Acute hypoxia produces a superoxide burst in cells

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dc.contributor.authorHernansanz-Agustín, Pablo
dc.contributor.authorIzquierdo-Álvarez, Alicia
dc.contributor.authorSánchez-Gómez, Francisco J.
dc.contributor.authorRamos, Elena
dc.contributor.authorVilla-Piña, Tamara
dc.contributor.authorLamas, Santiago
dc.contributor.authorBogdanova, Anna
dc.contributor.authorMartínez Ruiz, Antonio
dc.date.accessioned2024-05-08T12:34:24Z
dc.date.available2024-05-08T12:34:24Z
dc.date.issued2014-06
dc.description.abstractOxygen is a key molecule for cell metabolism. Eukaryotic cells sense the reduction in oxygen availability (hypoxia) and trigger a series of cellular and systemic responses to adapt to hypoxia, including the optimization of oxygen consumption. Many of these responses are mediated by a genetic program induced by the hypoxia-inducible transcription factors (HIFs), regulated by a family of prolyl hydroxylases (PHD or EGLN) that use oxygen as a substrate producing HIF hydroxylation. In parallel to these oxygen sensors modulating gene expression within hours, acute modulation of protein function in response to hypoxia is known to occur within minutes. Free radicals acting as second messengers, and oxidative posttranslational modifications, have been implied in both groups of responses. Localization and speciation of the paradoxical increase in reactive oxygen sp+ecies production in hypoxia remain debatable. We have observed that several cell types respond to acute hypoxia with a transient increase in superoxide production for about 10 min, probably originating in the mitochondria. This may explain in part the apparently divergent results found by various groups that have not taken into account the time frame of hypoxic ROS production. We propose that this acute and transient hypoxia-induced superoxide burst may be translated into oxidative signals contributing to hypoxic adaptation and preconditioning
dc.description.departmentDepto. de Bioquímica y Biología Molecular
dc.description.facultyFac. de Farmacia
dc.description.fundingtypeAPC financiada por la UCM
dc.description.refereedTRUE
dc.description.sponsorshipGobierno de España
dc.description.sponsorshipSwiss National Science Foundation
dc.description.sponsorshipInstituto de Salud Carlos III
dc.description.sponsorshipInstituto de Investigación Sanitaria Princesa
dc.description.sponsorshipMinisterio de Educación y Cultura
dc.description.statuspub
dc.identifier.doi10.1016/j.freeradbiomed.2014.03.011
dc.identifier.essn1873-4596
dc.identifier.issn0891-5849
dc.identifier.officialurlhttps://doi.org/10.1016/j.freeradbiomed.2014.03.011
dc.identifier.urihttps://hdl.handle.net/20.500.14352/103813
dc.journal.titleFree Radical Biology and Medicine
dc.language.isoeng
dc.page.final156
dc.page.initial146
dc.relation.projectIDinfo:eu-repo/grantAgreement/MSC//CP07%2F00143/ES/CP07%2F00143/
dc.relation.projectIDPS09/00101
dc.relation.projectIDinfo:eu-repo/grantAgreement/MINECO//PI12%2F00875/ES/Modificaciones postraduccionales oxidativas en fisiopatología molecular/
dc.relation.projectIDinfo:eu-repo/grantAgreement/MEC//SAF2009-7520
dc.relation.projectIDinfo:eu-repo/grantAgreement/SNSF//310030_124970/1
dc.relation.projectIDinfo:eu-repo/grantAgreement/COST//TD0901
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.cdu577.1
dc.subject.cdu577.2
dc.subject.keywordHypoxia
dc.subject.keywordFree radicals
dc.subject.keywordOxidative phosphorylation
dc.subject.keywordReactive oxygen species
dc.subject.keywordSuperoxide
dc.subject.keywordCell signaling
dc.subject.keywordIschemia
dc.subject.ucmBioquímica (Farmacia)
dc.subject.ucmBiología molecular (Farmacia)
dc.subject.unesco2302 Bioquímica
dc.titleAcute hypoxia produces a superoxide burst in cells
dc.typejournal article
dc.type.hasVersionVoR
dc.volume.number71
dspace.entity.typePublication
relation.isAuthorOfPublicationeec0b303-34c9-47dd-9ec6-704b6c6c7acd
relation.isAuthorOfPublication.latestForDiscoveryeec0b303-34c9-47dd-9ec6-704b6c6c7acd
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