Histidine excretion

Soupart s data for histidine excretion are lower than those of Stein and of Evered because they do not include 3-methylhistidine. The data of Stein and Evered include 3-methylhistidine because their figures were obtained with Moore and Stein s 1951 method and not their 1954 method which was used by Soupart (S24). 

Soupart (S22) showed that the output of histidine in the urine varies during the normal menstrual cycle and reaches a maximum value between the 15th and 20th day. This coincides with a similar peak of excretion of phenolic steroids, suggesting a possible relation between histidine excretion and hormonal activity. In still unpublished observations, he finds similar correlations during pregnancy and lactation. 

Experimental animals that have been exposed to ititrous oxide to deplete vitamin B12 show an increase in the proportion of liver folate present as methyl-tetrahydrofolate (85% rather than the normal 45%), largely at the expense of unsubstituted tetrahydrofolate and increased urinary loss of methyl-tetrahydrofolate (Horne et al., 1989). Tissue retention of folate is impaired because methyl-tetrahydrofolate is a poor substrate for polyglutamyl-folate synthetase, compared with unsubstituted tetrahydrofolate (Section 10.2.2.1). As a result of this, vitamin B12 deficiency is frequently accompanied by biochemical evidence of functional folate deficiency, including impaired metabolism of histidine (excretion of formiminoglutamate Section 10.3.1.2) and impaired thymidylate synthetase activity (as shown by abnormally low dUMP suppression Section 10.3.3.3), although plasma concentrations of methyl-tetrahydrofolate are normal or elevated. 

Saundersoa C.L Leslie, S. (1983). N -methyl histidine excretion by poultry not all species exaete N -methyl histidine quantitatively. Br. ]. Nutr., 50, 691-700. 

Saundersoa C.L. Whitehead, C.C. (1987). N Methyl histidine excretion and [U- C] amino acid oxidation in fully fed chickens from two lines for high and low body fat contents. Comp. Biochem. Physiol, 86B, 419-22. 

The amounts of single amino acids excreted in urine in the conjugated form, as determined independently by Stein and Muting, are given in Tables 1 and 2. According to Stein, glycine, glutamic acid, aspartic acid, histidine, and proline are quantitatively the most important amino acids liberated in the course of urine hydrolysis. Serine, lysine, tyrosine, cysteine and cystine, threonine, alanine, valine, phenylalanine, and leucine are... 

Granerus, G. (1968). Effects of oral histamine, histidine, and diet on urinary excretion of histamine, methylhistamine, and l-methyl-4-imidazoleacetic acid in man, Scand. J. Clin. Lab. Invest., 10, suppl., 49. 

Histamine is formed by decarboxylation of the amino acid l -histidine, a reaction catalyzed in mammalian tissues by the enzyme histidine decarboxylase. Once formed, histamine is either stored or rapidly inactivated. Very little histamine is excreted unchanged. The major metabolic pathways involve conversion to /V-methylhistamine, methylimidazoleacetic acid, and imidazoleacetic acid (IAA). Certain neoplasms (systemic mastocytosis, urticaria pigmentosa, gastric carcinoid, and occasionally myelogenous leukemia) are associated with increased numbers of mast cells or basophils and with increased excretion of histamine and its metabolites. 

Pentz et al. (P5) estimate taurine with fluorodinitrobenzene in urine passed through Dowex 50 H+ columns, but there are doubts as to whether this procedure is really specific for taurine (B38). Dent et al. have compared results obtained for the estimation of sulfur-containing amino acids in urine of cystinuric patients, by polarographic and microbiological methods (D18, D19). Hier (H12) and Schreier and Pliickthun (S10, Sll) have published data on amino acid excretion as determined microbiologically. Enzymatic methods have been used with success in the case of histidine in urine with specific decarboxylase preparations (S23). 

In regard to the urinary excretion of other free amino acids than histidine during normal pregnancy, the situation is as follows. There is hyperexcretion of glycine, glutamine (including glutamic acid), serine,... 

Fig. 7. Chromatogram of 24-hr urine specimen (sample 1 ml 170 ml/24 hr) in a case of common rachitis in a 9-month-old child (D24). The following features are to be noticed definitely increased excretion of threonine, serine, glycine, and histidine.

Soupart, P., Le dosage de l histidine dans I urine par une methode enzyma-tique specifique et son application a l etude de l excretion de l histidine chez la femme normale et la femme enceinte. Clin. Chim. Acta 3, 349-356 (1958). 

About 7% of dietary riboflavin is covalently bound to proteins (mainly as riboflavin-8-a-histidine or riboflavin-8-a-cysteine). The riboflavin-amino acid complexes released by proteolysis are not biologically available although they are absorbed from the gastrointestinal tract, they are excreted in the urine (Chia et al., 1978). 

Under normal conditions, about 25% of the urinary excretion of riboflavin is as the unchanged vitamin, with a small amount as a variety of glycosides of riboflavin and its metabolites. Riboflavin-8-a-histidine andriboflavin-8-a-cysteine arising from the catabofism of enzymes in which the coenzyme is covalently bound are excreted unchanged. 

Although catabolism of histidine is not a major source of substituted folate, the reaction is of interest because it has been exploited as a means of assessing folate nutritional stams. In folate deficiency, the activity of the formimi-notransferase is impaired by lack of cofactor. After a loading dose of histidine, there is impaired oxidative metabolism of histidine and accumulation of FIGLU, which is excreted in the urine (Section 10.10.4). 

The ability to metabolize a test dose of histidine provides a sensitive functional test of folate nutritional status as shown in Figure 10.6, forrnirninoglu-tamate (FIGLU) is an intermediate in histidine catabolism and is metabolized by the tetrahydrofolate-dependent enzyme FIGLU forrnirninotransferase. In folate deficiency, the activity of this enzyme is impaired, and FIGLU accumulates and is excreted in the urine, especially after a test dose of histidine - the FIGLU test. 

Although the FIGLU test depends on folate nutritional status, the metabolism of histidine wUl also be impaired and a positive result obtained, in vitamin B12 deficiency, because of the secondary deficiency of folate (Section 10.3.4.1). About 60% of vitamin Bi2-deficient subjects show increased FIGLU excretion after a histidine load. 

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