Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:3.5.1.5 (urease)
7,257 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A synthesis of roseoflavin by Streptomyces davawensis from guanine through riboflavin was demonstrated. The lines of evidence are (1)incorporations of 14C of [2-and U-14C] guanine and [2-14C] riboflavin into roseoflavin, (2) no incorporation of 14C of [8-14C] guanine into roseoflavin, (3) localizations of 14C in roseoflavin, and (4) a decrease of specific radioactivity of roseoflavin formed from [2-14C]guanine on addition of riboflavin to the culture. The 14C atoms in roseoflavin formed were localized by radioactivity analysis of the NaOH-hydrolysis products, i.e., urea and 1,2-dihydro-6-methyl-7-dimethylamino-2-keto-1-D-ribityl-3-quinox-alinecarboxylic acid (QC), a new substance. These hydrolysis products were identified by the isolation of dixanthylures, decomposition with urease, and from the properties of QC and QC tetraacetate isolated. These finding suggest that the pyrimidine ring of guanine is conserved in the formation of roseoflavin from guanine through riboflavin.
...
PMID:Formation of roseoflavin from guanine through riboflavin. 47 19

Urea has been shown to be an obligate intermediate in and the penultimate product of the catabolism of pyrimidine-ring nitrogen in Rhodosporidium toruloides (Rhodotorula). One of a series of mutants selected for its inability to utilize uracil as a sole source of nitrogen was unable to utilize urea also. The mutant accumulated urea and failed to form 14CO2 during supplementation with [2-14C]uracil. Radioautograms from the resulting cell extracts and media failed to reveal expected intermediates. Cell-free extracts of the mutant were shown to lack urease activity. Revertants of the mutant were essentially wild type in all tested attributes. Elements of the reductive pathway for pyrimidine catabolism are present in Rhodosporidium (O. A. Milstein and M. L. Bekker, J. Bacteriol. 127: 1-6, 1976), but is has not been determined whether this pathway is involved with production of urea.
...
PMID:Urea: obligate intermediate of pyrimidine-ring catabolism in Rhodosporidium toruloides. 57 31

Relative deficiencies of ornithine or arginine occur in the presence of excessive ammonia, excessive lysine, growth, pregnancy, trauma, or protein deficiency and malnutrition. Ammonia excess may occur in the presence of a normal liver when amino acid mixtures lacking ornithine, arginine, or citrulline are infused; when specific amino acids such as glycine are injected; when ammonium salts, urea, or urease are injected; or when the gastrointestinal tract contains an excess of protein, urea, or NH4+, as occurs after a gastrointestinal hemorrhage. In these states, ornithine is often rate-limiting for urea cycle function. Ornithine is also rate-limiting when ammonia excess occurs in the presence of hepatic failure. In three of the inherited urea cycle disorders, ornithine insufficiency and ammonia excess also occur. These disorders are citrullinemia, argininosuccinic aciduria, and argininemia. In the presence of excessive lysine the availability of arginine is reduced and the formation of ornithine is decreased in the liver; urea synthesis is reduced, but orotic acid synthesis is increased, and orotic aciduria results as carbamyl phosphate is directed toward the pyrimidine pathway. Hereditary lysinuric protein intolerance results in ornithine depletion, hyperammonemia, and orotic acid uria. Optimal growth in several species of animals requires 0.4-1.0% arginine in the diet. Diets deficient in arginine are associated with poor wound healing as well as stunted growth. The measurement of orotic acid excretion has been a convenient indicator of insufficiency of ornithine or arginine during growth or pregnancy in animals and should prove useful in assessing the requirement for arginine after trauma. Normal human pregnancy is associated with low-grade orotic aciduria. Protein deficiency and malnutrition increase the vulnerability of the animal or child to ammonia toxicity. This is presumably due to insufficient ornithine for normal urea cycle responsiveness.
...
PMID:Conditional deficiencies of ornithine or arginine. 308 83

