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dc.rights.licensehttp://creativecommons.org/licenses/by/4.0es_MX
dc.creatorADRIANA ALARCON AGUILARes_MX
dc.creatorVIRIDIANA YAZMIN GONZALEZ PUERTOSes_MX
dc.creatorARMANDO LUNA LOPEZes_MX
dc.creatorAMBAR LOPEZ MACAYes_MX
dc.creatorJulio Morán Andradees_MX
dc.creatorABEL SANTAMARIA DEL ANGELes_MX
dc.creatorMINA KONIGSBERG FAINSTEINes_MX
dc.date2014-
dc.date.accessioned2021-10-28T19:04:35Z-
dc.date.available2021-10-28T19:04:35Z-
dc.identifier.urihttp://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17292-
dc.descriptionOxidative stress has been recognized as a potential mediator of cell death. Astrocytes play an active role in brain physiology responding to harmful stimuli by activating astrogliosis, which in turn has been associated either with survival or degenerative events. The characterization of the mechanistic actions exerted by different toxins in astrocytes is essential to understand the brain function and pathology. As age plays a critical role in degenerative processes, the aim of this study was to determine whether the administration of equimolar concentrations of two neurotoxins evoking different toxic patterns can induce differential effects on primary astrocytes obtained either from newborn or adult rats, with particular emphasis on those events linked to oxidative stress as a potential source of damage. Primary cortical astrocyte cultures derived from rat brains were exposed to 1‐methyl‐4‐phenylpyridinium (MPP+) or beta‐amyloid peptide (β‐amyloid). Mitochondrial functionality and cell viability were determined as physiological parameters, whereas lipid and protein oxidation were used as markers of oxidative damage. The results of these experiments pointed towards a higher vulnerability to MPP + over β‐amyloid, on most of the tested markers. Hence, in order to allow a comprehensive evaluation of astrocytic responses against MPP + intoxication, a third astrocyte group was included for dose‐response experiments: astrocytes derived from aged rats. The present data indicate that the differences associated with age were mainly found in astrocytes exposed to MPP + (25 and 50 μM) at 1‐h treatment. Results are discussed in terms of the differential mechanisms involved in each model. Copyright © 2012 John Wiley & Sons, Ltd.es_MX
dc.formatAdobe PDFes_MX
dc.languageenges_MX
dc.publisherWileyes_MX
dc.relationhttps://onlinelibrary.wiley.com/doi/10.1002/jat.2841es_MX
dc.relation.requiresSies_MX
dc.rightsAcceso Abiertoes_MX
dc.sourceJournal of Applied Toxicology (1099-1263) Vol. 34 (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.subjectAstrocitoses_MX
dc.subjectAstrocyteses_MX
dc.subjectDaño de ADNes_MX
dc.subjectDNA damagees_MX
dc.titleComparing the effects of two neurotoxins in cortical astrocytes obtained fron rats of different ages: involvement of oxidative damagees_MX
dc.typeArtículoes_MX
dc.audienceResearcherses_MX
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dc.creator.idLOMA780323HMCPCM07es_MX
dc.creator.idCA1218690es_MX
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dc.creator.idKOFM650625MDFNNN02es_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercaes_MX
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