The effect of riboflavin deficiency upon the metabolism of tryptophan by liver and kidney tissue.

Riboflavin-deficient rats have been observed to excrete considerably more kynurenic acid than normal rats after the ingestion of n-tryptophan, but only slightly more kynurenine and xanthurenic acid (1). Increased excretion of anthranilic acid has also been noted (2, 3). Although the administration of tryptophan by injection also produces an increased excretion of xanthurenic acid in riboflavin deficiency, the injection of kynurenine is reported to yield somewhat less in the deficient than in the normal animal (4). Riboflavin is a component of the prosthetic groups of Dand n-amino acid oxidase. Its lack might therefore be assumed to alter the production of /3-3-indolepyruvic acid, and through such alteration to influence the production and output of other tryptophan metabolites. This hypothesis has been tested by determining the metabolite production after the incubation of liver and kidney slices from riboflavin-deficient and normal animals with L-, DL-, and n-tryptophan, Land n-kynurenine, and indolepyruvic acid. The study has required the preliminary development of a suitable method of measuring indolepyruvic acid quantitatively and the adaptation of other analytical procedures to the conditions employed. The purpose of this paper is to describe the results obtained by this approach.