The role of riboflavin and vitamin B6 in tryptophan metabolism

L M HENDERSON, R E KOSKI, F D'ANGELI
1955 Journal of Biological Chemistry  
From the pattern of urinary products excreted following the administration of tryptophan and some of its metabolites by vitamin-deficient, rats, certain suggestions regarding the r81e of riboflavin and vitamin Bs have been made. The most characteristic changes resulting from these de&. ciency states are decreased formation of pyridine derivatives (N'-methylnicotinamide (1, 2), quinolinic acid (2)) and pyridine nucleotides (3, 4)) and increased excretion of xanthurenic acid (5, 6). Impairment of
more » ... , 6). Impairment of the action of kynureninase, the enzyme which catalyzes the splitting of kynurenine and hydroxykynurenine as well as other a-amino-y-keto acids (7) to alanine and the corresponding anthranilic acid, has been offered as the explanation for the disturbed metabolism noted in vitamin Bs deficiency. The involvement of riboflavin in the hydroxylation of kynurenine was suggested by increased kynurenic acid (8) and decreased pyridine derivatives in the urine of deficient rats given tryptophan or kynurenine (2). Further support for this idea was provided by the observation that, riboflavin-deficient rats excreted more anthranilic acid and its derivatives in response to tryptophan (7, 9) . This suggested r61e of riboflavin has been questioned (7) on the basis of the finding that more xanthurenic acid @A) is excreted by riboflavin-deficient rats given tryptophan than by normal animals. Our earlier observations (2) involving the excretion patterns following the administration of tryptophan, kynurenine, and 3-hydroxyanthranilic acid have been extended to include 3-hydroxykynurenine. The quinolinic acid (&A) excretion findings support the postulated r81e of riboflavin in the hydroxylation of kynurenine. While riboflavin deficiency increased the xanthurenic acid response to tryptophan, it, decreased slightly the response to kynurenine. An explanation for the effect, of riboflavin deficiency on xanthurenic acid excretion is offered. * Supported by a grant in aid from E.
pmid:14392171 fatcat:trgi4ltv4zhslgl57r5ncaav34