Formation of indole-3-acetic acid and tryptamine in animals: a method for estimation of indole-3-acetic acid in tissues.

The original identification of indole-3-acetic acid as a growth factor for plants was made by Kogl et al. (1) on material isolated from human urine. The presence of IA’ in human urine has been amply verified by many investigators. Previous measurements of this substance in urine were determined by plant-growth bioassay or paper chromatography, no satisfactory chemical method being available. To date, an elevated excretion of IA has been reported in two clinical conditions. Armstrong and Robinson (2) reported an increased IA level in the urine of patients with phenylketonuria. Recently, Baron et al. (3) have demonstrated that patients with a hereditary syndrome (“H” disease) consisting of a pellagralike skin rash accompanied by intermittent cerebellar ataxia, mental deterioration, and renal amino-aciduria, excrete large amounts of this indole acid as well as excess amounts of tryptophan, indole-acetyl-glutamine, and indoxyl sulfate. From both chemical and physiological standpoints, it is important to determine the intermediates involved in the formation of IA in animals. The conversion of tryptophan to IA might occur through one or more of the following mechanisms: (a) the formation of indole pyruvic acid by transamination followed by decarboxylation, (b) oxidative deamination by L-amino acid oxidase or, (c) decarboxylation to tryptamine followed by oxidative deamination of the amine. This report describes sensitive and specific chemical methods for the measurement of IA in urine and tissues. Studies on the conversion of tryptophan to IA in vivo and in vitro indicate that whereas transamination is the major route, decarboxylation to tryptamine occurs to a significant extent. Catalysts for both metabolic pathways have been found in tissues and intestinal bacterial flora.