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Mitochondria, oxygen and reperfusion damage.

V M Darley-Usmar1, D Stone, D Smith

  • 1Department of Biochemical Sciences, Wellcome Research Laboratories, Beckenham, Kent U.K.

Annals of Medicine
|January 1, 1991
PubMed
Summary
This summary is machine-generated.

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Reperfusion of the heart causes calcium (Ca2+) uptake. Mitochondrial oxidants may affect Ca2+ handling during reoxygenation, but the cyclosporin-sensitive pore does not appear to be a major factor in hypoxic heart reoxygenation.

Area of Science:

  • Cardiology
  • Mitochondrial Physiology
  • Cellular Biology

Background:

  • Reperfusion of ischemic or hypoxic heart triggers oxygen-dependent processes like cell lysis and calcium (Ca2+) uptake.
  • Mitochondrial energization, requiring oxygen, is crucial for these processes, with mitochondria actively sequestering Ca2+.
  • Oxidants generated during mitochondrial electron transport may influence mitochondrial calcium handling during myocardial reoxygenation.

Purpose of the Study:

  • To review the mechanisms by which mitochondrial oxidants perturb calcium handling during hypoxic heart reoxygenation.
  • To investigate the role of the cyclosporin-sensitive mitochondrial pore in Ca2+ homeostasis disruption upon reoxygenation.

Main Methods:

  • Literature review on mitochondrial calcium handling and oxidative stress during cardiac reperfusion.

Related Experiment Videos

  • Experimental assessment of cyclosporin's effect on oxygen-dependent Ca2+ increase in reoxygenated hypoxic myocytes.

    • Main Results:

    • Mitochondrial oxidants are implicated in perturbing mitochondrial calcium handling during hypoxic myocardium reoxygenation.
    • Cyclosporin demonstrated minimal to no impact on the oxygen-dependent increase in total cell Ca2+ during reoxygenation of hypoxic myocytes.

    Conclusions:

    • The Ca2+-dependent mitochondrial pore, active under oxidative stress, does not seem to significantly contribute to Ca2+ homeostasis disruption in reoxygenated hypoxic hearts.
    • Further research is needed to fully elucidate the mechanisms of calcium dysregulation during cardiac reperfusion.