The effect of pyridoxine deficiency induced by desoxypyridoxine in human subjects upon the excretion of N 1-methylnicotinamide after tryptophan administration

Abstract

The urinary excretion of quinolinic acid and some other tryptophan metabolites has been determined after 2-g L-tryptophan load in a deoxypyridoxinetreated subject and in women receiving estrogen-containing oral contraceptives. In both situations there were increases in the excretion of quinolinic acid and 3-hydroxyanthranilic acid, as well as 3-hydroxykynurenine and xanthurenic acid. These changes were reversed by pyridoxine administration, and are considered to reflect an inhibitory effect of estrogens and deoxypyridoxine on vitamin B6-dependent enzymes. Although the principal enzyme of the tryptophan-nicotinic acid ribonucleotide pathway affected by impaired pyridoxal phosphate function is kynureninase, the present results are consistent with the existence of an unidentified enzyme beyond the formation of 3-hydroxyanthranilic acid which requires the coenzyme.