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

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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)

By counting the volatile molecules produced by an immobilized-enzyme catalyzed reaction which is interfaced to a mass spectrometer via a semi-permeable membrane, a general approach to biochemical measurement and detection is obtained which offers the potential of high sensitivity, specificity and speed. In combination with molecule microscopy, this method should allow, for example, a mapping of suitable enzyme distributions in non-stained and non-fixed tissue slices. Immobilized urease (urea amidohyrdrolase, EC 3.5.1.5) was used to assay urea using CO2 as the volatile product, and alcohol dehydrogenase (alcohol:NAD+ oxidoreductase, EC 1.1.1.1) was used to assay NADH using ethanol as the volatile product.
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PMID:Biochemical assay by immobilized enzymes and a mass spectrometer. 18 Oct 86

1. Urease from a sea urchin Lytechinus variegatus, was purified 300-fold, using heat precipitation, ethanol precipitation and gel filtration. 2. The pH optimum is 8.0. 3. The apparent Michaelis constant for urea is 0.13 mM at pH 8.0. 4. The inhibitory effects of seven reagents on urease were evaluated. The pattern of inhibition is similar to other invertebrate ureases. 5. L. variegatus urease is compared with that of several other invertebrates, and its possible significance in CaCO3 formation is discussed.
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PMID:Urease from a sea urchin Lytechinus variegatus: partial purification and kinetics. 31 93

1. Isolated hepatocytes were used to establish the reasons for the accumulation of aspartate, previously observed when the isolated rat liver was perfused with ethanol in the presence of alanine or ammonium lactate. 2. The isolated cells did not form aspartate when incubated with alanine and ethanol, but much aspartate was formed on incubation with ammonium lactate and ethanol. 3. Urea was the main nitrogenous product on incubation with alanine, in contrast with the perfused liver, where major quantities of NH4+ are also formed. When the formation of urea was nullified by the addition of urease, alanine plus ethanol caused aspartate formation, indicating that aspartate formation depends on the presence of critical concentrations of NH4+. 4. The accumulated aspartate was present in the cytosol. Ethanol halved the content of 2-oxoglutarate in the cytosol and more than trebled that of glutamate in the mitochondria. 5. The findings support the assumption that 2-oxoglutarate formed by the mitochondrial aspartate aminotransferase is not translocated to the cytosol in the presence of ethanol and NH4+, because it is rapidly converted into glutamate, the dehydrogenation of ethanol providing the required NADH. Aspartate, however, is translocated to the cytosol and accumulates there because of the lack of stoicheiometric amounts of oxoglutarate.
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PMID:The accumulation of aspartate in the presence of ethanol in rat liver. 120 Oct 7

Microbioassays using bacteria or enzymes are increasingly applied to measure chemical toxicity in the environment. Attractive features of these assays may include low cost, rapid response to toxicants, high sample throughput, modest laboratory equipment and space requirements, low sample volume, portability, and reproducible responses. Enzymatic tests rely on measurement of either enzyme activity or enzyme biosynthesis. Dehydrogenases are the enzymes most used in toxicity testing. Assay of dehydrogenase activity is conveniently carried out using oxidoreduction dyes such as tetrazolium salts. Other enzyme activity tests utilize ATPases, esterases, phosphatases, urease, luciferase, beta-galactosidase, protease, amylase, or beta-glucosidase. Recently, the inhibition of enzyme (beta-galactosidase, tryptophanase, alpha-glucosidase) biosynthesis has been explored as a basis for toxicity testing. Enzyme biosynthesis was found to be generally more sensitive to organic chemicals than enzyme activity. Bacterial toxicity tests are based on bioluminescence, motility, growth, viability, ATP, oxygen uptake, nitrification, or heat production. An important aspect of bacterial tests is the permeability of cells to environmental toxicants, particularly organic chemicals of hydrophobic nature. Physical, chemical, and genetic alterations of the outer membrane of E. coli have been found to affect test sensitivity to organic toxicants. Several microbioassays are now commercially available. The names of the assays and their basis are: Microtox (bioluminescence), Polytox (respiration), ECHA Biocide Monitor (dehydrogenase activity), Toxi-Chromotest (enzyme biosynthesis), and MetPAD (enzyme activity). An important feature common to these tests is the provision of standardized cultures of bacteria in freeze-dried form. Two of the more recent applications of microbioassays are in sediment toxicity testing and toxicity reduction evaluation. Sediment pore water may be assayed directly or solvents may be used to extract the toxicants. Some of the solvents used for extraction of organic chemicals are themselves toxic to bacteria (e.g., dichloromethane), requiring exchange with a less toxic solvent (e.g., ethanol, methanol, DMSO). A modification of the Microtox test allows direct assay of solid-phase samples such as sediments. The toxicity reduction evaluation (TRE) must be carried out at wastewater treatment plants whose effluents fail toxicity standards. The TREs require numerous and repeated toxicity assays, thus favoring application of microbioassays. Presently, no single microbioassay can detect all categories of environmental toxicants with equal sensitivity. Therefore, a battery of tests approach is recommended. The differential sensitivity of alternative tests may, in fact, be exploited. Further research is needed to construct strains of genetically engineered microorganisms or isolate microorganisms or enzymes that respond to specific classes of toxicants. These can be combined into batteries appropriate for different environments or test objectives.
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PMID:Bacterial and enzymatic bioassays for toxicity testing in the environment. 150 75

