Untersuchungen �ber den Tryptophan-Stoffwechsel beim Blasen-Carcinom

Kochen, W; Hochberg, K.

doi:10.1007/bf00524406

Cited by 7 publications

(3 citation statements)

References 14 publications

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“…Einzelheiten über den Trennungsgang siehe I.e. (16). Zur Analyse der Nicotinsäure-Derivate, der Chinaldin-und 8-Hydroxychinaldinsäure wird der Trockenrückstand einesTeils des 24-h-Urins (10 ml) mit ammoniakalischem Äthanol extrahiert, anschließend erfolgt eine Säulenchromatographie auf SP-Sephadex und Entwicklung mit Äthanol/Wasser (90 ml + 10 ml).…”

Section: Methodik Und Materialsunclassified

Tryptophan-Stoffwechseluntersuchungen bei unbehandelten Phenylketonurikern

Kochen¹,

Byrd²,

Bühner³

et al. 1975

Clinical Chemistry and Laboratory Medicine

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Studies on tryptophan metabolism in untreated phenylketonuric patientsThe products of the oxidative degradation of tryptophan via the kynurenine pathway were quantitatively determined in the urine of ten untreated patients with phenylketonuria, aged 4-35 years. All the patients were severely mentally retarded. The results of the analysis suggest a division of the patients into two groups, A and B.-The patients of group A showed a basal urinary excretion of kynurehine, kynurenic acid, 3-hydroxykynurenine and xanthurenic acid which lies in the lower part of the normal range. The increase in excretion of tryptophan metabolites under tryptophan loading was, however, significantly less than in controls. On the average, only 0.63 % of the load was excreted in the form of these assayed metabolites; in contrast, the control value is 1,13 %. In group B, the rate of excretion was higher than normal under basal and loading conditions. The post-tryptophan excretion was four times greater than that of controls (4.64 %). 3-hydroxyanthranilic acid could only be detected in group B after loading. The metabolite 8-hydroxyquinaldic acid, which is supposed to be an abnormal metabolic product of tryptophan, was excreted in milligram amounts. The analysis of the metabolites of 3-hydroxyanthranilic acid showed that the excretion of N r methylnicotinamide and Ni-methyl-2-pyridone-5-carboxamide was within'the normal range. The excretion of nicotinic acid and its amide was sporadic in both the patients and controls. Other theoretically possible metabolites in this pathway could not be found. A number of unidentified metabolites could be detected by thin-layer chromatography in the basal state. The excretion of these metabolites was greatly augmented after tryptophan loading. Other substances which were not detectable in the basal state became evident on loading. A number of these metabolites are characteristic either of group A or B. The structural identification of one of the new products has been hindered by its instability. A stable cleavage product was identified as o-aminoacetophenon by mass-spectroscopy. This metabolite is typical for group B. The possible influence of the blood phenylalanine on the metabolism of tryptophan in phenylketonuria is discussed.

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Section: Methodik Und Materialsunclassified

Tryptophan-Stoffwechseluntersuchungen bei unbehandelten Phenylketonurikern

Kochen¹,

Byrd²,

Bühner³

et al. 1975

Clinical Chemistry and Laboratory Medicine

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“…Recently, Radomski, Glass and Deichmann (1971) have given evidence supporting the role of tryptophan in bladder carcinogenesis by feeding 7 times the normal daily intake of DL-tryptophan to beagle dogs for periods of 3 5 months to 7 years. Marked local hyperplasia of the transitional bladder epithelium was observed in all cases.Several clinical studies of the metabolism of tryptophan have been carried out in patients with bladder cancer (Brown et al, 1960;Price and Brown, 1962;Benassi, Perissinotto and Allegri, 1963;Kochen and Hochberg, 1970). In these investigations one or more metabolites were determined in samples of 24-hour urine.…”

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“…Several clinical studies of the metabolism of tryptophan have been carried out in patients with bladder cancer (Brown et al, 1960;Price and Brown, 1962;Benassi, Perissinotto and Allegri, 1963;Kochen and Hochberg, 1970). In these investigations one or more metabolites were determined in samples of 24-hour urine.…”

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The Concentration of Free and Conjugated 3-Hydroxyanthranilic Acid in the Urine of Bladder Tumour Patients Before and After Therapy, Measured with an Enzymatic Method

Teulings¹,

Fokkens²,

Kaalen³

et al. 1973

Br J Cancer

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Summary.-The basal concentration of the tryptophan metabolite 3-hydroxyanthranilic acid (30HA), which has carcinogenic properties, was measured with an enzymatic method of determination which allowed separate measurement of free and conjugated 30HA. The concentration of free 30HA in untreated bladder cancer patients was significantly (P < 0.001) higher than in a healthy control group, but after local therapy the concentration was significantly lower than before treatment (P < 0-01). The concentration of conjugated 30HA was nearly constant in the three groups. It was concluded that other factors than a genetic determined abnormality might be operating in bladder cancer patients which could lead to an abnormal concentration of 30HA in their urine.'rHE role of tryptophan metabolites in the aetiology of human urinary bladder cancer has been the subject of numerous investigations. Twenty-two years ago a relationship was suggested by Dunning, Curtis and Maun (1950), who showed that a high incidence of bladder tumours resulted when rats were fed 2-acetylaminofluorene combined with DL-tryptophan. Several primary aromatic amine tryptophan metabolites, with a structure similar to known environmental human bladder carcinogens, are present in human urine (Brown and Price, 1956). Direct application to the mouse bladder of these metabolites by the " pellet technique " confirmed the carcinogenic activity of several of them (Bryan, 1971). Recently, Radomski, Glass and Deichmann (1971) have given evidence supporting the role of tryptophan in bladder carcinogenesis by feeding 7 times the normal daily intake of DL-tryptophan to beagle dogs for periods of 3 5 months to 7 years. Marked local hyperplasia of the transitional bladder epithelium was observed in all cases.Several clinical studies of the metabolism of tryptophan have been carried out in patients with bladder cancer (Brown et al., 1960;Price and Brown, 1962;Benassi, Perissinotto and Allegri, 1963;Kochen and Hochberg, 1970). In these investigations one or more metabolites were determined in samples of 24-hour urine. In most of the studies, loading with an oral dose of L-tryptophan was necessary because the analytical methods are working at lower limits of detection and sensitivity when used on basal urines. Because of the differences in method, it is difficult to compare the results obtained in the different laboratories. An abnormal metabolism was often observed in patients with spontaneous bladder cancer, but in other pathological conditions an abnormal excretion pattern was also found (Rose,.Moreover, the excretion of metabolites is related to tryptophan intake, hormonal regulation of the pathway, intake levels of pyridoxine and metabolic individualitv (Albanese et al., 1972). In a pilot study

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Umweltfaktoren als wesentliche Ursache des Blasenkarzinoms und seiner Epidemiologie — Ein historischer Überblick

Kälble

Blasenkarzinom

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Untersuchungen �ber den Tryptophan-Stoffwechsel beim Blasen-Carcinom

Cited by 7 publications

References 14 publications

Tryptophan-Stoffwechseluntersuchungen bei unbehandelten Phenylketonurikern

Tryptophan-Stoffwechseluntersuchungen bei unbehandelten Phenylketonurikern

The Concentration of Free and Conjugated 3-Hydroxyanthranilic Acid in the Urine of Bladder Tumour Patients Before and After Therapy, Measured with an Enzymatic Method

Umweltfaktoren als wesentliche Ursache des Blasenkarzinoms und seiner Epidemiologie — Ein historischer Überblick

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