dc.creatorFinamor, Isabela A.
dc.creatorOurique, Giovana M.
dc.creatorPês, Tanise S.
dc.creatorSaccol, Etiane M. H.
dc.creatorBressan, Caroline A.
dc.creatorScheid, Taína
dc.creatorBaldisserotto, Bernardo
dc.creatorLlesuy, Susana Francisca
dc.creatorPartata, Wânia A.
dc.creatorPavanato, Maria A.
dc.date.accessioned2017-12-15T17:34:36Z
dc.date.accessioned2018-11-06T15:27:32Z
dc.date.available2017-12-15T17:34:36Z
dc.date.available2018-11-06T15:27:32Z
dc.date.created2017-12-15T17:34:36Z
dc.date.issued2014-09
dc.identifierPavanato, Maria A.; Partata, Wânia A.; Llesuy, Susana Francisca; Baldisserotto, Bernardo; Scheid, Taína; Bressan, Caroline A.; et al.; The Protective Effect of N-Acetylcysteine on Oxidative Stress in the Brain Caused by the Long-Term Intake of Aspartame by Rats; Springer; Neurochemical Research; 39; 9; 9-2014; 1681-1690
dc.identifier0364-3190
dc.identifierhttp://hdl.handle.net/11336/30773
dc.identifier1573-6903
dc.identifierCONICET Digital
dc.identifierCONICET
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1897359
dc.description.abstractLong-term intake of aspartame at the acceptable daily dose causes oxidative stress in rodent brain mainly due to the dysregulation of glutathione (GSH) homeostasis. N-Acetylcysteine provides the cysteine that is required for the production of GSH, being effective in treating disorders associated with oxidative stress. We investigated the effects of N-acetylcysteine treatment (150 mg kg(-1), i.p.) on oxidative stress biomarkers in rat brain after chronic aspartame administration by gavage (40 mg kg(-1)). N-Acetylcysteine led to a reduction in the thiobarbituric acid reactive substances, lipid hydroperoxides, and carbonyl protein levels, which were increased due to aspartame administration. N-Acetylcysteine also resulted in an elevation of superoxide dismutase, glutathione peroxidase, glutathione reductase activities, as well as non-protein thiols, and total reactive antioxidant potential levels, which were decreased after aspartame exposure. However, N-acetylcysteine was unable to reduce serum glucose levels, which were increased as a result of aspartame administration. Furthermore, catalase and glutathione S-transferase, whose activities were reduced due to aspartame treatment, remained decreased even after N-acetylcysteine exposure. In conclusion, N-acetylcysteine treatment may exert a protective effect against the oxidative damage in the brain, which was caused by the long-term consumption of the acceptable daily dose of aspartame by rats.
dc.languageeng
dc.publisherSpringer
dc.relationinfo:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007/s11064-014-1360-9
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s11064-014-1360-9
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectN-Acetylcysteine Protective
dc.subjectAspartame
dc.subjectBrain
dc.subjectOxidative damage
dc.subjectGlutathione
dc.subjectProtective
dc.titleThe Protective Effect of N-Acetylcysteine on Oxidative Stress in the Brain Caused by the Long-Term Intake of Aspartame by Rats
dc.typeArtículos de revistas
dc.typeArtículos de revistas
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución