期刊
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
卷 385, 期 1, 页码 117-128出版社
ACADEMIC PRESS INC
DOI: 10.1006/abbi.2000.2066
关键词
ubiquinol; coenzyme Q; mitochondria; reperfusion; reactive oxygen species; aging; ubiquinol cytochrome c reductase; oxidation-reduction
资金
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK036069] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG012447, K04AG000676] Funding Source: NIH RePORTER
- NIA NIH HHS [1K04AG00676, 1RO1AG12447] Funding Source: Medline
- NIDDK NIH HHS [1RO1DK36069] Funding Source: Medline
- SAMHSA HHS [1POAG15885] Funding Source: Medline
The aging heart sustains greater injury during ischemia and reperfusion compared to adult hearts, Aging decreases oxidative function in interfibrillar mitochondria (IFM) that reside among the myofibers, while subsarcolemmal mitochondria (SSM), located beneath the plasma membrane, remain unaltered. Aging decreases complex III activity selectively in IFM via alteration of the cytochrome c binding site. With 25 min of global ischemia, complex III activity decreases in SSM and further decreases in IFM in the aging heart. Ischemia leads to a marked decrease in the electron paramagnetic resonance signal of the iron-sulfur protein (ISP) in both SSM and IFM, despite a preserved content of ISP peptide. Thus, ischemia results in a functional decrease in the iron-sulfur center in ISP without subunit peptide loss. In the aging heart, at the onset of reperfusion, IFM contain two tandem defects in the path of electron flow through complex III, providing a likely mechanism for enhanced oxidant production and reperfusion damage. (C) 2001 Academic Press.
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