000079326 001__ 79326
000079326 005__ 20200217133051.0
000079326 0247_ $$2doi$$a10.1016/j.fct.2018.07.014
000079326 0248_ $$2sideral$$a107038
000079326 037__ $$aART-2018-107038
000079326 041__ $$aeng
000079326 100__ $$0(orcid)0000-0002-3217-1424$$aLópez-Gallardo, E.$$uUniversidad de Zaragoza
000079326 245__ $$aFood derived respiratory complex I inhibitors modify the effect of Leber hereditary optic neuropathy mutations
000079326 260__ $$c2018
000079326 5060_ $$aAccess copy available to the general public$$fUnrestricted
000079326 5203_ $$aMitochondrial 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 > 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.
000079326 536__ $$9info:eu-repo/grantAgreement/ES/DGA-FEDER/B33-17R$$9info:eu-repo/grantAgreement/ES/ISCIII/PI14-00070$$9info:eu-repo/grantAgreement/ES/ISCIII/PI17-00021$$9info:eu-repo/grantAgreement/ES/ISCIII/PI17-00166$$9info:eu-repo/grantAgreement/ES/ISCIII/P114-00005
000079326 540__ $$9info:eu-repo/semantics/openAccess$$aby-nc-nd$$uhttp://creativecommons.org/licenses/by-nc-nd/3.0/es/
000079326 590__ $$a3.775$$b2018
000079326 591__ $$aTOXICOLOGY$$b18 / 93 = 0.194$$c2018$$dQ1$$eT1
000079326 591__ $$aFOOD SCIENCE & TECHNOLOGY$$b21 / 135 = 0.156$$c2018$$dQ1$$eT1
000079326 592__ $$a0.916$$b2018
000079326 593__ $$aFood Science$$c2018$$dQ1
000079326 593__ $$aToxicology$$c2018$$dQ1
000079326 593__ $$aMedicine (miscellaneous)$$c2018$$dQ1
000079326 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/acceptedVersion
000079326 700__ $$0(orcid)0000-0001-5964-6138$$aEmperador, S.$$uUniversidad de Zaragoza
000079326 700__ $$0(orcid)0000-0003-3524-5158$$aHernández-Ainsa, C.$$uUniversidad de Zaragoza
000079326 700__ $$0(orcid)0000-0003-1770-6299$$aMontoya, J.$$uUniversidad de Zaragoza
000079326 700__ $$0(orcid)0000-0002-8585-6371$$aBayona-Bafaluy, M.P.$$uUniversidad de Zaragoza
000079326 700__ $$0(orcid)0000-0002-0269-7337$$aRuiz-Pesini, E.$$uUniversidad de Zaragoza
000079326 7102_ $$11003$$2443$$aUniversidad de Zaragoza$$bDpto. Anatom.Histolog.Humanas$$cArea Histología
000079326 7102_ $$11002$$2060$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Bioquímica y Biolog.Mole.
000079326 773__ $$g120 (2018), 89-97$$pFood chem. toxicol.$$tFOOD AND CHEMICAL TOXICOLOGY$$x0278-6915
000079326 8564_ $$s631490$$uhttps://zaguan.unizar.es/record/79326/files/texto_completo.pdf$$yPostprint
000079326 8564_ $$s8683$$uhttps://zaguan.unizar.es/record/79326/files/texto_completo.jpg?subformat=icon$$xicon$$yPostprint
000079326 909CO $$ooai:zaguan.unizar.es:79326$$particulos$$pdriver
000079326 951__ $$a2020-02-17-12:42:59
000079326 980__ $$aARTICLE