dc.creator | Finamor, Isabela A. | |
dc.creator | Ourique, Giovana M. | |
dc.creator | Pês, Tanise S. | |
dc.creator | Saccol, Etiane M. H. | |
dc.creator | Bressan, Caroline A. | |
dc.creator | Scheid, Taína | |
dc.creator | Baldisserotto, Bernardo | |
dc.creator | Llesuy, Susana Francisca | |
dc.creator | Partata, Wânia A. | |
dc.creator | Pavanato, Maria A. | |
dc.date.accessioned | 2017-12-15T17:34:36Z | |
dc.date.accessioned | 2018-11-06T15:27:32Z | |
dc.date.available | 2017-12-15T17:34:36Z | |
dc.date.available | 2018-11-06T15:27:32Z | |
dc.date.created | 2017-12-15T17:34:36Z | |
dc.date.issued | 2014-09 | |
dc.identifier | Pavanato, 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.identifier | 0364-3190 | |
dc.identifier | http://hdl.handle.net/11336/30773 | |
dc.identifier | 1573-6903 | |
dc.identifier | CONICET Digital | |
dc.identifier | CONICET | |
dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/1897359 | |
dc.description.abstract | Long-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.language | eng | |
dc.publisher | Springer | |
dc.relation | info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007/s11064-014-1360-9 | |
dc.relation | info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s11064-014-1360-9 | |
dc.rights | https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ | |
dc.rights | info:eu-repo/semantics/restrictedAccess | |
dc.subject | N-Acetylcysteine Protective | |
dc.subject | Aspartame | |
dc.subject | Brain | |
dc.subject | Oxidative damage | |
dc.subject | Glutathione | |
dc.subject | Protective | |
dc.title | The Protective Effect of N-Acetylcysteine on Oxidative Stress in the Brain Caused by the Long-Term Intake of Aspartame by Rats | |
dc.type | Artículos de revistas | |
dc.type | Artículos de revistas | |
dc.type | Artículos de revistas | |