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Journal of Pharmacology And Experimental Therapeutics, Vol. 117, Issue 1, 39-51, 1956
Copyright © 1956 by American Society for Pharmacology and Experimental Therapeutics

ACTION OF SODIUM SALICYLATE AND RELATED COMPOUNDS ON TISSUE METABOLISM IN VITRO

Theodore M. Brody 1 and Willoughby Fouts 1

1 Department of Pharmacology, University of Michigan Medical School, Ann Arbor

Sodium salicylate, aspirin and methyl salicylate uncouple oxidative phosphorylation in liver, kidney and brain mitochondrial preparations. Liver and kidney are more sensitive to these agents than is brain. The uncoupling action is qualitatively similar to that seen with the classical uncoupling agent, 2,4-dinitro-phenol. The concentrations of salicylates used in these studies are comparable to toxic levels in the intact animal.

These compounds stimulate the oxygen consumption of brain mitochondria in an ortho phosphate and acceptor-saturated system, with pyruvate and malate as substrate. This effect is not abolished by incubation of brain mitochondria with ethylenediaminetetraacetate.

Salicylates stimulate the respiratory rate of an acceptor-deficient system and inhibit fatty acid oxidation of rat liver mitochondria. Like dinitrophenol, these agents enhance the liberation of inorganic phosphate from ATP.

Sodium salicylate, aspirin, methyl salicylate, and o-pyrocatechuate effectively depress oxidative phosphorylation while sodium benzoate, gentisate, beta-resorcylate, ggr-resorcylate, para-aminosalicylate, salicylamide, antipyrine and acetophenetidin are weak or ineffective uncoupling agents.

The oxygen consumption of liver and muscle slices from salicylate treated-rats is increased.

It is suggested that the above actions are responsible for many of the manifestations of salicylate poisoning.

Submitted on November 28, 1955




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Copyright © 1956 by the American Society for Pharmacology and Experimental Therapeutics.