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)

Lorazepam and oxazepam in plasma and urine were measured by gas chromatography-mass spectrometry. Oxazepam was used as an internal standard in the assay of lorazepam and vice versa. After removal of interfering substances with n-hexane, the drugs were extracted with benzene and converted to N1,O3-bistrimethylsilyl derivatives. Glucuronide forms of the drugs were extracted after hydrolysis with beta-glucuronidase. A common fragment ion at m/e 429 was used to monitor the two drugs. The sensitivity was 2 ng/ml for both drugs, which was sufficient to determine plasma and urine concentrations after therapeutic doses to humans.
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PMID:Simplified determination of lorazepam and oxazepam in biological fluids by gas chromatography-mass spectrometry. 4 99

Chronic exposure to benzene results in rats in the decrease of the lymphocyte count in the peripheral blood, the decrease of the beta-glucuronidase (BG) activity both in lymphocytes and neutrophilic granulocytes as well as in the damage to lysosomal apparatus of lymphocytes expressed in diffusion of the enzyme within the cell cytoplasm. Administration of selenium (sodium selenate) in dosis of 1.0 microgram/Kg during consecutive 10 days prior the exposure to benzene resulted in prevention of benzene-induced decrease of the BG activity in granulocytes and of a damage to lymphocyte lysosomes. Application of selenium in dosis of 5.0 microgram/Kg during the same time prior the exposure to benzene prevented the benzene-induced lymphocytopenia, induced the reactive increase of the granulocyte number, and caused, moreover, the prevention of the BG activity decrease in granulocytes. Simultaneously the increase of the BG-positive lymphocyte percentage was noted which was related to the increase of cells exhibiting the cytoplasmatic and extralysosomal localization of the enzyme. The results suggest that only smaller doses of sodium selenate prevented the damage to lysosomal membrane of lymphocytes induced by toxic effect of benzene.
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PMID:Activity of lysosomal beta-glucuronidase in leukocytes of rats exposed to benzene and sodium selenate. 7 28

Radiolabeled diethylstilbestrol (DES) was administered to one pregnant and three normal female rhesus monkeys. One normal female chimpanzee was also included in the study. Regardless of the mode of presentation (oral versus intravenous), the urine was the principal route of excretion for each species. The urine contained no non-polar radioactivity, and Sephadex LH-20 (MeOH/EtOH-50:50) resolved the radioactivity into five fractions (A, B, C, D, E). Fractions A,B, C, and D were hydrolyzable with beta-glucuronidase, and the principal aglycones were identified with GC/MS as cis-trans DES and dienestrol. The fecal excretory products were extracted with dimethoxy methane/methanol (50:50) and the radioactivity partitioned between benzene and H2O. The polar radioactivity was resolved by LH-20 (MeOH/EtOH-50:50) into chromatographic fractions similar to the urinary conjugates. These fecal conjugates were, however, less sensitive to beta-glucuronidase hydrolysis. The primary non-polar fecal radioactivity was chromatographically similar to DES (LH-20 and HPLC) in both species, and in the rhesus monkey the principal products identified were cis-trans DES and dienestrol.
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PMID:The metabolism of diethylstilbestrol in the rhesus monkey and chimpanzee. 10 73

A radioimmunoassay for the measurement of both unconjugated and conjugaged estetrol in plasma has been developed. The antiserum obtained after 6 months of immunization with 6-oxoestetrol-6-(O-carboxy-methyl)oxim-BSA was used at a final dilution of 1:90,000 and showed almost no cross reaction with other steroids except for estriol at 1.24%. Esterol-glucosiduronate was synthesized by incubating with adrenalectomized rat liver homogenate and uridine diphosphoglucuronic acid. Then, plasma estetrol-glucosiduronate was measured in the same manner for unconjugated estetrol after hydrolysis with beta-glucuronidase. Sephadex LH-20 column chromatography (7X110 mm, benzene:methanol, 85:15) was employed for accurate assessment. The sensitivity was 10 pg and the smallest amount measurable was 40 pg/sample. The method bland was consistently negligible. The intra and inter assay precision was 11.8% and 14.2% for unconjugated estetrol and that for estetrol-glucosiduronate was 13.5% and 17.1%.
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PMID:A radioimmunoassay of plasma unconjugated and conjugated estetrol. 20 82

In workers, aged 26--55, occupationally exposed for 80--118 months to organic solvents of paints and varnishes containing benzene, toluene and xylene, beta-glucuronidase (GR) and N-acetyl-beta-glucosaminidase (GZ activities were determined and glycogen content in peripheral blood lymphocytes was evaluated. In addition to lymphocytopenia, the number of lymphocytes with cytoplasmic localization of GR and GZ and a decrease in glycogen content in those cells were found. The authors suppose these changes are due to toxic effects of aromatic hydrocarbons, present in organic solvents of paints and varnishes, upon lymphocytes.
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PMID:[Cytochemical and immunological examinations of workers exposed to the effects of organic solvents of paints and varnishes. I. Activity of beta-glucuronidase and N-acetyl-beta-glucosaminidase. Glycogen content in lymphocytes]. 51 70

