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Preservation of cardiolipin content during aging in rat heart interfibrillar mitochondria

Shadi Moghaddas1, Maria S K Stoll, Paul E Minkler

  • 1Department of Medicine, Divisions of Cardiology, Case Western Reserve University, Cleveland, Ohio, USA.

The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
|January 5, 2002
PubMed

Insights

Aging does not alter cardiolipin content or composition in cardiac mitochondria. This finding suggests that changes in cardiolipin are not responsible for the age-related decline in oxidative phosphorylation in interfibrillar mitochondria.

Area of Science:

  • Mitochondrial biology
  • Aging research
  • Cardiovascular science

Background:

  • Aging selectively impairs oxidative phosphorylation in cardiac interfibrillar mitochondria (IFM), while subsarcolemmal mitochondria (SSM) remain unaffected.
  • Reduced activity of mitochondrial complexes III and IV in aged IFM suggests a potential defect in their lipid environment.
  • Cardiolipin, an oxidatively sensitive phospholipid, is crucial for the maximal activity of complexes III and IV.

Purpose of the Study:

  • To investigate whether aging alters cardiolipin content or composition in cardiac mitochondria.
  • To determine if cardiolipin alterations contribute to the age-related decline in IFM oxidative phosphorylation.

Main Methods:

  • Quantification of mitochondrial phospholipid content and composition in SSM and IFM from adult and aged Fischer 344 rats.
  • Analysis of cardiolipin acyl group and molecular species composition.
  • Assessment of lipid-mediated oxidative modification of complex III subunits.

Main Results:

  • Aging did not change the overall content of mitochondrial phospholipids, including cardiolipin, in either IFM or SSM.
  • The composition of cardiolipin, analyzed by acyl group and molecular species, remained unaltered by aging.
  • No evidence of cardiolipin-derived oxidative damage to complex III was detected.

Conclusions:

  • Alterations in cardiolipin content or composition do not explain the age-related decrease in oxidative phosphorylation in cardiac IFM.
  • The mechanism underlying the aging defect in IFM oxidative phosphorylation in Fischer 344 rats lies elsewhere, not in cardiolipin changes.

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