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The experiments described in this paper* were done in order to advance knowledge ofthe biochemistry of fluoroacetate poisoning. The proved failure of this compound to inhibit isolated enzymes made it difficult to relate the toxic action to an enzymic effect, until Bartlett & Barron (1947) made the important step of showing that in tissue slices fluoroacetate led to accumulations of acetate. Another significant point was made by Saunders (1947) and colleagues who found an alternation in the toxicity with increasing length of carbon chain in the w-fluoroesters; compounds with an even number of carbon atoms were toxic. Then Li6becq & Peters (1948, 1949) found an instance with centrifuged kidney homogenates where fluoroacetate caused depression of oxygen uptake without an increase of acetate but with accumulation of citiate; at the same time the oxidation of added citrate was inhibited by the poison. This led them to propose the jamnming hypothesis; according to this sodium fluoroacetate can be activated and condensed with oxaloacetate to form a fluorotricarboxylic acid, which either itself, or in the form of some derivative, inhibits the tricarboxylic acid cycle and so causes accumulation of citrate. A similar hypothesis was advanced independently by Martius (1949). Kal-nitsky & Barron (1948) later reported accumulation of citrate, but interpreted this differently. It was an important extension from these in vitro tests when Buffa & Peters (1949) found that the accumulation of citrate was also induced readily in vivo by injection of fluoroacetate into animals. This has been recently confirmed by Potter & Busch (1950). The best proof for the jamming hypothesis would be the isolation of a toxic fluorotricarboxylic acid either from the tissues of poisoned animals or from the products of some poisoned tissue preparation. Calculation showed that this was impracticable in vivo, owing to the small amount of substance present in poisoned tissues; attempts were therefore made to isolate the tricarboxylic acids formed during the oxidation of fumarate by a kidney homogenate in vitro in the presence of fluoroacetate. In this work, there will be described the isolation of a 'citrate' fraction from poisoned kidney tissue, a component of which has the power to inhibit citrate metabolism in vitro; this is not fluoroacetate, but is believed to be a tricarboxylic acid which contains fluorine in small amount. EXPERIMENTAL Determination of theinhibitory activity of tricarboxylic acidfractions using kidney homogenates The object of the test was to determine the capacity for inhibiting …

Biochemistry of fluoroacetate poisoning. Isolation of an active tricarboxylic acid fraction from poisoned kidney homogenates