The immunosuppressive drug, cyclosporin A (CsA), induces the generation of a transmembrane electrical potential difference (19) in deenergized plant mitochondria incubated in sucrose-based media.
Build up of 19 is prevented by external monovalent cations in the order K+ > Rb+ = Li+ > Na+, or by the protonophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone, which also collapses the 19 generated by CsA. Entry of K+ into mitochondria can be monitored as swelling by incubating the organelles in a medium containing KCl to maintain constant osmolarity. This swelling is inhibited by ATP and stimulated by CsA or valinomycin. In addition, in mitochondria energized by succinate, KCl causes a dissipation of 19, with sigmoidal kinetics, which is favored by CsA. Therefore, plant mitochondria appear to possess a K+ selective, voltage-dependent channel, which is opened by CsA, regulated by the redox state, and inhibited by nucleotides. The hypothetical roles of this new K+ ATP channel are discussed in relation to its potential involvement in mitochondrial volume regulation, thermogenesis, apoptosis, and/or prevention of reactive oxygen species formation in plants.