Trace levels of urethane, a cancer causing chemical, were detected in many kinds of wine, sherry, whisky, brandy and sake. Urethane formation from urea and ethanol in sake can be prevented by the treatment of acid urease, which is produced by Lactobacillus fermentum, but urethane, once formed, is very difficult to decompose. In order to keep the safety of alcoholic beverages, enzymatic removal of urethane has become an urgent problem. We found that Bacillus licheniformis sp., isolated from mouse gastrointestine, decomposed urethane to ethanol and ammonia. The enzyme showed higher urethanase activity at an acidic condition than at a neutral condition, and was resistant against ethyl alcohol of high concentrations. However, the enzyme had a low affinity to urethane for the industrial removal of the compound from alcoholic beverages.
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PMID:Urethanase of Bacillus licheniformis sp. isolated from mouse gastrointestine. 181 24

The anaerobic microflora of infected pulp cavities and chronic periapical abscesses was studied. A total of 19 infected nonvital teeth were subjected to this study. The coronal surface was swabbed with 70% ethanol to remove debris and to disinfect. Material in root canal chamber was obtained by sterilized paper points and suspended in reduced transport fluid. The samples were dispersed, diluted, and inoculated on blood agar plates. Isolates were identified by colony characteristics and cellular morphology, fermentation, indole production, nitrate reduction, gelatin digestion, urease production, ability to grow aerobically, API 20A System, and API ZYM System. Anaerobic bacteria were found in 14 pulp cavities. Anaerobic gram-negative rods, Actinomyces species, and Propionibacterium species were predominant in the root canals. Mixed infection with anaerobes and facultative anaerobes were demonstrated in most of the pulpal cavities of nonvital teeth.
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PMID:Isolation and classification of anaerobic bacteria from pulp cavities of nonvital teeth in man. 181 49

A plaque growth chamber was developed for long-term growth of five separate plaques from the same plaque or saliva sample under identical conditions of temperature and gas phase. Reagent addition and growth conditions for each plaque could be independently controlled, and each was accessible for sequential sampling and electrode insertion. Plaques were cultured for over six weeks on pellicle-coated Lux (TM) 25-mm diameter cover-slips at 35 degrees C under 5% CO2 in N2, and supplied with a medium containing 0.25% mucin (BMM) at 3.6 mL/h, and with periodic 5% sucrose. Electron microscopy and flora analysis of microcosm plaques showed that they had close similarities to reported characteristics of natural dental plaques. Diverse motile bacteria were present. Sucrose-induced Stephan pH curves and urea-induced pH rises were also similar to those reported for natural plaques. Changes in plaque urease, calcium, phosphate concentrations, and the flora were followed over five weeks in a plaque supplied with BMM containing additional 2.5 mmol/L calcium and 7.5 mmol/L phosphate. Despite this high environmental calcium phosphate concentration, there was no continuing increase in calcium levels, although plaque phosphate doubled. Urease levels fluctuated. Changes in the cultivable flora were minor. A urea-containing calcium phosphate/mono-fluorophosphate pH 5 solution, applied for six min every two h for seven days, increased plaque calcium, phosphate, and fluoride to high levels. Thus, plaques grown over several weeks in the multi-station artificial mouth exhibited metabolic and pH behavior typical of natural plaques, could be analyzed during development, and the system allowed manipulation of environmental variables important in plaque pH control and calcification.
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PMID:A multi-station dental plaque microcosm (artificial mouth) for the study of plaque growth, metabolism, pH, and mineralization. 196 Feb 50

