FEBS Letters
Volume 583, Issue 6 , Pages 997-1000, 18 March 2009

Reversible oxidation of mitochondrial peroxiredoxin 3 in mouse heart subjected to ischemia and reperfusion

Edited by Barry Halliwell

  • Vikas Kumar

      Affiliations

    • Department of Pathology, University of Otago Christchurch, Christchurch, New Zealand
    • ,
  • Nailya Kitaeff

      Affiliations

    • Department of Physiology, University of Auckland, Auckland, New Zealand
    • ,
  • Mark B. Hampton

      Affiliations

    • Department of Pathology, University of Otago Christchurch, Christchurch, New Zealand
    • ,
  • Mark B. Cannell

      Affiliations

    • Department of Physiology, University of Auckland, Auckland, New Zealand
    • ,
  • Christine C. Winterbourn

      Affiliations

    • Department of Pathology, University of Otago Christchurch, Christchurch, New Zealand
    • Corresponding Author InformationCorresponding author. Fax: +64 3 364 1083.

Received 14 January 2009; received in revised form 10 February 2009; accepted 11 February 2009. published online 20 February 2009.

Abstract 

Peroxiredoxins decompose peroxides through reversible oxidation of their active site cysteines. The redox state of the 2-Cys peroxiredoxins, 1, 2 and 3, was investigated in mouse hearts undergoing ischemia and reperfusion in a Langendorff system. The peroxiredoxins were predominantly reduced in control hearts. Mitochondrial peroxiredoxin 3 underwent significant oxidation to its disulfide-linked dimer during ischemia. Oxidation was largely reversed during reperfusion. No redox changes in cytoplasmic peroxiredoxins 1 and 2 were apparent. Peroxiredoxin 3 oxidation suggests localized mitochondrial generation of reactive oxidants during ischemia. This local antioxidant activity of peroxiredoxin 3 may have a role in maintaining cardiac function.

Keywords: Cardiac ischemia, Reperfusion injury, Mitochondria, Peroxiredoxin, Hydrogen peroxide

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PII: S0014-5793(09)00112-4

doi:10.1016/j.febslet.2009.02.018

FEBS Letters
Volume 583, Issue 6 , Pages 997-1000, 18 March 2009

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