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UCP3 overexpression neutralizes oxidative stress rather than nitrosative stress in mouse myotubes.

作者信息

Barreiro Esther, Garcia-Martínez Cèlia, Mas Sandra, Ametller Elisabet, Gea Joaquim, Argilés Josep M, Busquets Sílvia, López-Soriano Francisco J

机构信息

Muscle and Respiratory System Research Unit-Pneumology Department, IMIM-Hospital del Mar, Centro de Investigación en Red de Enfermedades Respiratorias (CibeRes), CEXS, Universitat Pompeu Fabra, Barcelona Biomedical Research Park, Barcelona, Spain.

出版信息

FEBS Lett. 2009 Jan 22;583(2):350-6. doi: 10.1016/j.febslet.2008.12.023. Epub 2008 Dec 25.

DOI:10.1016/j.febslet.2008.12.023
PMID:19101552
Abstract

The deleterious effects of oxidants on proteins may be modified by overexpression of uncoupling protein 3 (UCP3) in skeletal muscle cells exposed to hyperoxia or H(2)O(2). UCP3 overexpression significantly attenuated the increase in protein carbonylation in response to hyperoxia and H(2)O(2) exposures. However, antioxidant enzyme content and activity (superoxide dismutases, peroxiredoxins, glutathione peroxidase-I, and catalase) were reduced or not modified in UCP3-overexpressing myotubes exposed to oxidants. Protein nitration increased in UCP3-overexpressing cells exposed to hyperoxia, but not to H(2)O(2). We conclude that protein oxidation rather than nitration is neutralized by UPC3 overexpression in mouse myotubes exposed to abundant reactive oxygen species.

摘要

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