Abstract
In a sucrose medium, free from anions which are effective in the anion‐hydroxide exchange catalysed by trialkyltins, the effects of these compounds on mitochondrial respiration are similar to those of oligomycin, i.e. inhibition of respiration coupled to phosphorylation, and of arsenate stimulated respiration. They do not inhibit respiration stimulated by uncouplers nor respiration stimulated by uptake of divalent cations. They do not induce significant light scattering changes in this medium.In a medium containing potassium chloride similar oligomycin‐like effects are observed but in addition some release of respiratory control and marked swelling of the mitochondria are observed. A time‐dependent inhibition of uncoupler stimulated respiration appears to be a secondary effect consequent upon extensive swelling. The maximal rate of respiration attainable by the uncoupling effect of the trialkyltin compounds is independent of which compound is used. The concentration of trialkyltin compound required to produce uncoupling is correlated with the concentration required to mediate the chloride hydroxide exchange.In media containing other anions the maximal rate of respiration produced by trialkyltin compounds is correlated with the rate of electrogenic uniport of the anions through the mitochondrial membrane.Uncoupling by trialkyltin compounds is attributed to the action of the anion‐hydroxide exchange followed by leakage of the anion out of the mitochondria. These two processes result in the discharge of both the pH differential and electrical potential difference across the mitochondrial membrane.Apart from a lytic action of triphenyltin chloride and a potent respiratory inhibition in the presence of iodide or thiocyanate ions, it is proposed that all the observed effects of those compounds can be accounted for by the oligomycin‐like inhibition and the mediation of an anion hydroxide‐exchange across the mitochondrial membrane.
Published Version
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