Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hairless mouse epidermis was separated from the underlying dermis using a 2 h incubation in 20 mM ethylenediaminetetraacetic acid (EDTA). The basal epidermis, thus exposed, was then examined using scanning electron (SEM), transmission electron (TEM), and light microscopy (LM). Sheets were also stained for: (i) Langerhans cell adenosine triphosphatase (ATPase), beta-glucuronidase, and la antigens; and, (ii) melanocyte 3,4-dihydroxyphenylalanine (DOPA)-oxidase. A regular distribution of protruding dendritic cells was observed superficial to the basal epidermis. These external dendritic cells were identified as Langerhans cells on the basis of subcellular morphology and distribution in the TEM. ATPase staining was Langerhans cell specific. The Langerhans cell population in hairless mouse epidermis was large, and evenly distributed in the interfollicular epidermis and the outer root sheath of degenerate hair follicles. The melanocyte population, in comparison, was negligibly small (4-5 cells per mm2).
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PMID:The Langerhans cell in hairless mouse epidermis. 641 9

Activities of the neutrophil granule-associated proteins beta-glucuronidase, lysozyme and vitamin B12 binding protein were measured, serially, in the cells and serum of 10 patients undergoing total abdominal hysterectomy. The neutrophil leucocytosis which followed total abdominal hysterectomy was accompanied by a fall in the intraneutrophilic activities of all three granule-associated proteins. Intraneutrophilic lysozyme activity and intraneutrophilic vitamin B12 binding capacity were maximally reduced within 4 h of surgery and fell to 62 +/- 13% (mean +/- SEM) and 63 +/- 9% of their preoperative levels, respectively. This contrasted with the activity of intraneutrophilic beta-glucuronidase which was not maximally reduced until 24 h post-surgery when a fall to 80 +/- 6% of the preoperative level was observed. By the fifth postoperative day activities of the three intraneutrophilic granule proteins were increasing and approaching those observed preoperatively. Serum lysozyme and plasma unsaturated vitamin B12 binding capacity (UBBC) rose steadily following surgery and were significantly elevated by the fifth postoperative day. It is suggested that activation and in vivo degranulation of circulating neutrophils may be responsible for these changes in activity of neutrophil granule proteins following surgery.
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PMID:The effects of surgery on the activity of neutrophil granule proteins. 684 26

Arachidonate (1-300 microM) mobilized Ca2+ ions from an intracellular store and stimulated the entry of Ca2+ ions from the extracellular fluid in undifferentiated HL-60 cells that had been loaded with Fura-2. The integrated response was biphasic in form: arachidonate liberated Ca2+ ions from the intracellular store first, resulting in a transient increase in cytosolic free Ca2+ concentration ([Ca2+]i). Ca2+ entry from the extracellular fluid was not evident for a further 1-2 min. At baseline, [Ca2+]i was 48.1 +/- 14.0 nM (SEM, n = 5). Upon addition of arachidonate (100 microM), [Ca2+]i rose to a transient peak level of 217 +/- 38.6 nM (SEM, n = 5) and a later plateau level of 427 +/- 118 nM (SEM, n = 5). Removal of added Ca2+ ions from the extracellular fluid in the presence of EGTA (1.0 mM) had no effect on the initial transient response but abolished the second phase of the response. In HL-60 cells that had been loaded with BAPTA/AM, the initial transient phase of the response was abolished but the elevation in [Ca2+]i due to Ca2+ entry from the extracellular fluid was unaffected. Undifferentiated HL-60 cells also responded to arachidonate (100 microM) with an increase in the release of the lysosomal enzyme beta-glucuronidase. Arachidonate-induced beta-glucuronidase release from BAPTA-loaded cells or in control cells exposed to Ca(2+)-free solutions was inhibited by about 50%. In BAPTA-loaded cells that were incubated with Ca(2+)-free solutions, arachidonate-induced beta-glucuronidase release was inhibited by about 90%. Leukotriene B4 failed to elevate [Ca2+]i in the concentration range 0.01-1 microM and failed to activate beta-glucuronidase release in concentrations up to 10 microM. Furthermore, the cyclo-oxygenase/lipoxygenase inhibitor ETYA (100 microM) was without effect on secretion. Consistent with this finding, we found that a large number of unsaturated fatty acids could reproduce the effect of arachidonate on [Ca2+]i and beta-glucuronidase release. Fatty acids belonging to the omega-3, omega-6 and omega-7 unsaturated fatty acid families were effective in elevating [Ca2+]i and stimulating beta-glucuronidase release. However, three unsaturated fatty acids, all belonging to the omega-9 fatty acid family, were ineffective.
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PMID:Arachidonate and other fatty acids mobilize Ca2+ ions and stimulate beta-glucuronidase release in a Ca(2+)-dependent fashion from undifferentiated HL-60 cells. 852 54

