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Authordc.contributor.authorMancilla, Héctor 
Authordc.contributor.authorMaldonado, Rodrigo 
Authordc.contributor.authorCereceda, Karina 
Authordc.contributor.authorVillarroel Espíndola, Franz 
Authordc.contributor.authorMontes de Oca, Marco 
Authordc.contributor.authorAngulo, Constanza 
Authordc.contributor.authorCastro, Maite A. 
Authordc.contributor.authorSlebe, Juan C. 
Authordc.contributor.authorVera, Juan C. 
Authordc.contributor.authorLavandero González, Sergio
Admission datedc.date.accessioned2015-11-05T14:22:10Z
Available datedc.date.available2015-11-05T14:22:10Z
Publication datedc.date.issued2015
Cita de ítemdc.identifier.citationJournal of Cellular Biochemistry 116: 2283-2292, 2015en_US
Identifierdc.identifier.otherDOI: 10.1002/jcb.25178
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/134854
General notedc.descriptionArtículo de publicación ISIen_US
General notedc.descriptionSin acceso a texto completo
Abstractdc.description.abstractThe development and survival of male germ cells depend on the antioxidant capacity of the seminiferous tubule. Glutathione (GSH) plays an important role in the antioxidant defenses of the spermatogenic epithelium. Autophagy can act as a pro-survival response during oxidative stress or nutrient deficiency. In this work, we evaluated whether autophagy is involved in spermatogonia-type germ cell survival during severe GSH deficiency. We showed that the disruption of GSH metabolism with l-buthionine-(S,R)-sulfoximine (BSO) decreased reduced (GSH), oxidized (GSSG) glutathione content, and GSH/GSSG ratio in germ cells, without altering reactive oxygen species production and cell viability, evaluated by 2,7- dichlorodihydrofluorescein (DCF) fluorescence and exclusion of propidium iodide assays, respectively. Autophagy was assessed by processing the endogenous protein LC3I and observing its sub-cellular distribution. Immunoblot and immunofluorescence analysis showed a consistent increase in LC3II and accumulation of autophagic vesicles under GSH-depletion conditions. This condition did not show changes in the level of phosphorylation of AMPactivated protein kinase (AMPK) or the ATP content. A loss in S-glutathionylated protein pattern was also observed. However, inhibition of autophagy resulted in decreased ATP content and increased caspase-3/7 activity in GSH-depleted germ cells. These findings suggest that GSH deficiency triggers an AMPK-independent induction of autophagy in germ cells as an adaptive stress response.en_US
Patrocinadordc.description.sponsorshipFONDECYT (Fondo Nacional de Desarrollo Cientifico y Tecnologico) 1110508 1141033 1110571 DID-1330-32-06 FONDAP (Fondo de Financiamiento de Centros de Investigacion en Areas Prioritarias) 15130011 Direccion de Postgrado, Universidad Austral de Chile Escuela de Graduados, Facultad de Ciencias, Universidad Austral de Chile CONICYT (Comision Nacional de Investigacion Cientifica y Tecnologica)en_US
Lenguagedc.language.isoenen_US
Publisherdc.publisherWiley-Blackwellen_US
Keywordsdc.subjectAutophagyen_US
Keywordsdc.subjectGerm Cellsen_US
Keywordsdc.subjectGlutathioneen_US
Títulodc.titleGlutathione Depletion Induces Spermatogonial Cell Autophagyen_US
Document typedc.typeArtículo de revistaen_US


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