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

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

Autor Nunes, V. A. Google Scholar
Gozzo, A. J. Google Scholar
Cruz-Silva, I Google Scholar
Juliano, M. A. Google Scholar
Viel, T. A. Google Scholar
Godinho, R. O. Google Scholar
Meirelles, F. V. Google Scholar
Sampaio, M. U. Google Scholar
Sampaio, CAM Google Scholar
Araujo, M. S. Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Resumo 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.
Palavra-chave apoptosis
oxidative stress
vitamin E
muscle cells
Bax and Bcl-2
Idioma Inglês
Data de publicação 2005-07-01
Publicado em Comparative Biochemistry and Physiology C-toxicology & Pharmacology. New York: Elsevier B.V., v. 141, n. 3, p. 225-240, 2005.
ISSN 1532-0456 (Sherpa/Romeo, fator de impacto)
Publicador Elsevier B.V.
Extensão 225-240
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000231895400002
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