Modulation of a plant mitochondrial K+ATP channel and its involvement in cytochrome c release.
Pea stem mitochondria, resuspended in a KCl medium (de-energized mitochondria), underwent a swelling, as a consequence of K+ entry, that was inhibited by ATP. This inhibition was partially restored by GTP and diazoxide (K+ATP channel openers). In addition, glyburide and 5-hydroxydecanate (K+ATP channel blockers) induced an inhibition of the GTP-stimulated swelling. Mitochondrial swelling was inhibited by H2O2, but stimulated by NO. The same type of responses was also obtained in succinate-energized mitochondria. When the succinate-dependent transmembrane electrical potential (deltapsi) had reached a steady state, the addition of KCl induced a dissipation that was inhibited by H2O2 and stimulated by NO. The latter stimulation was prevented by carboxy-PTIO, a NO scavenger. Phenylarsine oxide (a thiol oxidant) and NEM (a thiol blocker) stimulated the KCl-induced dissipation of deltapsi, while DTE prevented this effect in both cases. In addition, DTE transiently inhibited the NO-induced dissipation of deltapsi, but then it caused a more rapid collapse. These results, therefore, show that the plant mitochondrial K+ATP channel resembles that present in mammalian mitochondria and that it appears to be modulated by dithiol-disulfide interconversion, NO and H2O2. The aperture of this channel was linked to the partial rupture of the outer membrane. The latter effect led to a release of cytochrome c, thus suggesting that this release may be involved in the manifestation of programmed cell death.
Chiandussi
Elisa
E
Department of Biology and Agro-industrial Economics, University of Udine, Italy.
Petrussa
Elisa
E
Macrì
Francesco
F
Vianello
Angelo
A
D003574:Cytochrome c Group / Q000378:metabolism*; D004220:Disulfides; D006861:Hydrogen Peroxide / Q000494:pharmacology; D024101:Mitochondrial Proteins / Q000187:drug effects*; D008933:Mitochondrial Swelling / Q000187:drug effects; D009569:Nitric Oxide / Q000494:pharmacology; D010084:Oxidation-Reduction; D018532:Pisum sativum / Q000648:ultrastructure; D010940:Plant Proteins / Q000187:drug effects*; D011188:Potassium / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects*
D003574:Cytochrome c Group; D004220:Disulfides; D024101:Mitochondrial Proteins; D010940:Plant Proteins; D015221:Potassium Channels; D009569:Nitric Oxide; D006861:Hydrogen Peroxide; D011188:Potassium