Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 14C-urea breath test analogous to its clinical counterpart is described for use in ferrets naturally or experimentally infected with Helicobacter mustelae. The test is performed within a sealed glass metabolism chamber through which air is drawn at a constant rate and expired breath collected into sodium hydroxide. Peak 14CO2 production occurred approximately 1 hour after substrate administration. Both inter- and intra-animal responses were highly reproducible, with mean coefficients of variation less than 10%. Other than enhancing peak 14CO2 levels very slightly, fasting had little influence on the response. In infant animals challenged with H mustelae, breath test activity increased linearly with the total count of culturable bacteria isolated from the antrum. Treatment of established infections with colloidal bismuth subcitrate (DeNol) for 4 weeks resulted in clearance of all detectable bacteria but retention of some breath test activity. Subsequent regrowth of bacteria was parallelled by an increase in the breath test response. Inclusion of amoxycillin and metronidazole in the treatment regimen, however, eradicated all the bacteria and almost totally eliminated 14CO2 production. This response parallels the clinically observed suppressive effect on H pylori achieved with bismuth alone relative to the total eradication seen with triple therapy. A single oral dose of the urease inhibitor, flurofamide, inhibited over 90% of the response for at least 24 hours. Acetohydroxamic acid was less effective. These findings suggest that in the ferret H mustelae model, breath test analysis can be a useful, non-invasive alternative to endoscopy for evaluation of agents affecting either growth of the organism or urease activity.
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PMID:Development of a 14C-urea breath test in ferrets colonised with Helicobacter mustelae: effects of treatment with bismuth, antibiotics, and urease inhibitors. 843 69

Growth of the yeast Phaffia rhodozyma was carried out in a simplified medium based on less expensive nutrient sources, such as diluted sugar cane juice, urea, and sodium phosphate. The usual content of the astaxanthin, an oxygenated pink carotenoid useful for fish flesh staining, was improved along with with good cell yields (respective values of > 1300 micrograms/g cells and > 5 g cells/L were observed). Yeast invertase and urease must therefore play an important role in the implementation of low-cost culture media.
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PMID:Culture of the astaxanthinogenic yeast Phaffia rhodozyma in low-cost media. 866 8

Helicobacter pylori exhibits a complex system of enzymes which serve a range of functions, such as colonization, damage of the host epithelium and provision of essential metabolic substrates. Colonization is favoured by urease and by the action on mucus and the mucosal barrier exerted by phospholipases and proteases, although this latter mechanism is controversial. Toxic effects are effected by urease, alcohol dehydrogenase (ADH), phospholipases and proteolytic enzymes. ADH produces acetaldehyde that is toxic to the mucosal cells, while phospholipases induce generation of products such as lysolecithin, which damage the gastric epithelium. Catalase and sodium dismutase of H. pylori are mainly involved in transforming toxic oxygen metabolites to harmless water; they protect the bacterium from the killing effect of neutrophils. Metabolic enzymes (for example, phosphatases, ATPases) are essential for the generation of energy, for synthesis and transport of cell products and for ion fluxes. In addition, they influence cell growth and the expression of virulence factors.
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PMID:Helicobacter pylori enzymes. 873 Feb 61

The urease from the ascomycetous fission yeast Schizosaccharomyces pombe was purified about 4000-fold (34% yield) to homogeneity by acetone precipitation, ammonium sulfate precipitation, DEAE-Sepharose ion-exchange column chromatography, and if required, Mono-Q ion-exchange fast protein liquid chromatography. The enzyme was intracellular and only one species of urease was detected by nondenaturing polyacrylamide gel electrophoresis (PAGE). The native enzyme had a M(r) of 212 kDa (Sepharose CL6B-200 gel filtration) and a single subunit was detected with a M(r) of 102 kDa (PAGE with sodium dodecyl sulfate). The subunit stoichiometry was not specifically determined, but the molecular mass estimations indicate that the undissociated enzyme may be a dimer of identical subunits. The specific activity was 700-800 micromols urea.min-1.mg protein-1, the optimum pH for activity was 8.0, and the Km for urea was 1.03 mM. The sequence of the amino terminus was Met-Gln-Pro-Arg-Glu-Leu-His-Lys-Leu-Thr-Leu-His-Gln-Leu-Gly-Ser-Leu-Ala and the sequence of two tryptic peptides of the enzyme were Phe-Ile-Glu-Thr-Asn-Glu-Lys and Leu-Tyr-Ala-Pro-Glu-Asn-Ser-Pro-Gly-Phe-Val-Glu-Val-Leu-Glu-Gly-Glu-Ile- Glu- Leu-Leu-Pro-Asn-Leu-Pro. The N-terminal sequence and physical and kinetic properties indicated that S. pombe urease was more like the plant enzymes than the bacterial ureases.
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PMID:Purification and characterization of urease from schizosaccharomyces pombe. 874 56

The current AOAC method (963.28) for large-scale (50 g) testing of urine on grain is based on the reaction of sodium in urine with magnesium uranyl acetate. Detection of sodium suggests that urine is present and that a test for urea is appropriate. Urea is detected with urease-bromothymol blue-paper and is confirmed through its reaction with xanthydrol to form dixanthylurea crystals, which are detected microscopically. The initial nonspecific test for sodium can be influenced by the presence of salt or other sodium compounds. Furthermore, the magnesium uranyl acetate spray used in Method 963.28 potentially exposes the analyst to the aerosol of a volatile, toxic uranium compound. Excess reagents and analyzed test portions must be disposed of as radioactive waste. In addition, Method 963.28 requires several steps to determine the presence of urea. The alternative AOAC method (972.41) tests for the presence of urea from urine on individual seeds. Urea is enzymatically decomposed to ammonia and carbon dioxide by urease. Liberated ammonia shifts the pH, changing the color of the indicator in the agar from yellow to blue. This study adapts Method 972.41 to larger test samples. Up to 25 g grains and seeds are sprayed with urease test agar instead of being individually immersed in the urease test agar. The modified method was used to analyze urea on seeds and grains of 24 plants from 4 families. The method has a limit of detection of one seed contaminated with 1 microgram urea.
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PMID:Use of urease-bromothymol blue-agar method for large-scale testing of urine on grain and seeds. 875 45

