Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/327996
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dc.contributor.CRUESPUNIVERSIDADE DE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authoremailheloisa.ferreira@slmandic.edu.brpt_BR
dc.typeArtigopt_BR
dc.titleIncreased Glutathione Levels Contribute To The Beneficial Effects Of Hydrogen Sulfide And Inducible Nitric Oxide Inhibition In Allergic Lung Inflammationen
dc.contributor.authorCampospt_BR
dc.contributor.authorDaiana; Ravagnanipt_BR
dc.contributor.authorFelipe G.; Gurgueirapt_BR
dc.contributor.authorSonia A.; Vercesipt_BR
dc.contributor.authorAnibal E.; Teixeirapt_BR
dc.contributor.authorSimone A.; Costapt_BR
dc.contributor.authorSoraia K. P.; Muscarapt_BR
dc.contributor.authorMarcelo N.; Ferreirapt_BR
dc.contributor.authorHeloisa H. A.pt_BR
unicamp.authorVercesi, Anibal E.] Univ Estadual Campinas, Fac Med Sci, Dept Clin Pathol, Lab Bioenerget, Campinas, SP, Brazilpt_BR
unicamp.author.external[Campos, Daianapt_BR
unicamp.author.externalFerreira, Heloisa H. A.] Sao Leopoldo Mand Inst & Res Ctr, Inflammat Res Lab, Rua Jose Rocha Junqueira 13, BR-13045755 Campinas, SP, Brazilpt_BR
unicamp.author.external[Ravagnani, Felipe G.pt_BR
unicamp.author.externalGurgueira, Sonia A.pt_BR
unicamp.author.external[Teixeira, Simone A.pt_BR
unicamp.author.externalCosta, Soraia K. P.pt_BR
unicamp.author.externalMuscara, Marcelo N.] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, Sao Paulo, SP, Brazilpt_BR
dc.subjectReduced Glutathione (gsh)/oxidized Glutathione (gssg) Ratioen
dc.subjectAconitaseen
dc.subjectOvalbuminen
dc.subjectOxidative Stressen
dc.subject1400 Wen
dc.subjectSodium Hydrosulfideen
dc.description.abstractThe interaction between nitric oxide (NO) and hydrogen sulfide (H2S) in the airways could have significant implications for the pathogenesis and therapeutic effects of both on lung diseases. In this study we investigated whether the beneficial effects of H2S on asthma could be comparable to that inhibition of inducible NO synthase (iNOS). Methods: Female BALB/C mice sensitized with ovalbumin (OVA) received either the H2S donor sodium hydrosulfide (NaHS, 14 mu mol/kg) or the iNOS inhibitor 1400W (1 mg/kg), 30 min before each OVA challenge during six days. On the first, second and sixth days, the leucocyte infiltration in lung parenchyma and bronchoalveolar lavage was evaluated. The aconitase activity (a sensor of O-2(center dot-) formation) and lipid peroxidation, as well as levels of reduced glutathione (GSH) and oxidized glutathione (GSSG) were determined in the lung tissues. Results: OVA-challenge caused a significant and time-dependent increase in the eosinophil number in the airways, which was accompanied by a significant decrease of aconitase activity and GSH/GSSG ratio along with enhanced lipid peroxidation in the lungs. Treatment with NaHS or 1400 W significantly attenuated the airways eosinophilia that was paralleled by an increase in aconitase activity and decrease of lipid peroxidation. NaHS or 1400 W treatments also reversed the decreased GSH/GSSG ratio seen after OVA-challenge. Conclusions: The present study shows for the first time that the increased GSH/GSSG ratio caused by either H2S supplementation or iNOS-inhibition is a potential mechanism protecting airways against oxidative stress and inflammatory lung diseases. (C) 2016 Elsevier B.V. All rights reserved.en
dc.relation.ispartofInternational Immunopharmacologypt_BR
dc.publisherElsevier Science BVpt_BR
dc.publisherAmsterdampt_BR
dc.date.issued2016pt_BR
dc.date.monthofcirculationoutpt_BR
dc.identifier.citationInternational Immunopharmacology. Elsevier Science Bv, v. 39, p. 57 - 62, 2016.pt_BR
dc.language.isoEnglishpt_BR
dc.description.volume39pt_BR
dc.description.firstpage57pt_BR
dc.description.lastpage62pt_BR
dc.rightsfechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn1567-5769pt_BR
dc.identifier.eissn1878-1705pt_BR
dc.identifier.wosidWOS:000383932000008pt_BR
dc.identifier.doi10.1016/j.intimp.2016.07.009pt_BR
dc.identifier.urlhttp://www-sciencedirect-com.ez88.periodicos.capes.gov.br/science/article/pii/S1567576916302788?via%3Dihubpt_BR
dc.description.sponsorshipSao Paulo Research Foundation (FAPESP), Brazil [2012/02145-3]pt_BR
dc.description.sponsorshipNational Council for Scientific and Technological Development (CNPq) [2013/04151-3, 2014/24518-1]pt_BR
dc.description.sponsorship1Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorship1Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.date.available2017-11-13T13:22:53Z-
dc.date.accessioned2017-11-13T13:22:53Z-
dc.description.provenanceMade available in DSpace on 2017-11-13T13:22:53Z (GMT). No. of bitstreams: 1 000383932000008.pdf: 840673 bytes, checksum: 6618db08f54b306aeb286596465a5ac1 (MD5) Previous issue date: 2016en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/327996-
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