Mephenoxalone (5-(o-methoxyphenoxymethyl)-2-oxazolidone) is degraded by various routes in the human, and some is excreted unchanged. In the metabolism of mephenoxalone, the phenoxymethyl ether bond is cleaved; thus o-methoxyphenol (metabolite I) was identified in urine, and 3-amino-1,2-propanediol (IIa) was found after alkaline hydrolysis. Hydroxylation of the benzene ring produces a phenolic hydroxymephenoxalone (metabolite III), and demethylation converts mephenoxalone into demethylmepheonxalone (metabolite IV). Opening of the oxazolidone ring leads to the production of 1-(o-methoxyphenoxy)-3-aminopropane-2-ol(metabolite V). Urine contains two further substances: 1-(o-hydroxyphenoxy)-3-aminopropene (metabolite VI) and dehydromephenoxalone (metabolite VII). Metabolite VI may be an artefact. Compounds III, IV and VII could only be detected after acid hydrolysis and enzymic cleavage with beta-glucuronidase/aryl sulphatase, whereas V and VI were detected only after acid hydrolysis. Thin layer chromatography revealed three further metabolites, which were not identified.
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PMID:[Isolation and identification of some metabolites of mephenoxalone (Control-OM) from human urine (author's transl)]. 57 73

Initial excretion studies with orally administered [monoethyl-1-3H] DES demonstrated the feces to be the principal mode of elimination of DES in the C3H mouse. Metabolic studies with tritiated DES and/or [UL-14C] DES were performed with orally dosed C3H high (MTV+) and low (MTV-) titer MMTV female mice. Extraction and partitioning of the fecal radioactivity demonstrated 77 to 86% (n = 4) to be benzene soluble and the remainder H2O soluble. The principal product in the organic phase following Sephadex LH-20 and HPLC purification was DES. The aqueous phase was resolved by LH-20 into two conjugate fractions that were partially hydrolyzed by beta-glucuronidase. The principal aglycone was chromatographically identical with authentic DES. The urinary conjugates were resolved into six fractions. The four major fractions were 80% hydrolyzable with beta-glucuronidase. Two of these fractions had trans-DES as the principal aglycone, whereas the other two had a major peak similar to but not chromatographically coincident with cis-DES. In certain experiments mice were sequentially dosed with tritium (24 hr) followed by a 14C dose (24 hr). Two mice (MTV+) were also previously fed 1000 ppb DES prior to these experiments. The tritated and 14C products were combined and analyzed simultaneously. This experiment did not reveal significant differences in the metabolism due to the modes of radioactive labeling, MMTV titer, or the prior feeding of DES. The developed methodology was judged to purify quantitatively 90% or more of the DES radioactive products.
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PMID:Metabolism of diethylstilbestrol in the C3H mouse: chromatographic systems for the quantitative analysis of DES metabolic products. 66 80

The activity of some enzymes of neutrophils in peripheral blood of rats in subacute benzene vapour poisoning (an exposure to the concentration of benzene vapour of 27.000 mg/m3, 6 hr daily for 10 consecutive days) was determined cytochemically. Increase in the activity of alkaline phosphatase and decrease in that of acid hydrolases: acid phosphatase, beta-glucuronidase and beta-glucosaminidase were found. The results obtained indicate destructive action of benzene on lysosomes of peripheral blood neutrophils.
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PMID:Enzymatic changes in peripheral blood leukocytes in rats in subacute benzene vapours poisoning. II. The activity of neutrophils enzymes. 74 May 49

A quantitative GLC-mass spectrometric procedure was developed for the determination of phenacetin and its O-desethyl metabolite, acetaminophen, in human plasma. The assay utilizes selective ion detection to monitor, in a GLC effluent, the MH+ molecular ions of both phenacetin and the methyl derivative of acetaminophen, p-acetanisidine, generated by isobutane chemical ionization. Deuterated analogs of phenacetin and acetaminophen, phenacetin-d3 and acetaminophen-d3, respectively, are added to the plasma before extraction to serve as internal standards. To determine phenacetin and unconjugated acetaminophen, 1.0 ml of plasma is extracted with 5 ml of benzene-dichloroethane (7:3). The extraction solvent is removed, and the residue is methylated with diazomethane. Th solution is again evaporated to dryness, and the residue is reconstituted in ethyl acetate. A portion of this solution is then analyzed by GLC-mass spectrometry, with the mass spectrometer set to monitor m/e 166 (p-acetanisidine), 169 (p-acetanisidine-d3), 180 (phenacetin), and 183 (phenacetin-d3). To determine total acetaminophen, 0.1 ml of plasma is treated with a mixture of beta-glucuronidase and sulfatase, extracted with ethyl acetate, methylated, and analyzed by GLC-mass spectrometry. The procedure has a sensitivity limit of 1 ng of phenacetin/ml and 0.1 mug of acetaminophen/ml. The curves relating the amount of phenacetin and acetaminophen added versus the amount of phenacetin and acetaminophen found for 12 known phenacetin concentrations over the 9.9-246.6-ng/ml range and for 16 known acetaminophen concentrations over the 0.52-13.10-mug/ml range are straight lines with intercepts of nearly zero and with slopes of unity. Analyses of six separate plasma samples, each containing 25 ng of phenacetin/ml and 1.31 mug of acetaminophen/ml, had a precision of +/- ng/ml for phenacetin and +/- 0.08 mug/ml for acetaminophen.
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PMID:Quantitative determination of phenacetin and its metabolite acetaminophen by GLC-chemical ionization mass spectrometry. 84 98

The biotransformation of croconazole, a potent new antimycotic agent, was studied in the rabbit. Croconazole was excreted in the urine primarily as conjugates. Most of the radioactive metabolites in the urine could be extracted with organic solvent after hydrolysis with beta-glucuronidase. As many as 16 metabolites in the organic extracts were separated by TLC. Thirteen were identified by comparison of their mass and/or proton NMR spectra with those of synthetic samples. Aromatic ring hydroxylation of each benzene ring, O-dechlorobenzylation, and loss of the imidazole ring were found to occur.
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PMID:Metabolism of the antimycotic agent, croconazole, in rabbits. 256 15


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