期刊
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
卷 43, 期 4, 页码 411-419出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2007.05.019
关键词
mitochondria; calcium; hypoxia; reoxygenation; mtNOS; oxidative stress
资金
- NIA NIH HHS [R03 AG023264-02, R03 AG023264, R03 AG023264-04, R03 AG023264-03, R03 AG023264-01A1] Funding Source: Medline
The objective of the present study was to delineate the molecular mechanisms for mitochondrial contribution to oxidative stress induced by hypoxia and reoxygenation in the heart. The present study introduces a novel model allowing real-time study of mitochondria under hypoxia and reoxygenation, and describes the significance of intramitochondrial calcium homeostasis and mitochondrial nitric oxide synthase (mtNOS) for oxidative stress. The present study shows that incubating isolated rat heart mitochondria under hypoxia followed by reoxygenation, but not hypoxia per se, causes cytochrome c release from the mitochondria, oxidative modification of mitochondrial lipids and proteins, and inactivation of mitochondrial enzymes susceptible to inactivation by peroxynitrite. These alterations were prevented when mtNOS was inhibited or mitochondria were supplemented with antioxidant peroxynitrite scavengers. The present study shows mitochondria independent of other cellular components respond to hypoxia/reoxygenation by elevating intramitochondrial ionized calcium and stimulating mtNOS. The present study proposes a crucial role for heart mitochondrial calcium homeostasis and mtNOS in oxidative stress induced by hypoxia/reoxygenation. (C) 2007 Elsevier Inc. All rights reserved.
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