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<publisher>HAL CCSD</publisher>
<title lang=en>Protective action of n-3 fatty acids on benzo[a]pyrene-induced apoptosis through the plasma membrane remodeling-dependent NHE1 pathway</title>
<creator>Dendelé, Béatrice</creator>
<creator>Tekpli, Xavier</creator>
<creator>Hardonnière, Kévin</creator>
<creator>Holme, Jørn A</creator>
<creator>Debure, Laure</creator>
<creator>Catheline, Daniel, </creator>
<creator>Arlt, Volker M</creator>
<creator>Nagy, Eszter</creator>
<creator>Phillips, David H</creator>
<creator>Ovrebø, Steinar</creator>
<creator>Mollerup, Steen</creator>
<creator>Poët, Mallory</creator>
<creator>Chevanne, Martine</creator>
<creator>Rioux, Vincent, </creator>
<creator>Dimanche-Boitrel, Marie-Thérèse</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>Stress, membrane, signalisation ; 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 ) - 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>Norwegian Institute of Public Health ; Division of Environmental Medicine</contributor>
<contributor>Récepteur de mort et échappement tumoral ; 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 ) - 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>UPSC Biochimie ; AGROCAMPUS OUEST</contributor>
<contributor>King's College London ; MRC-HPA Centre for Environment & Health</contributor>
<contributor>Institut de pharmacologie moléculaire et cellulaire (IPMC) ; Université Nice Sophia Antipolis (UNS) ; Université Côte d'Azur (UCA) - Université Côte d'Azur (UCA) - Centre National de la Recherche Scientifique (CNRS)</contributor>
<contributor>This study was financially supported by the Ligue Nationale contre le Cancer (FR) and Cancer Research UK.</contributor>
<description>International audience</description>
<source>ISSN: 0009-2797</source>
<source>Chemico-Biological Interactions</source>
<publisher>Elsevier</publisher>
<identifier>hal-00950341</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00950341</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00950341/document</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00950341/file/DENDELE_et_al_2013-unmarked.pdf</identifier>
<source>https://hal.archives-ouvertes.fr/hal-00950341</source>
<source>Chemico-Biological Interactions, Elsevier, 2014, 207, pp.41-51. 〈10.1016/j.cbi.2013.11.002〉</source>
<identifier>PUBMED : 24246761</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/24246761</relation>
<identifier>DOI : 10.1016/j.cbi.2013.11.002</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.cbi.2013.11.002</relation>
<language>en</language>
<subject lang=es>lipid rafts</subject>
<subject lang=es>apoptosis</subject>
<subject lang=es>benzo[a]pyrene</subject>
<subject lang=es>eicosapentaenoic acid</subject>
<subject lang=es>docosahexaenoic acid</subject>
<subject lang=es>Na+/H+ exchanger 1</subject>
<subject>[SDV.MHEP] Life Sciences [q-bio]/Human health and pathology</subject>
<subject>[SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biomolecules [q-bio.BM]</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Plasma membrane is an early target of polycyclic aromatic hydrocarbons (PAH). We previously showed that the PAH prototype, benzo[a]pyrene (B[a]P), triggers apoptosis via DNA damage-induced p53 activation (genotoxic pathway) and via remodeling of the membrane cholesterol-rich microdomains called lipid rafts, leading to changes in pH homeostasis (non-genotoxic pathway). As omega-3 (n-3) fatty acids can affect membrane composition and function or hamper in vivo PAH genotoxicity, we hypothesized that addition of physiologically relevant levels of polyunsaturated n-3 fatty acids (PUFAs) might interfere with B[a]P-induced toxicity. The effects of two major PUFAs, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), were tested on B[a]P cytotoxicity in the liver epithelial cell line F258. Both PUFAs reduced B[a]P-induced apoptosis. Surprisingly, pre-treatment with DHA increased the formation of reactive B[a]P metabolites, resulting in higher levels of B[a]P-DNA adducts. EPA had no apparent effect on B[a]P metabolism or related DNA damage. EPA and DHA prevented B[a]P-induced apoptotic alkalinization by affecting Na(+)/H(+) exchanger 1 activity. Thus, the inhibitory effects of omega-3 fatty acids on B[a]P-induced apoptosis involve a non-genotoxic pathway associated with plasma membrane remodeling. Our results suggest that dietary omega-3 fatty acids may have marked effects on the biological consequences of PAH exposure.</description>
<date>2014-01-25</date>
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