Formation of Citrate in vivo Induced by Fluoroacetate Poisoning

Abstract

THE intensely toxic action of the rat poison sodium fluoroacetate (CH₂F.COONa) upon the central nervous system and heart is of special interest because of the stability of the carbon – fluorine link. Bartlett and Barron¹ have suggested that it competes with acetate ion in intermediary metabolism, and Saunders² and colleagues that larger chain compounds of this type must be convertible to CH₂F.CO to show toxicity. Recently Liébecq and Peters^3,4, using centrifuged guinea pig kidney homogenates, have found that the oxidation of citrate formed from fumarate is inhibited by fluoroacetate. They have proposed the further hypothesis that this poison is metabolized like acetate and enters the tricarboxylic cycle, eventually 'jamming' this and causing accumulation of citrate.