Codeine and morphine pharmacokinetics among different CYP2D6 genotypes was compared in this study. Polymerase chain reaction tests were used to determine CYP2D6 genotypes in leukocyte deoxyribonucleic acid in 32 unrelated volunteers. Based on the genotypes, subjects were categorized into three groups: homozygous C/C188 (n = 8), heterozygous C/T188 (n = 12), and homozygous T/T188 (n = 12). Each subject was given a single oral dose of 30 mg codeine phosphate tablet after overnight fasting. Plasma concentration of codeine and 24-hour urinary morphine recovery were measured with HPLC. All three genotypes of subjects showed almost identical time profiles of plasma codeine. Urinary morphine glucuronide was hydrolyzed with beta-glucuronidase. The total recovered amount of morphine and glucuronides was 4349 +/- 646, 2564 +/- 242, and 1127 +/- 164 nmol (mean +/- SEM), respectively, for C/C188, C/T188, and T/T188 subjects (p < 0.05). The significant lower amount of urinary morphine but identical codeine plasma concentration suggested a lower partial clearance of the formation of morphine from codeine in T/T188 subjects. The results suggest a future study to assess the analgesic effect of codeine in different genotypes of CYP2D6 extensive metabolizers.
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PMID:Formation of morphine from codeine in Chinese subjects of different CYP2D6 genotypes. 882 35

The present study examined the degradation behaviour of poly(beta-hydroxy octanoate) (PHO), a bacterial poly(beta-hydroxy alkanoate), following incubation under hydrolytic or enzymatic conditions in vitro. Solution-cast PHO films were incubated in a citrate buffer solution with and without acid phosphatase and in an acetate buffer with and without beta-glucuronidase for periods ranging from 7 to 60 days. The physical characterization of the PHO films was analyzed by SEM and tensile strength studies. In addition, various analytical methods were used to detect modifications in the chemical and morphological structure of the PHO, namely, ESCA, FTIR, DSC, X-ray diffraction, and SEC. The results indicate that the enzymatic conditions selected in the present study induced no significant surface morphological or chemical modifications, and no significant weight loss was observed after 60 days of incubation. However, as revealed by weight average molecular weight Mw and number average molecular weight Mn decreases, changes in the bulk structure of the PHO were observed with acid phosphatase at 28 and 60 days, in contrast to smaller Mw and Mn decreases recorded in both the buffers and the beta-glucuronidase. The tensile properties had decreased following incubation, yet showed no difference under all of the selected conditions. With no weight loss or surface changes, the PHO films incubated in acid phosphatase showed only a chemical hydrolytic process characterized by Mw and Mn decreases with time of incubation. The present study demonstrated that the degradation of PHO films is one of slow, chemical hydrolysis only, perhaps requiring several months of incubation. The hydrophobic nature of the long alkyl pendent chain in PHO may be responsible for this slow process. The inability of enzymes to degrade PHO may be attributed to the latter's poor adsorption capacity, due to its hydrophobic nature, and to a lack of specificity in the catalytic activity of these enzymes.
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PMID:Hydrolytic and enzymatic incubation of polyhydroxyoctanoate (PHO): a short-term in vitro study of a degradable bacterial polyester. 1022 69

Little is known about flavonoid metabolism and excretion in man. In the present study, the urinary excretion of a major flavonoid in wine, catechin, and its metabolites, were measured after nine human subjects each consumed 120 ml red wine (RW) on one day and de-alcoholized red wine (DRW) on a separate day. Both the RW and DRW contained 120 (SEM 3) micromol catechin (35 mg). GC-MS analyses of the trimethylsilylated derivatives of catechin and 3' and 4' methylcatechin were performed before and after hydrolysis of conjugates by beta-glucuronidase and sulfatase. Baseline urine samples collected prior to wine consumption contained 0.013 (SEM 0.005) micromol catechin and metabolites. During the 8 h period following consumption of RW and DRW, 6.6 (SEM 0.9) and 5.3 (SEM 0.6) micromol catechin and metabolites were excreted in 893 (SEM 94) and 740 (SEM 101) ml urine respectively. This corresponded to 3.0-10.3% of the dose after RW and 2.1-8.2% of the dose after DRW. The amount of catechin and metabolites excreted in urine was 20% higher after RW compared with DRW (P=0.06). Catechin in all urine samples was present as metabolites and there were no differences in the proportions of individual metabolites after RW and DRW. As with other flavonoids, the fate of most ingested catechin is not yet known.
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PMID:Urinary excretion of catechin metabolites by human subjects after red wine consumption. 1189 12

