Interfibrillar cardiac mitochondrial comples III defects in the aging rat heart

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Updated: Oct 1, 2026

Measuring Mitochondrial Electron Transfer Complexes in Previously Frozen Cardiac Tissue from the Offspring of Sow: A Model to Assess Exercise-Induced Mitochondrial Bioenergetics Changes
08:04

Measuring Mitochondrial Electron Transfer Complexes in Previously Frozen Cardiac Tissue from the Offspring of Sow: A Model to Assess Exercise-Induced Mitochondrial Bioenergetics Changes

Published on: August 16, 2021

Charles L Hoppel1, Shadi Moghaddas, Edward J Lesnefsky

  • 1Department of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. clh5@po.cwru.edu

Biogerontology
|May 17, 2002
PubMed

Insights

Aging hearts show reduced mitochondrial function in interfibrillar mitochondria (IFM), leading to increased oxidative stress and injury during reperfusion. Subsarcolemmal mitochondria (SSM) function remained unaffected by aging.

Area of Science:

  • Cardiovascular biology
  • Mitochondrial function
  • Aging research

Background:

  • Aging impacts cardiac function, with mitochondria playing a key role.
  • Mitochondria are categorized into subsarcolemmal (SSM) and interfibrillar (IFM) populations, potentially having distinct aging responses.
  • Cardiac ischemia-reperfusion injury is exacerbated in aged hearts.

Purpose of the Study:

  • To investigate age-related changes in cardiac mitochondrial function, specifically oxidative phosphorylation.
  • To compare the effects of aging on interfibrillar mitochondria (IFM) versus subsarcolemmal mitochondria (SSM).
  • To elucidate the mechanisms underlying increased cardiac injury during ischemia-reperfusion in aging hearts.

Main Methods:

  • Utilized Fischer 344 rats at different ages (6 vs. 24 months) as an aging model.
  • Isolated cardiac mitochondria (IFM and SSM) for assessment of protein yield and oxidative phosphorylation.
  • Analyzed electron transport chain complex activity, cardiolipin content, and superoxide production.

Main Results:

  • Elderly rats exhibited decreased protein yield and impaired oxidative phosphorylation (complex III and IV) in cardiac IFM, but not SSM.
  • Aging specifically reduced electron transport complex III activity in IFM.
  • Increased superoxide production and electron leakage at complex III were observed in aging IFM, despite unchanged cardiolipin levels.

Conclusions:

  • Aging selectively impairs cardiac interfibrillar mitochondria (IFM) function, particularly electron transport complex III.
  • Combined aging-related defects in IFM complex III and ischemia-reperfusion injury exacerbate oxidative damage in aging hearts.
  • Defects in IFM complex III, exacerbated by ischemia, prime mitochondria for enhanced oxidant production during reperfusion, increasing cardiac injury.

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