Role of reactive oxygen species and cardiolipin in the release of cytochrome c from mitochondria. (Articolo in rivista)

Type
Label
  • Role of reactive oxygen species and cardiolipin in the release of cytochrome c from mitochondria. (Articolo in rivista) (literal)
Anno
  • 2003-01-01T00:00:00+01:00 (literal)
Alternative label
  • Petrosillo G 1, Ruggiero FM 1, 2, Paradies G 1,2. (2003)
    Role of reactive oxygen species and cardiolipin in the release of cytochrome c from mitochondria.
    in The FASEB journal
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Petrosillo G 1, Ruggiero FM 1, 2, Paradies G 1,2. (literal)
Pagina inizio
  • 2202 (literal)
Pagina fine
  • 2208 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 17 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#descrizioneSinteticaDelProdotto
  • Viene proposto un meccanismo a due tappe di rilascio del citocromo c dai mitocondri integri indotto dai ROS: perossidazione della cardiolipina, distacco del citocromo c dalla membrana e rilascio nel citosol attraverso il VDAC. (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1 Department of Biochemistry and Molecular Biology, University of Bari, 2 CNR Institute of Biomembranes and Bioenergetics, Bari, Italy. (literal)
Titolo
  • Role of reactive oxygen species and cardiolipin in the release of cytochrome c from mitochondria. (literal)
Abstract
  • Several lines of evidence indicate that mitochondria-mediated reactive oxygen species (ROS) generation is a major source of oxidative stress in the cell. Release of cytochrome c from mitochondria is a central event in apoptosis induction and appears to be mediated by ROS. Dissociation of cytochrome c from the IMM, where it is bound to cardiolipin, represents a necessary first step for cytochrome c release. In the present study, the role of ROS and cardiolipin in the release of cytochrome c from rat liver mitochondria was investigated. ROS were produced by mitochondria oxidizing succinate in the nonphosphorylating state. Cytochrome c was quantitated by a new, very sensitive and rapid reverse-phase HPLC method. We found that succinate-supported ROS production resulted in a release of cytochrome c from mitochondria and a parallel loss of cardiolipin content. These effects were directly and significantly correlated and also abolished by ADP, which prevents succinate-mediated ROS production. The ROS-induced cytochrome c release was independent from MPT and appears to involve VDAC. It is suggested that mitochondrial-induced ROS production promotes cytochrome c release from mitochondria by a two-steps process, consisting of the dissociation of this protein from cardiolipin, followed by permeabilization of the outer membrane, probably by interaction with VDAC. The data may help clarify the molecular mechanism underlying the release of cytochrome c from the mitochondria to the cytosol and the role of ROS and cardiolipin in this release. (literal)
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