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Early modulation of the transcription factor Nrf2 in rodent striatal slices by quinolinic acid, a toxic metabolite of the kynurenine pathway

dc.rights.licensehttp://creativecommons.org/licenses/by/4.0es_MX
dc.creatorANA LAURA COLIN GONZALEZes_MX
dc.creatorARMANDO LUNA LOPEZes_MX
dc.creatorMINA KONIGSBERG FAINSTEINes_MX
dc.creatorJOSE PEDRAZA CHAVERRIes_MX
dc.creatorABEL SANTAMARIA DEL ANGELes_MX
dc.date2014
dc.date.accessioned2021-11-01T17:23:02Z
dc.date.available2021-11-01T17:23:02Z
dc.identifier.urihttp://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17294
dc.descriptionNuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a transcription factor involved in the orchestration of antioxidant responses. Although its pharmacological activation has been largely hypothesized as a promising tool to ameliorate the progression of neurodegenerative events, the actual knowledge about its modulation in neurotoxic paradigms remains scarce. In this study, we investigated the early profile of Nrf2 modulation in striatal slices of rodents incubated in the presence of the toxic kynurenine pathway metabolite, quinolinic acid (QUIN). Tissue slices from rats and mice were obtained and used throughout the experiments in order to compare inter-species responses. Nuclear Nrf2 protein levels and oxidative damage to lipids were compared. Time– and concentration–response curves of all markers were explored. Nrf2 nuclear activation was corroborated through phase 2 antioxidant protein expression. The effects of QUIN on Nrf2 modulation and oxidative stress were also compared between slices of wild-type (Nrf2+/+) and Nrf2 knock-out (Nrf2−/−) mice. The possible involvement of the N-methyl-d-aspartate receptor (NMDAr) in the Nrf2 modulation and lipid peroxidation was further explored in mice striatal slices. In rat striatal slices, QUIN stimulated the Nrf2 nuclear translocation. This effect was accompanied by augmented lipid peroxidation. In the mouse striatum, QUIN per se exerted an induction of Nrf2 factor only at 1 h of incubation, and a concentration–response effect on lipid peroxidation after 3 h of incubation. QUIN stimulated the striatal content of phase 2 enzymes. Nrf2−/− mice were slightly more responsive than Nrf2+/+ mice to the QUIN-induced oxidative damage, and completely unresponsive to the NMDAr antagonist MK-801 when tested against QUIN. Findings of this study indicate that: (1) Nrf2 is modulated in rodent striatal tissue in response to QUIN; (2) Nrf2−/− striatal tissue was moderately more vulnerable to oxidative damage than the Wt condition; and (3) early Nrf2 up-regulation reflects a compensatory response to the QUIN-induced oxidative stress in course as part of a general defense system, whereas Nrf2 down-regulation might contribute to more intense oxidative cell damage.es_MX
dc.formatAdobe PDFes_MX
dc.languageenges_MX
dc.publisherElsevier & Pergamones_MX
dc.relationhttps://www.sciencedirect.com/science/article/abs/pii/S0306452213010415#!es_MX
dc.relation.requiresSies_MX
dc.rightsAcceso Abiertoes_MX
dc.sourceNeuroscience (0306-4522) Vol. 260 (2014)es_MX
dc.subjectBIOLOGÍA Y QUÍMICAes_MX
dc.subjectCiencias de la vidaes_MX
dc.subjectEnvejecimientoes_MX
dc.subjectAginges_MX
dc.subjectEstrés oxidativoes_MX
dc.subjectOxidative Stresses_MX
dc.subjectDaño de ADNes_MX
dc.subjectDNA damagees_MX
dc.subjectAntioxidanteses_MX
dc.subjectAntioxidantses_MX
dc.titleEarly modulation of the transcription factor Nrf2 in rodent striatal slices by quinolinic acid, a toxic metabolite of the kynurenine pathwayes_MX
dc.typeArtículoes_MX
dc.audienceResearcherses_MX
dc.creator.idCOGA860125MDFLNN04es_MX
dc.creator.idLULA690630HDFNPR02es_MX
dc.creator.idKOFM650625MDFNNN02es_MX
dc.creator.idPECJ561020HTSDHS07es_MX
dc.creator.idSAAA661010HDFNNB07es_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX


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