Beta-glucuronidase hydrolyzes glucuronide moieties from steroids and xenobiotics, such that circulating glucuronyl conjugates can interact with target tissues. In animal models, dietary constituents can alter beta-glucuronidase activity. In humans, serum beta-glucuronidase activity reflects liver enzyme loss during cell turnover, and thus is a surrogate for hepatic beta-glucuronidase. We recruited 83 men and 120 women, who were nonsmokers, 20-40 y of age, with self-reported vegetable and fruit (V&F) intakes of < or = 2.5 or > or = 4.5 servings/d. Diet was assessed by 3-d food record and serum carotenoids were measured as biomarkers of V&F intake (e.g., servings V&F vs. alpha-carotene; r = 0.47, P = 0.0001). Serum beta-glucuronidase activity (Modified Sigma Units/L), determined in blood samples collected on two consecutive days from fasting subjects, was higher in men than women (mean +/- SEM: 20.4 x 10(3) +/- 1.0 x10(3) and 17.0 x 10(3) +/- 0.6 x 10(3), P = 0.002). beta-Glucuronidase activity (adjusted for sex) was inversely associated with intakes of plant protein, fruit, dietary fiber (r = -0.24 to -0.30; P < 0.001), botanical groupings Cucurbitaceae, Rosaceae, and Leguminosae (r = -0.16 to -0.19; P < 0.05), and serum alpha- and beta-carotene and beta-cryptoxanthin (r = -0.18 to -0.26; P < or = 0.01). Activity was not associated with overall vegetable intake. Although these associations are modest, the data suggest that plant foods, particularly constituents of fruits and fiber-containing foods, may influence human beta-glucuronidase activity in a potentially favorable direction.
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PMID:Serum beta-glucuronidase activity is inversely associated with plant-food intakes in humans. 1204 56

1: The use of fluorine-19 nuclear magnetic resonance (19F-NMR) and gas chromatography-electron capture detection (GC-ECD) in the analysis of fluorine-containing products in the urine of sevoflurane-exposed patients was explored. 2: Ten patients were anaesthetized by sevoflurane for 135-660 min at a flow rate of 6 l min(-1). Urine samples were collected before, directly after and 24 h after discontinuation of anaesthesia. 3: 19F-NMR analysis of the urines showed the presence of several fluorine-containing metabolites. The main oxidative metabolite, hexafluoroisopropanol (HFIP)-glucuronide, showed two strong quartet signals in the 19F-NMR spectrum. HFIP concentrations after beta-glucuronidase treatment were quantified by (19)F-nuclear magnetic resonance. Concentrations directly after and 24 h after discontinuation of anaesthesia were 131 +/- 41 (mean +/- SEM) and 61 +/- 19 mol mg(-1) creatinine, respectively. Urinary HFIP excretions correlated with sevoflurane exposure. 4: Longer scanning times enabled the measurement of signals from two compound A-derived metabolites, i.e. compound A mercapturic acid I (CAMA-I) and compound A mercapturic acid II (CAMA-II), as well as products from beta-lyase activation of the respective cysteine conjugates of compound A. The signals of the mercapturic acids, 3,3,3-trifluoro-2-(fluoromethoxy)-propanoic acid and 3,3,3-trifluorolactic acid were visible after combining and concentrating the patient urines. CAMA-I and -II excretions in patients were completed after 24 h. 5: Since 19F-nuclear magnetic resonance is not sensitive enough, urinary mercapturic acids concentrations were quantified by gas chromatography-electron capture detection. CAMA-I and -II urinary concentrations were 2.3 +/- 0.7 and 1.4 +/- 0.4 mol mg(-1) creatinine, respectively. Urinary excretion of CAMA-I showed a correlation with sevoflurane exposure, whereas CAMA-II did not. 6. The results show that 19F-nuclear magnetic resonance is a very selective and convenient technique to detect and quantify HFIP in non-concentrated human urine. 19F-nuclear magnetic resonance can also be used to monitor the oxidative biotransformation of sevoflurane in anaesthetized patients. Compound A-derived mercapturic acids and 3,3,3-trifluoro-2-(fluoromethoxy)-propanoic acid and 3,3,3-trifluorolactic acid, however, require more sensitive techniques such as gas chromatography-electron capture detection and/or gas chromatography-mass spectrometry for quantification.
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PMID:Use of 19F-nuclear magnetic resonance and gas chromatography-electron capture detection in the quantitative analysis of fluorine-containing metabolites in urine of sevoflurane-anaesthetized patients. 1520 1


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