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dc.contributor.authorDiniz, Yeda S.
dc.contributor.authorRocha, Katiucha K. H. R.
dc.contributor.authorSouza, Gisele A.
dc.contributor.authorGalhardi, Cristiano M.
dc.contributor.authorEbaid, Geovana M. X.
dc.contributor.authorRodrigues, Hosana G.
dc.contributor.authorNovelli Filho, Jose Luiz V. B.
dc.contributor.authorCicogna, Antonio Carlos [UNESP]
dc.contributor.authorNovelli, Ethel L. B.
dc.date.accessioned2014-05-20T13:53:19Z
dc.date.available2014-05-20T13:53:19Z
dc.date.issued2006-08-14
dc.identifierhttp://dx.doi.org/10.1016/j.ejphar.2006.05.039
dc.identifier.citationEuropean Journal of Pharmacology. Amsterdam: Elsevier B.V., v. 543, n. 1-3, p. 151-157, 2006.
dc.identifier.issn0014-2999
dc.identifier.urihttp://hdl.handle.net/11449/19025
dc.description.abstractThis study examined whether sucrose-rich diet (SRD)-induced hyperglycaemia, dyslipidemia and oxidative stress may be inhibited by N-acetylcysteine (C5H9-NO3S), an organosulfur from Allium plants. Male Wistar 40 rats were divided into four groups (n = 10): (C) given standard chow and water; (N) receiving standard chow and 2 mg/l N-acetylcysteine in its drinking water; (SRD) given standard chow and 30% sucrose in its drinking water; and (SRD-N) receiving standard chow, 30% sucrose and N-acetylcysteine in its drinking water. After 30 days of treatment, SRD rats had obesity with increased abdominal circumference, hyperglycaemia, by dyslipidemia and hepatic triacylglycerol accumulation. These adverse effects were associated with oxidative stress and depressed lipid degradation in hepatic tissue. The SRD adverse effects were not observed in SDR-N rats. N-Acetylcysteine reduced the oxidative stress, enhancing glutathione-peroxidase activity, and normalizing lipid hydroperoxyde, reduced glutathione and superoxide dismutase in hepatic tissue of SRD-N rats. The beta-hydroxyacyl coenzyme-A dehydrogenase and citrate-synthase activities were increased in SRD-N rats, indicating enhanced lipid degradation in hepatic tissue as compared to SRD. SRD-N rats had reduced serum oxidative stress and diminished glucose, triacylglycerol, very-low-density lipoprotein (VLDL), oxidized low-density lipoprotein (alpha-LDL) and cholesterol/highdensity lipoprotein (HDL) ratio in relation to SRD. In conclusion, NAC offers promising therapeutic values in prevention of dyslipidemic profile and alleviation of hyperglycaemia in high-sucrose intake condition by improving antioxidant defences. N-Acetylcysteine had also effects preventing metabolic shifting in hepatic tissue, thus enhancing fat degradation and reducing body weight gain in conditions of excess sucrose intake. The application of this agent in food system via exogenous addition may be feasible and beneficial for antioxidant protection. (c) 2006 Elsevier B.V All rights reserved.en
dc.format.extent151-157
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofEuropean Journal of Pharmacology
dc.sourceWeb of Science
dc.subjectN-acetylcysteinept
dc.subjectsucrosept
dc.subjectlipid profilept
dc.subjectglycaemiapt
dc.subjectoxidative stresspt
dc.titleEffects of N-acetylcysteine on sucrose-rich diet-induced hyperglycaemia, dyslipidemia and oxidative stress in ratsen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.description.affiliationUniv São Paulo, UNESP, Inst Biol Sci, Dept Chem & Biochem, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUniv São Paulo, UNESP, Fac Med, Post Grad Course Dept Clin & Cardiol, Botucatu, SP, Brazil
dc.description.affiliationUniv São Paulo, UNESP, Fac Med, Dept Orthopaed Surg, Botucatu, SP, Brazil
dc.description.affiliationUnespUniv São Paulo, UNESP, Inst Biol Sci, Dept Chem & Biochem, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespUniv São Paulo, UNESP, Fac Med, Post Grad Course Dept Clin & Cardiol, Botucatu, SP, Brazil
dc.description.affiliationUnespUniv São Paulo, UNESP, Fac Med, Dept Orthopaed Surg, Botucatu, SP, Brazil
dc.identifier.doi10.1016/j.ejphar.2006.05.039
dc.identifier.wosWOS:000239684700021
dc.rights.accessRightsAcesso restrito
unesp.campusUniversidade Estadual Paulista (UNESP), Instituto de Biociências, Botucatupt
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Medicina, Botucatupt
dc.identifier.lattes9418970103564137
unesp.author.lattes9418970103564137
unesp.author.orcid0000-0002-6122-0379[6]
unesp.author.orcid0000-0001-8741-1336[4]
dc.relation.ispartofjcr3.040
dc.relation.ispartofsjr1,057
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