Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/8661
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dc.contributor.authorValdivieso, Ángel Gabrieles
dc.contributor.authorDugour, Andrea V.es
dc.contributor.authorSotomayor, Verónicaes
dc.contributor.authorClauzure, Mariángeleses
dc.contributor.authorFigueroa, Juan M.es
dc.contributor.authorSanta Coloma, Tomás Antonioes
dc.date.accessioned2019-08-29T20:37:04Z-
dc.date.available2019-08-29T20:37:04Z-
dc.date.issued2018-
dc.identifier.citationValdivieso ÁG, Dugour AV, Sotomayor V, Clauzure M, Figueroa JM, Santa-Coloma TA. N-acetyl cysteine reverts the proinflammatory state induced by cigarette smoke extract in lung Calu-3 cells [en línea]. Redox Biology. 2018;16:294-302. doi:10.1016/j.redox.2018.03.006 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8661es
dc.identifier.issn2213-2317-
dc.identifier.urihttps://repositorio.uca.edu.ar/handle/123456789/8661-
dc.description.abstractAbstract: Chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF) are lethal pulmonary diseases. Cigarette consumption is the main cause for development of COPD, while CF is produced by mutations in the CFTR gene. Although these diseases have a different etiology, both share a CFTR activity impairment and proinflammatory state even under sterile conditions. The aim of this work was to study the extent of the protective effect of the antioxidant N-acetylcysteine (NAC) over the proinflammatory state (IL-6 and IL-8), oxidative stress (reactive oxygen species, ROS), and CFTR levels, caused by Cigarette Smoke Extract (CSE) in Calu-3 airway epithelial cells. CSE treatment (100 µg/ml during 24 h) decreased CFTR mRNA expression and activity, and increased the release of IL-6 and IL-8. The effect on these cytokines was inhibited by N-acetyl cysteine (NAC, 5 mM) or the NF-kB inhibitor, IKK-2 (10 µM). CSE treatment also increased cellular and mitochondrial ROS levels. The cellular ROS levels were normalized to control values by NAC treatment, although significant effects on mitochondrial ROS levels were observed only at short times (5´) and effects on CFTR levels were not observed. In addition, CSE reduced the mitochondrial NADH-cytochrome c oxidoreductase (mCx I-III) activity, an effect that was not reverted by NAC. The reduced CFTR expression and the mitochondrial damage induced by CSE could not be normalized by NAC treatment, evidencing the need for a more specific reagent. In conclusion, CSE causes a sterile proinflammatory state and mitochondrial damage in Calu-3 cells that was partially recovered by NAC treatment.es
dc.formatapplication/pdf-
dc.language.isoenges
dc.publisherElsevieres
dc.rightsAcceso Abierto*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.sourceRedox Biology. 2018;16:294-302es
dc.subjectFIBROSIS QUISTICAes
dc.subjectEPOCes
dc.subjectANTIOXIDANTESes
dc.titleN-acetyl cysteine reverts the proinflammatory state induced by cigarette smoke extract in lung Calu-3 cellses
dc.typeArtículoes
dc.identifier.doi10.1016/j.redox.2018.03.006-
dc.identifier.pmid29573703-
uca.disciplinaMEDICINA-
uca.issnrd1es
uca.affiliationFil: Valdivieso, Ángel Gabriel. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentinaes
uca.affiliationFil: Valdivieso, Ángel Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Dugour, Andrea V. Fundación Pablo Cassará; Argentinaes
uca.affiliationFil: Sotomayor, Verónica. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentinaes
uca.affiliationFil: Sotomayor, Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Clauzure, Mariángeles. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentinaes
uca.affiliationFil: Clauzure, Mariángeles. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Figueroa, Juan M. Fundación Pablo Cassará; Argentinaes
uca.affiliationFil: Santa Coloma, Tomás Antonio. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Biología Celular y Molecular; Argentinaes
uca.affiliationFil: Santa Coloma, Tomás Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.versionpublishedVersiones
item.languageiso639-1en-
item.grantfulltextopen-
item.fulltextWith Fulltext-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Biología Celular y Molecular-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.deptLaboratorio de Biología Celular y Molecular-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Biología Celular y Molecular-
crisitem.author.deptLaboratorio de Nanotecnología-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.orcid0000-0002-3266-1095-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
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