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

Author Nunes, Viviane A. Autor UNIFESP Google Scholar
Gozzo, Andrezza Justino Autor UNIFESP Google Scholar
Cruz-Silva, Ilana Autor UNIFESP Google Scholar
Juliano, Maria Aparecida Autor UNIFESP Google Scholar
Viel, Tania A. Autor UNIFESP Google Scholar
Godinho, Rosely O. Autor UNIFESP Google Scholar
Meirelles, Flavio V. Google Scholar
Sampaio, Misako U. Autor UNIFESP Google Scholar
Sampaio, Claudio A M Autor UNIFESP Google Scholar
Araujo, Mariana S. Autor UNIFESP Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
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.
Keywords apoptosis
oxidative stress
vitamin E
muscle cells
Bax and Bcl-2
Language English
Date 2005-07-01
Published in 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, impact factor)
Publisher Elsevier B.V.
Extent 225-240
Access rights Closed access
Type Article
Web of Science ID WOS:000231895400002

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