Urea-sensitive enzyme field effect transistors (ENFETs) were prepared by cross-linking urease with bovine serum albumin in saturated glutaraldehyde vapor on the sensitive surface of a pH-FET. The linear part of the biosensor dynamic range is between 5 x 10(-5) and 10(-3) M of urea. The influence of pH on the sensor response, stability and reproducibility of the urea sensor were examined. The addition of EDTA, glycerol, sodium azide and dithiothreitol in the storage buffer solution was studied. In these specific storage conditions, an increase of sensor sensitivity and stability was observed, which means that the enzyme is inhibited during the immobilisation procedure and can be partially restored. Furthermore such reagents do not affect the operational characteristics of the sensor when working in serum.
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PMID:Performance of urea-sensitive enzyme field effect transistors: influence of the storage conditions. 876 74

Ecabet sodium (ecabet), a new agent that has protective effects on the gastric mucosa has anti-Helicobacter pylori effects, binding with urease to inhibit H. pylori activity, and causing the bacterial to become non-viable. Ecabet monotherapy eradicates H. pylori infection in Japanese monkeys. We investigated a new regimen that included ecabet to eradicate H. pylori infection in gastric ulcer patients. Fifty-five H. pylori-positive patients with gastric ulcer were randomly assigned to one of two groups: group 1 received dual therapy with lansoprazole (30 mg o.d.) for 8 weeks plus clarithromycin (200 mg b.i.d.) or amoxicillin (250 mg q.i.d.) for 2 weeks. Group 2 received triple therapy with lansoprazole (30 mg o.d.) and ecabet sodium (1.0 g b.i.d.) for 8 weeks plus clarithromycin (200 mg b.i.d.) or amoxicillin (250 mg q.i.d.) for 2 weeks. Four weeks after the treatment was withdrawn, H. pylori status was evaluated by histological examination, rapid urease test, and culture. The eradication rate was 26% (7 out of 27 patients) in group 1 and 79% (22 out of 28 patients) in group 2. All patients completed the treatment. The addition of ecabet to the regimen increased the eradication rate of H. pylori infection, and there were no associated major side effects.
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PMID:Ecabet sodium eradicates Helicobacter pylori infection in gastric ulcer patients. 895 22

The effect of aminoglycosides on renal function was evaluated in 30 full-term infants who were treated within 24 h of birth with either amikacin (10 infants, group A), gentamicin (9 infants, group B), or netilmicin (10 infants, group C). Renal function was assessed before, during, and 48 h after discontinuation of therapy by measuring the plasma creatinine concentration (PCr), the fractional excretion of sodium (FENa), potassium, magnesium, phosphate (FEP), uric acid, and the urinary excretion of calcium (UCA/UCr ratio) immediately before (trough) and after (peak) the infusion of the aminoglycosides. The results were compared with 10 control newborns who did not receive antibiotics. Significant alterations in renal function were observed only during therapy with gentamicin (group B). These consisted of a sustained elevation of FENa and UCa/UCr ratio throughout therapy, a latent increase in FEP on the 7th day (P < 0.05), and lack of the normal postnatal decline of PCr in 3 of 9 infants (P < 0.01). These abnormalities persisted up to 2 days after discontinuation of therapy. Therapeutic doses of gentamicin may result in significant electrolyte disturbances in sick full-term infants.
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PMID:Effect of aminoglycoside therapy on renal function in full-term infants. 897 4

Helicobacter pylori adhere to Kato III and Hela S3 cells in monolayer cultures. To explore whether cell surface glycoconjugates on these two cell lines mediate binding of H. pylori, various carbohydrates, glycoproteins, and glycolipids were tested to inhibit H.pylori cell adhesion. The adhesion was measured (i) with a urease-based assay and (ii) by cells stained with fluorescein. Sodium periodate and sialidase treatment (but not alpha- or beta-galactosidase, heparitinase,lysozyme, or trypsin) inhibited H. pylori binding to both cell lines. Sulfatides and sulfated glycoconjugates (50 microg/ml) but not heparin or a number of simple carbohydrates inhibited binding (1 mg/ml). The two H.pylori strains studied (CCUG 17874 and strain 25) showed high binding of soluble 125I-labeled heparin and other sulfated carbohydrate compounds.
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PMID:Sulfatides inhibit binding of Helicobacter pylori to the gastric cancer Kato III cell line. 909 25

Helicobacter pylori CPY3401 and an isogenic urease-negative mutant, HPT73, showed chemotactic responses to urea, flurofamide (a potent urease inhibitor), and sodium bicarbonate. Since urea and sodium bicarbonate are secreted through the gastric epithelial surface and hydrolysis of urea by urease on the bacterial surface is essential for colonization, the chemotactic response of H. pylori may be crucial for its colonization and persistence in the stomach.
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PMID:Urease-independent chemotactic responses of Helicobacter pylori to urea, urease inhibitors, and sodium bicarbonate. 911 96


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