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The immunosuppressive drug, cyclosporin A (CsA), induces the generation of a transmembrane electrical potential difference (Δ Ψ) in deenergized plant mitochondria incubated in sucrose-based media. Build up of Δ Ψ 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 Δ Ψ 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 Δ Ψ, 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+ATPchannel are discussed in relation to its potential involvement in mitochondrial volume regulation, thermogenesis, apoptosis, and/or prevention of reactive oxygen species formation in plants.

The roles of mild uncoupling caused by free fatty acids (mediated by plant uncoupling mitochondrial protein (PUMP) and ATP/ADP carrier (AAC)) and non‐coupled respiration (alternative oxidase (AO)) on H2O2formation by plant mitochondria were examined. Both laurate and oleate prevent H2O2formation dependent on the oxidation of succinate. Conversely, these free fatty acids (FFA) only slightly affect that dependent on malate plus glutamate oxidation. Carboxyatractylate (CAtr), an inhibitor of AAC, completely inhibits oleate‐ or laurate‐stimulated oxygen consumption linked to succinate oxidation, while GDP, an inhibitor of PUMP, caused only a 30% inhibition. In agreement, CAtr completely restores the oleate‐inhibited H2O2formation, while GDP induces only a 30% restoration. Both oleate and laurate cause a mild uncoupling of the electrical potential (generated by succinate), which is then followed by a complete collapse with a sigmoidal kinetic. FFA also inhibit the succinate‐dependent reverse electron transfer. Diamide, an inhibitor of AO, favors the malate plus glutamate‐dependent H2O2formation, while pyruvate (a stimulator of AO) inhibits it. These results show that the succinate‐dependent H2O2formation occurs at the level of Complex I by a reverse electron transport. This generation appears to be prevented by mild uncoupling mediated by FFA. The anionic form of FFA appears to be shuttled by AAC rather than PUMP. The malate plus glutamate‐dependent H2O2formation is, conversely, mainly prevented by non‐coupled respiration (AO).