Urine aspartic acid

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... 

As early as 1905 Abderhalden (Al) isolated from the hydrolyzate of the nondiffusible fraction of human urine four amino acids, i.e., leucine, alanine, glycine, and glutamic acid, and detected two others phenylalanine and aspartic acid. Some amino acids derived from this fraction have been quantitatively determined by Albanese et al. (A3) who found in the amount of the nondiffusible fraction corresponding to one liter of urine as much as 32.8 mg tryptophan, 18.0 mg phenylalanine, 16.2 mg methionine, 15.2 mg cystine, 13.1 mg arginine, 6.7 mg histidine, and 3.9 mg tyrosine. 

Stein et al. found in the course of experiments dealing with free and conjugated urinary amino acids in Wilson s disease (S9) that besides a marked aminoaciduria, almost a twofold increase in the excretion of all bound amino acids could be observed. As compared with normal urine (S8), unusual amounts of conjugated leucine, isoleucine, and valine are excreted in cases of Wilson s disease. Also the increase of glutamic acid, aspartic acid, and phenylalanine after urine hydrolysis is much more distinct in this disease than in normal conditions. Other bound amino acids are at or below normal levels. 

In the course of studies on aminoaciduria in Fanconi s syndrome, Dent (Dl) isolated from the urine of the subject investigated a simple peptide identified as serylglycylglycine. Carsten (Cl) found in normal urine several peptides containing in every case one of the dicarboxylic amino acids. He discovered also two tetrapeptides, one of them consisting of equimolar amounts of aspartic acid and glycine, and the second composed of glycine, alanine, and glutamic acid in the ratio 2 1 1. The first of these tetrapeptides was also found in the urine of a patient with rheumatoid arthritis. 

By means of a procedure described above, Hanson and Fittkau (HI) isolated seventeen different peptides from normal urine. One of them, not belonging to the main peptide fraction, consisted of glutamic acid, and phenylalanine with alanine as the third not definitely established component. The remaining peptides contained five to ten different amino acid residues and some unidentified ninhydrin-positive constituents. Four amino acids, i.e., glutamic acid, aspartic acid, glycine, and alanine, were found in the majority of the peptides analyzed. Twelve peptides contained lysine and eight valine. Less frequently encountered were serine, threonine, tyrosine, leucine, phenylalanine, proline, hydroxyproline, and a-aminobutyric acid (found only in two cases). The amino acid composi-... 

Orotic acid is an intermediate in pyrimidine synthesis. It is synthesized from the transcar-bamylation of aspartic acid and subsequent intramolecular condensation. Any defect in ureagenesis causing accumulation of intracellular carbamoyl phosphate provides substrate for orotic acid synthesis. Therefore, a defect of OTC, or any defect distal to this step, can cause orotic aciduria. The detection of elevated orotic acid in the urine is most useful in differentiating between patients with OTC deficiency and either CPSI- or NAGS-deficient patients in whom orotic aciduria is not present. 

A second, cytosolic CPS activity (CPSII) occurs in mammals as part of the CAD trifunctional protein that catalyzes the first three steps of pyrimidine synthesis (CPSII, asparate tran-scarbamoylase, and dihydroorotase). The activities of these three enzymes—CPSII, aspartate transcarbamoylase, and dihydroorotase—result in the production of orotic acid from ammonium, bicarbonate, and ATP. CPSII has no role in ureagenesis, but orotic aciduria results from hepatocellular accumulation of carbamyl phosphate and helps distinguish CPSI deficiency from other UCDs. Defects in CPSI classically present with neonatal acute hyperammonemic encephalopathy. The plasma citrulline and urine orotic acid concentrations are both low. A definitive diagnosis can be established by enzyme assay of biopsied liver tissue or by mutation analysis. 

Following oral administration 7-22% of alitame is unabsorbed and excreted in the feces. The remaining amount is hydrolyzed to aspartic acid and alanine amide. The aspartic acid is metabolized normally and the alanine amide excreted in the urine as a sulfoxide isomer, as the sulfone, or conjugated with glucuronic acid. 

The evaluated methods were apphed to detect thiols in blood serum, urine, and food samples " aspartic acid in drugs free sulfur traces in chemical reagents that include sulfur in their structure " ores and products of their flotation tire treads and rubber vulcanizates (Table 2). 

Quantitation of the Antitumor Agent N-(Phosphonacetyl)-L-aspartic Acid in Human Plasma and Urine by Gas Chromatography-Mass Spectrometry-Selected Ion Monitoring J. Chromatogr. 182(2) 163-169 (1980) CA 93 18827e... 

Quinolinic acid is synthesized not only from tryptophan in mammals (50) but also from aspartic acid and dihydroxyacetone phosphate in microorganisms (51). Therefore, quinolinic acid is the key intermediate in the de novo NAD biosyn-thethic pathway. Furthermore, quinolinic acid has been shown to excite nerve cells in rodents and primates on iontophoretic application (52) and intracerebral injection of quinolinic acid in rats results in selective axon-sparing neuronal lesions (53). The quinolinic acid content in biological materials is very low, so its content cannot be measured by the HPLC-UV method described under (28) in Section III.B. Recently, Mawatari et al. (54) found that quinolinic acid induces fluorescence by photoirradiation in the presence of hydrogen peroxide and established a system based on HPLC with detection by the fluorescence reaction. The detection limit was 1.1 pmol. Chromatograms of reference quinolinic acid and of quinolinic acid in urine are shown in Figure 18. 

A few indole derivatives are phytohormones. The most important of them is /3-indolylacetic acid, indole-3-acetic acid or, abbreviated, lAA (Fig. 160). It was detected in 1934 by Kogl in human urine, then in microorganisms, and, finally, also in higher plants. lAA occurs in plants either free or bound, e.g. esterifield to glucose or in peptide linkage with aspartic acid and glutamic acid. 

Biochemical characteristics (plasma levels of alanine and aspartate transminases, alkaline phosphatase, triglycerides, cholesterol, urea, uric acid, allantoin, glucose, protein, albumin, sodium, potassium, calcium, magnesium, phosphorus urine levels of protein and glucose). 

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