Mitochondrial Reactive Oxygen Species in Myocardial Pre- and Postconditioning

  • Ariel R. Cardoso
  • Bruno B. Queliconi
  • Alicia J. Kowaltowski
Part of the Oxidative Stress in Applied Basic Research and Clinical Practice book series (OXISTRESS)


Myocardial ischemia followed by reperfusion is a well established condition of medical importance in which reactive oxygen species (ROS) are determinant for the pathological outcome. Indeed, oxidative damage during reperfusion is causative of many of the complications found after ischemia. ROS leading to postischemic myocardial damage come from many sources, including mitochondria, NADPH oxidase, xanthine oxidase, and infiltrated phagocytes [1]. ROS also can act as signaling molecules in the cardiovascular system, including protecting the heart against myocardial ischemic damage, secondarily to ischemic pre- and postconditioning. In this case, there is ample evidence that the source of signaling ROS is mitochondrial [2–7]. This chapter will briefly review aspects of mitochondrial ROS signaling relevant to myocardial ischemic protection by pre- and postconditioning.


Electron transport chain Oxidative phosphorylation Uncoupling proteins Mitochondrial KATP channels Mitochondrial membrane potential Mitochondrial free radical production 


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Copyright information

© Springer Science+Business Media, LLC 2010

Authors and Affiliations

  • Ariel R. Cardoso
    • 1
  • Bruno B. Queliconi
    • 1
  • Alicia J. Kowaltowski
    • 1
  1. 1.Departamento de BioquímicaInstituto de Química, Universidade de São PauloSão PauloBrazil

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