Decrease in mitochondrial complex I activity in ischemic/reperfused rat heart. Involvement of reactive oxygen species and cardiolipin (Articolo in rivista)

Type
Label
  • Decrease in mitochondrial complex I activity in ischemic/reperfused rat heart. Involvement of reactive oxygen species and cardiolipin (Articolo in rivista) (literal)
Anno
  • 2004-01-01T00:00:00+01:00 (literal)
Alternative label
  • Paradies G, Petrosillo G, Pistolese M, Di Venosa N, Federici A, Ruggiero FM (2004)
    Decrease in mitochondrial complex I activity in ischemic/reperfused rat heart. Involvement of reactive oxygen species and cardiolipin
    in Circulation research
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Paradies G, Petrosillo G, Pistolese M, Di Venosa N, Federici A, Ruggiero FM (literal)
Pagina inizio
  • 53 (literal)
Pagina fine
  • 59 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 94 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Department of Biochemistry and Molecular Biology and CNR Institute of Biomembranes and Bioenergetics,Department of Emergency and Transplantation and Department of Pharmacology and Human Physiology, University of Bari, Bari Italy (literal)
Titolo
  • Decrease in mitochondrial complex I activity in ischemic/reperfused rat heart. Involvement of reactive oxygen species and cardiolipin (literal)
Abstract
  • Reactive oxygen species (ROS) are considered an important factor in ischemia-reperfusion injury to cardiac myocytes. Mitochondrial respiration is an important source of ROS production and hence a potential contributor to cardiac reperfusion injury. In this work, we have examined the effect of ischemia and ischemia followed by reperfusion of rat hearts on various parameters related to mitochondrial function, such as complex I activity, oxygen consumption, ROS production and cardiolipin content. The activity of complex I was reduced by 25 and 48 % in mitochondria isolated from ischemic and reperfused rat heart respectively, compared to the controls. These changes in complex I activity were associated to parallel changes in state 3 respiration. The capacity of mitochondria to produce H2O2 increased upon reperfusion. The mitochondrial content of cardiolipin, which is required for optimal activity of complex I, decreased by 28 % and by 50 % as function of ischemia and reperfusion respectively. The lower complex I activity in mitochondria from reperfused rat heart could be completely restored to the level of normal heart by exogenous added cardiolipin. This effect of cardiolipin could not be replaced by other phospholipids nor by peroxidized cardiolipin. It is proposed that the defect in complex I activity in ischemic/reperfused rat heart could be ascribed to a ROS –induced cardiolipin damage. These findings may provide an explanation for some of the factors responsible for myocardial reperfusion injury. (literal)
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