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<dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:invenio="http://invenio-software.org/elements/1.0" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><dc:identifier>doi:10.1016/j.fct.2018.07.014</dc:identifier><dc:language>eng</dc:language><dc:creator>López-Gallardo, E.</dc:creator><dc:creator>Emperador, S.</dc:creator><dc:creator>Hernández-Ainsa, C.</dc:creator><dc:creator>Montoya, J.</dc:creator><dc:creator>Bayona-Bafaluy, M.P.</dc:creator><dc:creator>Ruiz-Pesini, E.</dc:creator><dc:title>Food derived respiratory complex I inhibitors modify the effect of Leber hereditary optic neuropathy mutations</dc:title><dc:identifier>ART-2018-107038</dc:identifier><dc:description>Mitochondrial DNA mutations in genes encoding respiratory complex I polypeptides can cause Leber hereditary optic neuropathy. Toxics affecting oxidative phosphorylation system can also cause mitochondrial optic neuropathy. Some complex I inhibitors found in edible plants might differentially interact with these pathologic mutations and modify their penetrance. To analyze this interaction, we have compared the effect of rotenone, capsaicin and rolliniastatin-1 on cybrids harboring the most frequent Leber hereditary optic neuropathy mutations and found that m.3460G &gt; A mutation increases rotenone resistance but capsaicin and rolliniastatin-1 susceptibility. Thus, to explain the pathogenicity of mitochondrial diseases due to mitochondrial DNA mutations, their potential interactions with environment factors will have to be considered.</dc:description><dc:date>2018</dc:date><dc:source>http://zaguan.unizar.es/record/79326</dc:source><dc:doi>10.1016/j.fct.2018.07.014</dc:doi><dc:identifier>http://zaguan.unizar.es/record/79326</dc:identifier><dc:identifier>oai:zaguan.unizar.es:79326</dc:identifier><dc:relation>info:eu-repo/grantAgreement/ES/DGA-FEDER/B33-17R</dc:relation><dc:relation>info:eu-repo/grantAgreement/ES/ISCIII/PI14-00070</dc:relation><dc:relation>info:eu-repo/grantAgreement/ES/ISCIII/PI17-00021</dc:relation><dc:relation>info:eu-repo/grantAgreement/ES/ISCIII/PI17-00166</dc:relation><dc:relation>info:eu-repo/grantAgreement/ES/ISCIII/P114-00005</dc:relation><dc:identifier.citation>FOOD AND CHEMICAL TOXICOLOGY 120 (2018), 89-97</dc:identifier.citation><dc:rights>by-nc-nd</dc:rights><dc:rights>http://creativecommons.org/licenses/by-nc-nd/3.0/es/</dc:rights><dc:rights>info:eu-repo/semantics/openAccess</dc:rights></dc:dc>

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