The effect of cycloserine on pyridoxine-dependent metabolism in tuberculosis.
Measurements were made of urinary tryptophan metabolites of 13 tuberculosis patients in order to reveal characteristics of pyridoxine-dependent metabolism before and during cycloserine treatment. The abnormally high level of xanthurenic acid excretion in untreated patients suggests a decreased availability of pyridoxal phosphate related to the disease process. Although plasma cycloserine levels were kept high once therapy began, xanthurenic acid excretion before and after tryptophan load became progressively more normal as symptoms diminished. This observation suggests that the convulsions which may sometimes accompany cycloserine administration are not due to a direct pyridoxine antagonism by the drug. Throughout the study, no significant changes in 5-hydroxyindoleacetic acid excretion were observed. Presumably, the metabolic pathway of serotonin is unaffected by tryptophan loading, cycloserine administration, or the apparent pyridoxine depletion associated with tuberculosis.
D003523:Cycloserine / Q000494:pharmacology*; D006801:Humans; D006897:Hydroxyindoleacetic Acid / Q000652:urine; D011736:Pyridoxine / Q000378:metabolism*; D013997:Time Factors; D014364:Tryptophan / Q000378:metabolism; D014376:Tuberculosis / Q000378:metabolism*; D014977:Xanthurenates / Q000652:urine
D014977:Xanthurenates; D006897:Hydroxyindoleacetic Acid; D014364:Tryptophan; D003523:Cycloserine; D011736:Pyridoxine