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Preservation of Cardiolipin Content During Aging in Rat Heart Interfibrillar Mitochondria

^a Departments of Medicine (Divisions of Cardiology, Case Western Reserve University, Cleveland, Ohio
^b Departments of Medicine (Divisions of Clinical Pharmacology), Case Western Reserve University, Cleveland, Ohio
^c Departments of Medicine (Divisions of Pharmacology, Case Western Reserve University, Cleveland, Ohio
^d Departments of Medicine (Divisions of Chemistry, Case Western Reserve University, Cleveland, Ohio
^e Medical Services and Geriatric Research, Education and Clinical Center, Louis Stokes Veterans Affairs Medical Center, Cleveland, Ohio

Edward J. Lesnefsky, Cardiology Section/Medical Service 111B(W), Louis Stokes Veterans Affairs Medical Center, 10701 East Boulevard, Cleveland, OH 44106 E-mail: EXL9{at}po.cwru.edu.

Decision Editor: John Faulkner, PhD

Aging selectively decreases the rate of oxidative phosphorylation in the interfibrillar population of cardiac mitochondria (IFM) located between the myofibers. In contrast, subsarcolemmal mitochondria (SSM), located below the plasma membrane, remain unaffected. IFM from elderly (24-month-old) Fischer 344 rats have a decreased specific activity of complexes III and IV. Complexes III and IV require an inner mitochondrial membrane lipid environment enriched in the oxidatively sensitive phospholipid cardiolipin for maximal activity. We asked if aging decreases the content or alters the composition of cardiolipin as a potential mechanism of the aging defect in IFM. The content and composition of mitochondrial phospholipids were measured in SSM and IFM from adult and aging rat hearts. Aging did not alter the content of mitochondrial phospholipids, including cardiolipin, in either population of mitochondria. The composition of cardiolipin based on characterization of both acyl group and the individual molecular species of cardiolipin was also unaltered by aging. Lipid-mediated oxidative modification of complex III subunits was not detected, making cardiolipin-derived oxidative damage to complex III unlikely. Thus, alterations in cardiolipin are not the mechanism for the aging defect in IFM in Fischer 344 rats.

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