Helicobacter pylori (H. pylori), ex-Campylobacter pylori, is now considered to be the causative agent of active chronic gastritis in humans and may be diagnosed by histology, gram-stain, culture, urease test or noninvasively by 14C-urea breath test. The aim of this study was to determine the sensitivity, specificity, and reproducibility of the breath test as compared with the microbiological (culture) "gold standard". Forty-one subjects were studied. Gastroscopy was performed in all participants and 2 antral mucosa biopsy specimens were taken for urease test and microbiological (gram-stain and culture) studies. The breath test was performed within one week after the gastroscopy. After fasting overnight, a control breath sample was obtained and a standard meal was offered to delay gastric emptying. Then, the participants drank 5 microCi of 14C-urea in 20 ml of water and breath samples were collected at 10, 15, 30 and 60 min in a hyamine-ethanol solution with a p-H indicator. A repeat test was performed in 9 subjects to assess test reproducibility. Twenty-nine subjects (71 percent) were Hp positive and 12 (29 percent) H. pylori negative. A highly significant difference (p less than 0.0001) was observed in 14CO2 exhalation in colonized and non-colonized subjects in samples collected at all times studied. As compared with culture we found that the breath test was 97 percent sensitive and 100 percent specific. We conclude that 14C-urea breath test is a simple, inexpensive, sensitive, and reliable method to detect H. pylori colonization. It is a useful test to epidemiologic and therapeutic trials.
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PMID:[14C-urea breath test to diagnose gastric Helicobacter pylori colonization]. 227 58

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.
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PMID:Orotic acid, arginine, and hepatotoxicity. 352 4

1. Yeast alcohol dehydrogenase was used to determine ethanol in the portal and hepatic veins and in the contents of the alimentary canal of rats given a diet free from ethanol. Measurable amounts of a substance behaving like ethanol were found. Its rate of interaction with yeast alcohol dehydrogenase and its volatility indicate that the substance measured was in fact ethanol. 2. The mean alcohol concentration in the portal blood of normal rats was 0.045mm. In the hepatic vein, inferior vena cava and aorta it was about 15 times lower. 3. The contents of all sections of the alimentary canal contained measurable amounts of ethanol. The highest values (average 3.7mm) were found in the stomach. 4. Infusion of pyrazole (an inhibitor of alcohol dehydrogenase) raised the alcohol concentration in the portal vein 10-fold and almost removed the difference between portal and hepatic venous blood. 5. Addition of antibiotics to the food diminished the ethanol concentration of the portal blood to less than one-quarter and that of the stomach contents to less than one-fortieth. 6. The concentration of alcohol in the alimentary canal and in the portal blood of germ-free rats was much decreased, to less than one-tenth in the alimentary canal and to one-third in the portal blood, but detectable quantities remained. These are likely to arise from acetaldehyde formed by the normal pathways of degradation of threonine, deoxyribose phosphate and beta-alanine. 7. The results indicate that significant amounts of alcohol are normally formed in the gastro-intestinal tract. The alcohol is absorbed into the circulation and almost quantitatively removed by the liver. Thus the function, or a major function, of liver alcohol dehydrogenase is the detoxication of ethanol normally present. 8. The alcohol concentration in the stomach of alloxan-diabetic rats was increased about 8-fold. 9. The activity of liver alcohol dehydrogenase is generally lower in carnivores than in herbivores and omnivores, but there is no strict parallelism between the capacity of liver alcohol dehydrogenase and dietary habit. 10. The activity of alcohol dehydrogenase of gastric mucosa was much decreased in two out of the three germ-free rats tested. This is taken to indicate that the enzyme, like gastric urease, may be of microbial origin. 11. When the body was flooded with ethanol by the addition of 10% ethanol to the drinking water the alcohol concentration in the portal vein rose to 15mm and only a few percent of the incoming ethanol was cleared by the liver.
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PMID:The physiological role of liver alcohol dehydrogenase. 548 98


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