This communication presents evidence from the literature and recent experiments that describe circumstances wherein arginine may be a conditional dietary essential. Previous work has established that the synthesis of orotic acid (OA), the first pyrimidine formed in the de novo pathway of nucleic acid synthesis, becomes elevated whenever the ammonia load exceeds the capacity of the urea cycle. Under these circumstances, the common intermediate, carbamyl phosphate, leaks from the mitochondria and induces OA synthesis in the cytoplasm. This leads to increased OA excretion in the urine as pyrimidine synthesis escapes feedback control. A deficiency of urea cycle substrates such as arginine, and administration of certain drugs, ammonium salts, urease, or excess amino acids raises orotic acid excretion. Our recent experiments in rats show that OA excretion is also elevated after partial hepatectomy following galactosamine administration, exposure to carbon tetrachloride, or feeding 36% of calories as ethanol. The elevation in OA excretion was suppressed by dietary supplementation with arginine, implying that arginine is conditionally essential. Adult human male alcoholics showed elevated urinary orotic acid-to-creatinine ratios early after drinking episodes, which declined with time following abstinence. Such evidence shows that well studied hepatotoxins and surgical liver injury affect pathways of ammonia metabolism and suggests that urinary orotic acid can be an indicator of hepatotoxicity and increased needs for arginine. Arginine-deficient diets and alcohol feeding both enhance fatty deposition in the liver, which can be worsened by high fat intakes in rats. Alcoholism, various other diseases, and fasting and realimentation change orotic acid excretion. Such responses will have to be taken into account in establishing "normal values" for OA excretion.
...
PMID:Orotic acid, arginine, and hepatotoxicity. 352 4

After the urine was treated with urease, lyophilized, and trimethylsilylated, it was examined for metabolic profiles in Dalmatian dogs and Shetland sheepdogs by gas chromatography-mass spectrometry (GC/MS), which simultaneously analyzes organic acids, amino acids, sugars, sugar alcohols, purine and pyrimidine bases, and nucleosides. The profiles were compared with those from human specimens. As clarified in past studies, Dalmatian dogs showed an extreme decrease in allantoin, which is the final product of purine metabolism in the canine of other species, and a marked detection of uric acid peak. This finding suggests that purine metabolism in Dalmatian dogs is different from that in the other species. Only two Shetland sheepdogs, whose mother had chronic renal failure, showed a marked excretion of uric acid, as in Dalmatian dogs. In addition, some Dalmatian dogs, who were maintained on a protein-restricted diet, showed a little excretion of uric acid. A large amount of uric acid is detected in combination with pentose-monosaccharides, hexose-monosaccharides and sugar alcohols in neonatal human urine in comparison with the present dog samples. A marked difference between the canine and the humans is that phenylacetylglycine, which is derived from the aromatic amino acid phenylalanine, is excreted in the canine urine. Phenylacetylglycine is not detected in the human urine, and there have been no reports of its excretion in canine urine.
...
PMID:Gas chromatography-mass spectrometric studies of canine urinary metabolism. 749 34

The aim of this study was the identification of 181 Citrobacter strains on the basis of the recently proposed taxonomic changes of Brenner. All strains were isolated from diarrhoeic patients; 124 strains were originally sent for identification to Laboratory of Enterobacteriaceae DB NIH, 57 strains was isolated in Czech Republic. Citrobacter isolates were initially identified as C. koseri (3 strains), C. amalonaticus (1 strain) or as members of the C. freundii complex (177 strains). Additionally some biochemical tests were performed. The ability to grow in medium containing KCN, lysine decarboxylase production, lactose fermentation and PYR test were examined. Strains belonging to the C. freundii complex were identified to the species level by biochemical methods on the basis of the results of Brenner, who found some tests to be useful in separating Citrobacter species. These test included citrate and acetate utilization, arginine dihydrolase and ornithine decarboxylase activities, motility, urease production, esculin hydrolysis, and acid production from sucrose, dulcitol, melibiose, raffinose and salicin. On the basis of the criteria described above, 96.6% of the strains tested could be assigned to one of the recently named species of C. freundii complex. Using biochemical tests suggested by Brenner we were able to identify Citrobacter strains members of newly recognised species. A five-test system is proposed to identify the most frequently encountered species currently residing in the C. freundii complex.
...
PMID:[Taxonomy of Citrobacter rods found in human specimens]. 1080 58

