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

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Thu, Vu Thi Kim, Hyoung Kyu Ha, Seung Hee Yoo, Ji-Young Park, Won Sun Kim, Nari Oh, Goo Taeg Han, Jin
Description	Author Affiliation: Thu VT ( National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, FIRST Mitochondrial Research Group, Inje University, 633-165 Gaegeum-Dong, Busanjin-Gu, Busan, 613-735, Korea.)
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.
File Format	HTM / HTML
ISSN	00316768
Issue Number	1
Volume Number	460
e-ISSN	14322013
Journal	Pflügers Archiv - European Journal of Physiology
Language	English
Publisher	Springer
Publisher Date	2010-06-01
Publisher Place	Germany
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Physiology Glutathione Peroxidase Metabolism Mitochondria, Muscle Enzymology Myocardial Reperfusion Injury Prevention & Control Myocardium Reactive Oxygen Species Adenosine Triphosphate Animals Blotting, Western Cell Hypoxia Cytoprotection Dna Damage Dna, Mitochondrial Electrophoresis, Gel, Two-dimensional Deficiency Genetics Hydrogen Peroxide Male Membrane Potential, Mitochondrial Mice Mice, Inbred C57bl Mice, Knockout Pathology Nad Oxygen Consumption Perfusion Protein Interaction Domains And Motifs Protein Interaction Mapping Proteomics Methods Superoxides Time Factors Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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