wish to thank the Faculté des Sciences pharmaceutiques et biologiques de Rennes (University of Rennes 1) for financial support to KH, and the Ligue Nationale contre le Cancer (committees 22, 35, 49, 85) and the French National Academy of Medicine for financial support to our work.</contributor>
<description>International audience</description>
<source>ISSN: 0887-2333</source>
<source>Toxicology in Vitro</source>
<publisher>Elsevier</publisher>
<identifier>hal-01163757</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01163757</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01163757/document</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01163757/file/Benzo%5Ba%5Dpyrene-induced%20nitric.pdf</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01163757</source>
<source>Toxicology in Vitro, Elsevier, 2015, 29 (7), pp.1597-1608. 〈10.1016/j.tiv.2015.06.010〉</source>
<identifier>DOI : 10.1016/j.tiv.2015.06.010</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.tiv.2015.06.010</relation>
<identifier>PUBMED : 26086121</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/26086121</relation>
<language>en</language>
<subject lang=en>AhR</subject>
<subject lang=en>Apoptosis</subject>
<subject lang=en>benzo[a]pyrene</subject>
<subject lang=en>Mitochondrial membrane hyperpolarization</subject>
<subject lang=en>Nitric Oxide</subject>
<subject lang=en>Survival</subject>
<subject>[SDV] Life Sciences [q-bio]</subject>
<subject>[SDV.TOX] Life Sciences [q-bio]/Toxicology</subject>
<subject>[SDV.CAN] Life Sciences [q-bio]/Cancer</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Benzo[a]pyrene (B[a]P), the prototype molecule of polycyclic aromatic hydrocarbons, exhibits genotoxic and carcinogenic effects, which has led the International Agency for Research on Cancer to recognize it as a human carcinogen. Besides the well-known apoptotic signals triggered by B[a]P, survival signals have also been suggested to occur, both signals likely involved in cancer promotion. Our previous work showed that B[a]P induced an hyperpolarization of mitochondrial membrane potential (ΔΨm) in rat hepatic epithelial F258 cells. Elevated ΔΨm plays a role in tumor development and progression, and nitric oxide (NO) has been suggested to be responsible for increases in ΔΨm. The present study therefore aimed at evaluating the impact of B[a]P on NO level in F258 cells, and at testing the putative role for NO as a survival signal, notably in link with ΔΨm. Our data demonstrated that B[a]P exposure resulted in an NO production which was dependent upon the activation of the inducible NO synthase. This enzyme activation involved AhR and possibly p53 activation. Preventing NO production not only increased B[a]P-induced cell death but also blocked mitochondrial hyperpolarization. This therefore points to a role for NO as a survival signal upon B[a]P exposure, possibly targeting ΔΨm</description>
<date>2015</date>
</dc>
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