This review will be concerned primarily with a practical yet comprehensive diagnostic procedure for the diagnosis or even mass screening of a variety of metabolic disorders. This rapid, highly sensitive procedure offers possibilities for clinical chemistry laboratories to extend their diagnostic capacity to new areas of metabolic disorders. The diagnostic procedure consists of the use of urine or filter paper urine, preincubation of urine with urease, stable isotope dilution, and gas chromatography-mass spectrometry. Sample preparation from urine or filter paper urine, creatinine determination, stable isotope-labeled compounds used, and GC-MS measurement conditions are described. Not only organic acids or polar ones but also amino acids, sugars, polyols, purines, pyrimidines and other compounds are simultaneously analyzed and quantified. In this review, a pilot study for screening of 22 target diseases in newborns we are conducting in Japan is described. A neonate with presymptomatic propionic acidemia was detected among 10,000 neonates in the pilot study. The metabolic profiles of patients with ornithine carbamoyl transferase deficiency, fructose-1,6-bisphosphatase deficiency or succinic semialdehyde dehydrogenase deficiency obtained by this method are presented as examples. They were compared to those obtained by the conventional solvent extraction methods or by the tandem mass spectrometric method currently done with dried filter blood spots. The highly sensitive, specific and comprehensive features of our procedure are also demonstrated by its use in establishing the chemical diagnosis of pyrimidine degradation defects in order to prevent side effects of pyrimidine analogs such as 5-flurouracil, and the differential diagnosis of three types of homocystinuria, orotic aciduria, uraciluria and other urea cycle disorders. Evaluation of the effects of liver transplantation or nutritional conditions such as folate deficiency in patients with inborn errors of metabolism is also described.
...
PMID:Diagnosis of inborn errors of metabolism using filter paper urine, urease treatment, isotope dilution and gas chromatography-mass spectrometry. 1148 33

Inborn errors of pyrimidine degradation, dihydropyrimidine dehydrogenase deficiency and dihydropyrimidinase deficiency, are less rare than has generally been assumed. Many asymptomatic cases have been reported, and in patients with symptoms, the clinical abnormalities are variable and nonspecific. Withdrawal of pyrimidine analogues such as 5-fluorouracil (5FU), a commonly used anticancer drug, from the cancer chemotherapy regimens of patients with pyrimidine degradation deficiencies, however, is critical because 5FU is degraded in vivo by pyrimidine-degradative enzymes. Patients with these deficiencies suffer from severe neurotoxicity, sometimes leading to death, following administration of 5FU, and even otherwise asymptomatic homozygotes or heterozygotes may develop severe clinical symptoms upon administration of such medication. Therefore, a rapid and specific method for identifying cancer patients with these enzyme deficiencies prior to treatment with 5FU is critical. To address this problem, we established methods for highly sensitive yet specific determinations of thymine, uracil, dihydrothymine, dihydrouracil, orotate and creatinine simultaneously in 0.1-ml liquid urine or filter-paper urine. This method involves stable isotope dilution, a simplified urease treatment previously described and gas chromatography-mass spectrometry without prior fractionation. The high recovery and low C.V. values were obtained and healthy control values were also determined for these metabolites. Using artificially prepared urine specimens simulating these disorders. the chemical diagnosis can be made clearly, and no further analysis appears to be required for differential chemical diagnosis.
...
PMID:Simple gas chromatographic-mass spectrometric procedure for diagnosing pyrimidine degradation defects for prevention of severe anticancer side effects. 1148 36

