Vitamin E prevents cell death induced by mild oxidative stress in chicken skeletal muscle cells

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dc.contributor.author Nunes, Viviane A. [UNIFESP]
dc.contributor.author Gozzo, Andrezza Justino [UNIFESP]
dc.contributor.author Cruz-Silva, Ilana [UNIFESP]
dc.contributor.author Juliano, Maria Aparecida [UNIFESP]
dc.contributor.author Viel, Tania A. [UNIFESP]
dc.contributor.author Godinho, Rosely O. [UNIFESP]
dc.contributor.author Meirelles, Flavio V.
dc.contributor.author Sampaio, Misako U. [UNIFESP]
dc.contributor.author Sampaio, Claudio A M [UNIFESP]
dc.contributor.author Araujo, Mariana S. [UNIFESP]
dc.date.accessioned 2016-01-24T12:37:57Z
dc.date.available 2016-01-24T12:37:57Z
dc.date.issued 2005-07-01
dc.identifier http://dx.doi.org/10.1016/j.cca.2005.06.001
dc.identifier.citation Comparative Biochemistry and Physiology C-toxicology & Pharmacology. New York: Elsevier B.V., v. 141, n. 3, p. 225-240, 2005.
dc.identifier.issn 1532-0456
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/28370
dc.description.abstract Apoptosis and necrosis are two forms of cell death that can occur in response to various agents and oxidative damage. in addition to necrosis, apoptosis contributes to muscle fiber loss in various muscular dystrophies as well participates in the exudative diathesis in chicken, pathology caused by dietary deficiency of vitamin E and selenium, which affects muscle tissue. We have used chicken skeletal muscle cells and bovine fibroblasts to study molecular events involved in the cell death induced by oxidative stress and apoptotic agents. the effect of vitamin E on cell death induced by oxidants was also investigated. Treatment of cells with anti-Fas antibody (50 to 400 ng/mL), staurosporine (0.1 to 100 mu M) and TNF-alpha (10 and 50 ng/mL) resulted in a little loss of Trypan blue exclusion ability. Those stimuli conducted cells to apoptosis detected by an enhancement in caspase activity upon fluorogenic substrates but this activity was not fully blocked by the caspase inhibitor Z-VAD-fmk. Oxidative stress induced by menadione (10, 100 and 250 mu M) promoted a significant reduction in cell viability (10%, 20% and 35% for fibroblasts; 20%, 30% and 75% for muscle cells, respectively) and caused an increase in caspase activity and DNA fragmentation. H2O2 also promoted apoptosis verified by caspase activation and DNA fragmentation, but in higher doses induced necrosis. Vitamin E protected cells from death induced by low doses of oxidants. Although it was ineffective in reducing caspase activity in fibroblasts, this vitamin diminished the enzyme activity in muscle cells. These data suggested that oxidative stress could activate apoptotic mechanisms; however the mode of cell death will depend on the intensity and duration of the stimulus, and on the antioxidant status of the cells. (C) 2005 Elsevier Inc. All rights reserved. en
dc.format.extent 225-240
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof Comparative Biochemistry and Physiology C-toxicology & Pharmacology
dc.rights Acesso restrito
dc.subject apoptosis en
dc.subject necrosis en
dc.subject oxidative stress en
dc.subject vitamin E en
dc.subject muscle cells en
dc.subject fibroblasts en
dc.subject chicken en
dc.subject Bax and Bcl-2 en
dc.title Vitamin E prevents cell death induced by mild oxidative stress in chicken skeletal muscle cells en
dc.type Artigo
dc.rights.license http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.contributor.institution Universidade de São Paulo (USP)
dc.description.affiliation Universidade Federal de São Paulo, Escola Paulista Med, Dept Biochem, São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Escola Paulista Med, Dept Pharmacol, São Paulo, Brazil
dc.description.affiliation Univ São Paulo, Dept Sci, Fac Zootecnia & Engn Alimentos, Pirassununga, SP, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Escola Paulista Med, Dept Biochem, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Escola Paulista Med, Dept Pharmacol, São Paulo, Brazil
dc.identifier.doi 10.1016/j.cca.2005.06.001
dc.description.source Web of Science
dc.identifier.wos WOS:000231895400002



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