The indole acids of human urine; paper chromatography of indole acids.

Nencki and Sieber (1) first reported the formation of a red pigment in urine which had been made strongly acid by the addition of mineral acids, and they named the pigment “urorosein.” At one time considerable import was attached to the appearance of a strongly positive urorosein reaction (2, 3). Herter (2), however, established that this reaction frequently could be associated with gastrointestinal disturbances, succeeded in isolating indoleacetic acid as the urinary chromogen in one such case (4), and inferred that indoleacetic acid of intestinal origin was responsible for the urorosein reaction. This view was widely accepted, and for many years little further work was done on the nature and significance of this reaction. The observation that a strongly positive urorosein reaction always can be demonstrated in the urine of patients with phenylketonuria led to the identification of indoleacetic and indolelactic acids as the major indole compounds in their urine (5). In addition, paper chromatograms of extracts revealed the presence of 5-hydroxyindoleacetic acid and many other indole acids. Recently, the excretion of greatly increased amounts of indoleacetic acid, N-(indole-3-acetyl)glutamine, and tryptophan by patients with Hartnup disease was reported (6). Hartnup disease is a newly described hereditary abnormality in the metabolism of tryptophan and is characterized by pellagra-like skin rashes accompanied by intermittent cerebellar ataxia and mental deterioration (7). In addition, it may be recalled that Ross (8) observed that a greatly increased urorosein reaction could be observed with the urine of insane patients, as compared with that of normal individuals, and that the occurrence of this strongly increased reaction in two patients probably did not occur as the result of differences in the food intake or in intestinal putrefaction in the case of the patients (9).