Dihydropyrimidine dehydrogenase (DHPDase), dihydropyrimidinase (DHPase) and beta-ureidopropionase (betaUPase) are the enzymes that catalyze the first, second, and third steps of the degradation of pyrimidines, respectively. beta-Ureidopropionate (betaUP) and beta-ureidoisobutyrate (betaUIB) are increased in the urine of patients with betaUPase deficiency. The original case in which betaUPase deficiency was discovered by NMR spectroscopy was an 11-month-old patient who presented with hypotonia and dystonic movement. We detected a second but asymptomatic case during a pilot study of neonatal screening with filter-paper urine, urease pretreatment and gas chromatography/mass spectrometry (GC/MS). The urease pretreatment of urine without fractionation resulted in a high recovery of these polar ureide compounds and allowed the highly sensitive GC/MS detection and diagnosis of betaUPase deficiency. betaUP and betaUIB were identified using GC/MS techniques. In the urine of the neonate with betaUPase deficiency, betaUP and betaUIB were persistently increased. Thymine, 5,6-dihydrothymine and 5,6-dihydrouracil were increased only moderately but significantly. It is known that thymine and uracil increase markedly in DHPDase deficiency, and 5,6-dihydrothymine and 5,6-dihydrouracil increase in DHPase deficiency. Therefore, betaUPase deficiency can be differentially diagnosed from the first and second enzyme deficiencies. Application of this specific and sensitive diagnostic procedure will lead to an understanding of the clinical heterogeneity of betaUPase deficiency. Furthermore, the identification of patients with defects in pyrimidine metabolism will enable doctors to avoid cancer chemotherapy with pyrimidine analogues such as 5-fluorouracil, which could be dangerous for these patients.
...
PMID:Screening and diagnosis of beta-ureidopropionase deficiency by gas chromatographic/mass spectrometric analysis of urine. 1227 38

Diazinon [O,O-diethyl O-2-isopropyl-6-methyl(pyrimidine-4-yl) phosphorothioate] and imidacloprid [1-(1-[6-chloro-3-pyridinyl]methyl)-N-nitro-2-imidazolidinimine] are applied to lawns for insect control simultaneously with nitrogenous fertilizers such as urea, but their potential effect on urease activity and nitrogen availability in turfgrass management has not been evaluated. Urease activity in enzyme assays, washed cell assays, and soil slurries was examined as a function of insecticide concentration. Intact cores from field sites were used to assess the effect of insecticide application on urease activity in creeping bentgrass (Agrostis palustris Huds.) and bluegrass (Poa pratensis L.) sod. Bacterial urease from Bacillus pasteurii and plant urease from jack bean [Canavalia ensiformis (L.) DC.] were unaffected by the insecticides. Both insecticides inhibited the growth of Proteus vulgaris, a urease-producing bacterium, but only diazinon significantly reduced urease activity in washed cells; neither insecticide inhibited urease activity in sonicated cells. Neither diazinon nor imidacloprid inhibited urease activity in Woolper soil (fine, mixed, mesic Typic Argiudoll) slurries, but diazinon slightly inhibited urease activity in Maury soil (fine, mixed, semiactive, mesic Typic Paleudalf) slurries. Imidacloprid had no effect on urease activity in creeping bentgrass or bluegrass sod at up to 10 times the commercial application rate. Diazinon briefly, but significantly, reduced urease activity in bluegrass sod. Co-application of imidacloprid and urea appears to be benign with respect to urease activity in soil and sod. Diazinon, in contrast, appears to have a significant, short-term, inhibitory effect on the microbial urease-producing community, but that effect depends on soil type.
...
PMID:Effects of commercial diazinon and imidacloprid on microbial urease activity in soil and sod. 1609 10


1 2 Next >>

---