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THE metabolic mechanism by which tryptophan is converted into nicotinic acid appears to be altered in several human diseases. Yet it has not been possible to demonstrate specific excretory patterns for the various diseases. The excretory pattern in the urines of patients with cancer of the bladder is certainly the one which presents the most specific and relevant alterations (Quagliariello, 1963). Several authors have shown the presence of 3-hydroxyanthranilic acid in the urine of patients with cancer of the bladder: Boyland and Williams using column (1956a) and paper chromatography (1956b); Quagliariello, Auricchio, Casale and Tancredi (1958) by means of paper chromatography; Tompsett (1959) and Abul-Fadl and Khalafallah (1961) with a colorimetric method. Quagliariello, Tancredi, Fedele and Saccone (1961) found that the amounts of 3-hydroxyanthra-nilic acid, 3-hydroxynurenine and anthranilic acid excreted by bladder cancer patients were reduced by giving large doses of nicotinamide. Allen, Boyland, Dukes, Horning and Watson (1957) have shown that biological ortho-amino-phenols, such as 3-hydroxyanthranilic acid and 3-hydroxykynurenine, can induce experimental cancer of the bladder. Dunning, Curtis and Maun (1950) reported that cancer of the urinary bladder, caused by 2-acetamido-fluorene, arose in practically all cases in rats fed on a diet containing a high quantity of tryptophan. Further, Quagliariello, Auricchio and Rinaldi (1958) found that on oral administration of 2-acetamido-fluorene, 3-hydroxyanthranilic acid > quinolinic acid conversion in rat liver was inhibited to a large extent. This metabolic block would be expected to cause accumulation of carcinogenic substances such as 3-hydroxyanthranilic acid and 3-hydroxynurenine; this could give a tentative explanation of the above reported findings of Dunning et al. Recently Ehrhart and Georgii (1959) reported that 3-hydroxyanthranilic acid can induce myeloid forms of leukaemia in mice (RFH-strain) with a low incidence of spontaneous leukaemia. The leukaemia rate following the administration of 3-hydroxyanthra-nilic acid could be increased by blocking 3-hydroxyanthranilic acid oxidase with 2-acetamido-fluorene (Ehrhart, 1962). These studies prompted our further researches on the eventual connection between tryptophan metabolism and carcinogenesis. In the present work the excretion of 3-hydroxyanthranilic acid in the urine of patients with tumours of the urinary bladder and of the kidney has been studied. None of the patients with bladder cancer was engaged in the handling of aromatic amines.

Tryptophan-Nicotinic Acid Metabolism in Patients with Tumours of the Bladder and Kidney