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Glutathione peroxidase 1 protects mitochondria against hypoxia/ reoxygenation damage in mouse hearts

Title
Glutathione peroxidase 1 protects mitochondria against hypoxia/ reoxygenation damage in mouse hearts
Authors
Thu V.T.Kim H.K.Ha S.H.Yoo J.-Y.Park W.S.Kim N.Oh G.T.Han J.
Ewha Authors
오구택
SCOPUS Author ID
오구택scopus
Issue Date
2010
Journal Title
Pflugers Archiv European Journal of Physiology
ISSN
0031-6768JCR Link
Citation
vol. 460, no. 1, pp. 55 - 68
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Glutathione peroxidase 1 (GPx1) plays an important role in preventing cardiac dysfunction following ischemia-reperfusion injury. However, its role in protecting cardiac mitochondria against reoxygenation-induced reactive oxygen species (ROS) generation in vivo is unclear. We examined the role of GPx1 in protecting cardiac mitochondria against hypoxia-reoxygenation (HR) damage by testing for alterations in cardiac mitochondrial function. We used a two-dimensional gel electrophoresis proteomics analysis to examine the effects of reoxygenation on cardiac protein in wild-type (GPx1 +/+) and GPx1 knockout (GPx1 -/-) mouse hearts. We identified 42 protein spots showing differential expression in the two groups. Sixteen of the proteins identified were located in mitochondria and were involved in a number of key metabolic pathways. To verify our proteomics findings functionally, we performed NADH autofluorescence measurements and ATP production assays. The reduced expression of oxidative phosphorylation proteins in GPx1 -/- mice following HR treatment resulted in loss of the mitochondrial membrane potential and decreased mitochondrial respiration. Mitochondrial ROS production and oxidative mtDNA damage were increased markedly during reoxygenation in GPx1 -/- hearts. We also found morphological abnormalities in cardiac mitochondria and myocytes in HR-treated GPx1 -/-. This is the first report of the role of GPx1 in protecting cardiac mitochondria against reoxygenation damage in vivo. These findings will help clarify the mechanisms of HR injury and will aid in the development of antioxidant therapies to prevent cardiac mitochondrial dysfunction associated with reoxygenation. © 2010 Springer-Verlag.
DOI
10.1007/s00424-010-0811-7
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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