Changes in Contractile Proteins under Oxidative Stress

  • Masanori Kaneko
  • Yuji Matsumoto
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 168)


Oxygen free radicals have been demonstrated to have the capacity to cause cardiac contractile dysfunction [1–4]. It is well known that cardiac contraction is produced by the interaction between actin and myosin and that the energy for the contraction is supplied through the myosin ATPase reaction [5]. Myofibrillar creatine kinase has been demonstrated to be functionally coupled to myosin ATPase [6–8] and serves as an important intramyofibrillar ATP-regenerating system (phosphocreatine energy shuttle) [5]. Therefore, alterations in myofibrillar creatine kinase activity may disturb energy utilization by the myocardium and may result in contractile dysfunction. In fact, it has been reported that inhibition of creatine kinase activity can result in dysfunction of the heart, especially at increased work loads [9].


Creatine Kinase Xanthine Oxidase Oxygen Free Radical Sulfhydryl Group Creatine Kinase Activity 
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© Kluwer Academic Publishers 1996

Authors and Affiliations

  • Masanori Kaneko
  • Yuji Matsumoto

There are no affiliations available

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