Acetylsalicylate (2-5 mM) inhibited phosphorylating (condition III) and uncoupled respiration of rat liver mitochondria in vitro, when succinate and glutamate were used as substrates of oxidation. Lower concentrations of acetylsalicylate did not cause the uncoupling effect. Antirheumatic drug 2,3-dihydroxybenzoate activated the phosphorylation in mitochondria, if it was added up to concentrations of 0.5-5.0 mM for succinate and 0.5 mM for glutamate. An increase of 2,3-dihydroxybenzoate concentration was accompanied by gradual inhibition of phosphorylating and uncoupled oxidation of succinate; activation of the respiration was completely abolished by addition of ADP, DNP and 2,3-dihydroxybenzoate (20 mM). The data obtained suggest that the uncoupling effect of salicylate, which is formed by hydrolysis of acetylsalicylate in the organism, might be responsible for the toxic effect of the latter.