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

An improved method for the simultaneous gas-chromatographic determination of individual 17-oxosteroids and of pregnanediol in the same sample of urine is described. The method involves the following steps. The urinary sample is chromatographed on Amberlite XAD-2. The fraction containing the steroid conjugates is evaporated; the residue is dissolved in n-heptane and the organic phase extracted with water. The steroid glucuronides are hydrolysed by a bacterial beta-glucuronidase; subsequently, the steroid sulphates are solvolysed in ethyl acetate. Free 17-oxosteroids and pregnanediol are separated by two-dimensional thin-layer chromatography. The zone containing the steroids to be investigated is eluted; after evaporation, the residue is treat with N-methyl N-trimethyl silyl trifluoroacetamide. The reaction mixture is injected into a gas chromatograph; the trimethyl silyl ethers of the individual 17-oxosteroids and of pregnanediol are quantitated by measuring the peak heights.
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PMID:An improved method for the simultaneous determination of individual 17-oxosteroids and of pregnanediol in urine by gas-liquid chromatography. 86 85

Cyclophellitol [1S,2R,3S,4R,5R,6R)-5-hydroxymethyl-7-oxabicyclo[4,1,0] heptane-2,3,4-triol) was tested against 9 glycosidases and found to be a specific inhibitor of almond beta-glucosidase. Cyclophellitol inhibited almond beta-glucosidase activity by 50% at 0.8 micrograms/ml and was a competitive inhibitor of almond beta-glucosidase as revealed by Lineweaver-Burk plot. Cyclophellitol was inactive against yeast alpha-glucosidase, beta-galactosidase, beta-glucuronidase, alpha-L-fucosidase, end-beta-N-acetyl glucosaminidase, alpha-mannosidase, and cellulase. It was weakly active toward fungal beta-xylosidase. Cyclophellitol-treated almond beta-glucosidase was equally suppressed after dialysis; thus cyclophellitol is likely to bind to almond beta-glucosidase irreversibly. The inhibitor was found by fluorimetric assay to be active against beta-glucosidase but inactive toward alpha-glucosidase in Molt-4 microsomal fraction. It also inhibited Molt-4 beta-glucocerebrosidase completely at 2 micrograms/ml when the enzyme was assayed with a synthetic labeled substrate, and the inhibitory activity was more than one hundred times higher than that of nojirimycin, castanospermine, or of deoxynojirimycin. Mice administered 1 mg of cyclophellitol daily for 5 days began to exhibit severe abnormalities of nervous system similar to those found in Gaucher's mouse.
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PMID:Biological activities of cyclophellitol. 214 35

Urine from sawmill workers exposed to alpha-pinene, beta-pinene and delta-3-carene was collected and hydrolyzed with beta-glucuronidase at pH 5.0 for 24 h at 37 degrees C. After hydrolysis the urine was cleaned on a SEP-PAK C18 cartridge. The cartridge was eluted with n-heptane. The eluate was injected onto a gas chromatograph equipped with a 25-m (0.32-mm ID) SP-1000 capillary column. The major peak in the chromatogram was identified by GC-MS as trans-verbenol by electron impact at 70 eV. cis-Verbenol was also identified. These metabolites could not be detected in non-hydrolyzed urine from the exposed workers or in hydrolyzed urine from an unexposed individual. The recoveries of the verbenols from hydrolyzed urine were in the range of 85 to 94% and the metabolites were stable both in urine and in n-heptane after sample cleaning at -20 degrees C for at least 12 weeks. We suggest that these metabolites are formed from alpha-pinene by hydroxylation.
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PMID:Identification of cis- and trans-verbenol in human urine after occupational exposure to terpenes. 222 58

A sensitive capillary electrophoretic method was developed and validated for the simultaneous determination of dextromethorphan and its metabolites, dextrorphan, 3-hydroxymorphinan, and 3-methoxymorphinan, in human plasma. After cleavage of conjugates by enzymatic hydrolysis with beta-glucuronidase, dextromethorphan and its metabolites were extracted from 1.5 ml of plasma by a liquid liquid extraction procedure using heptane-ethylacetate (50:50, v/v) and re-extracted to aqueous phase. The compounds were separated within 8 min on a fused silica capillary, 75 microm internal diameter using sodium borate (pH 9.4; 50 mM) as running buffer, and measured by UV-detection at 195 nm using a detection cell with a path length of 1.2 mm. The method was accurate and precise. Linear relationships were observed between the peak response and the concentration in the range of 1-400 ng ml(-1) plasma with correlation coefficients above 0.998. The limit of detection was 0.5-1 ng ml(-1) plasma for all compounds. The method was used for determination of plasma levels of dextromethorphan and its metabolites after transdermal and oral administration of dextromethorphan.
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PMID:Simultaneous determination of dextromethorphan and its metabolites in human plasma by capillary electrophoresis. 991 85

Increasing evidence suggests that a continuous release of histamine from mast cells occurs in the airways of asthmatic patients and that histamine may modulate functions of other inflammatory cells such as macrophages. In the present study histamine (10(-9)-10(-6) M) increased in a concentration-dependent fashion the basal release of beta-glucuronidase (EC(50) = 8.2 +/- 3.5 x 10(-9) M) and IL-6 (EC(50) = 9.3 +/- 2.9 x 10(-8) M) from human lung macrophages. Enhancement of beta-glucuronidase release induced by histamine was evident after 30 min and peaked at 90 min, whereas that of IL-6 required 2-6 h of incubation. These effects were reproduced by the H(1) agonist (6-[2-(4-imidazolyl)ethylamino]-N-(4-trifluoromethylphenyl)heptane carboxamide but not by the H(2) agonist dimaprit. Furthermore, histamine induced a concentration-dependent increase of intracellular Ca(2+) concentrations ([Ca(2+)](i)) that followed three types of response, one characterized by a rapid increase, a second in which [Ca(2+)](i) displays a slow but progressive increase, and a third characterized by an oscillatory pattern. Histamine-induced beta-glucuronidase and IL-6 release and [Ca(2+)](i) elevation were inhibited by the selective H(1) antagonist fexofenadine (10(-7)-10(-4) M), but not by the H(2) antagonist ranitidine. Inhibition of histamine-induced beta-glucuronidase and IL-6 release by fexofenadine was concentration dependent and displayed the characteristics of a competitive antagonism (K(d) = 89 nM). These data demonstrate that histamine induces exocytosis and IL-6 production from human macrophages by activating H(1) receptor and by increasing [Ca(2+)](i) and they suggest that histamine may play a relevant role in the long-term sustainment of allergic inflammation in the airways.
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PMID:Histamine induces exocytosis and IL-6 production from human lung macrophages through interaction with H1 receptors. 1123 57