ArticleJournal of bioenergetics and biomembranes2002
Modulation of a plant mitochondrial K+ATP channel and its involvement in cytochrome c release.
Article in Journal of bioenergetics and biomembranes, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 40 citations in OpenAlex.
- Redox Regulation of Mitochondrial Potassium Channels Activity.Antioxidants (Basel, Switzerland) · 2024Review
- Reactive oxygen species- and nitric oxide-dependent regulation of ion and metal homeostasis in plants.Journal of experimental botany · 2023Article
- Modulation of Potassium Channel Activity in the Balance of ROS and ATP Production by Durum Wheat Mitochondria-An Amazing Defense Tool Against Hyperosmotic Stress.Frontiers in plant science · 2015Review
- Transport pathways--proton motive force interrelationship in durum wheat mitochondria.International journal of molecular sciences · 2014Review
- Physiology of potassium channels in the inner membrane of mitochondria.Pflugers Archiv : European journal of physiology · 2012Review
- The activity of plant inner membrane anion channel (PIMAC) can be performed by a chloride channel (CLC) protein in mitochondria from seedlings of maize populations divergently selected for cold tolerance.Journal of bioenergetics and biomembranes · 2011Article
- Mechanisms of xylanase-induced nitric oxide and phosphatidic acid production in tomato cells.Planta · 2011Article
- Article
- Nitric oxide block of outward-rectifying K+ channels indicates direct control by protein nitrosylation in guard cells.Plant physiology · 2004Article
- A highly active ATP-insensitive K+ import pathway in plant mitochondria.Journal of bioenergetics and biomembranes · 2004Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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