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dc.contributor.authorRibas, Vicent-
dc.contributor.authorGarcía-Ruiz, Carmen-
dc.contributor.authorFernández-Checa, José C.-
dc.date.accessioned2015-03-03T11:42:38Z-
dc.date.available2015-03-03T11:42:38Z-
dc.date.issued2014-07-01-
dc.identifierdoi: 10.3389/fphar.2014.00151-
dc.identifierissn: 1663-9812-
dc.identifier.citationFrontiers in Pharmacology 5:151 (2014)-
dc.identifier.urihttp://hdl.handle.net/10261/111680-
dc.description.abstractGlutathione (GSH) is the main non-protein thiol in cells whose functions are dependent on the redox-active thiol of its cysteine moiety that serves as a cofactor for a number of antioxidant and detoxifying enzymes. While synthesized exclusively in the cytosol from its constituent amino acids, GSH is distributed in different compartments, including mitochondria where its concentration in the matrix equals that of the cytosol. This feature and its negative charge at physiological pH imply the existence of specific carriers to import GSH from the cytosol to the mitochondrial matrix, where it plays a key role in defense against respiration-induced reactive oxygen species and in the detoxification of lipid hydroperoxides and electrophiles. Moreover, as mitochondria play a central strategic role in the activation and mode of cell death, mitochondrial GSH has been shown to critically regulate the level of sensitization to secondary hits that induce mitochondrial membrane permeabilization and release of proteins confined in the intermembrane space that once in the cytosol engage the molecular machinery of cell death. In this review, we summarize recent data on the regulation of mitochondrial GSH and its role in cell death and prevalent human diseases, such as cancer, fatty liver disease, and Alzheimer's disease. © 2014 Ribas, Garcia-Ruiz and Fernandez-Checa.-
dc.description.sponsorshipVicent Ribas is recipient of an Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) Post-doctoral Fellowship-BIOTRACK, supported by the European Community’s Seventh Framework Programme (EC FP7/2007-2013) under the grant agreement number 229673 and the Spanish Ministry of Economy and Competitiveness (MINECO) through the grant COFUND2013-40261. The work was supported by Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Fundació la Marató de TV3 and grants PI11/0325 (META) from the Instituto Salud Carlos III and grants, SAF2011-23031, and SAF2012-34831 from Plan Nacional de I+D, Spain; Fundación Mutua Madrileña and the center grant P50-AA-11999 (Research Center for Liver and Pancreatic Diseases, NIAAA/NIH)-
dc.publisherFrontiers Media-
dc.relationinfo:eu-repo/grantAgreement/EC/FP7/229673-
dc.relation.isversionofPublisher's version-
dc.rightsopenAccess-
dc.subjectGlutathione-
dc.subjectCholasteral-
dc.subjectMitochondrail-
dc.subjectReactive oxygen species-
dc.subjectSteatohepatitis-
dc.subjectAlzheimier disease-
dc.titleGlutathione and mitochondria-
dc.typeartículo-
dc.identifier.doi10.3389/fphar.2014.00151-
dc.relation.publisherversionhttp://dx.doi.org/10.3389/fphar.2014.00151-
dc.date.updated2015-03-03T11:42:38Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.identifier.pmid25024695-
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