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:3.2.1.31 (beta-glucuronidase)
7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolism of [3H]benzo[a]pyrene (BP) and (-)-trans-[14C]7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene (BP-7,8-diol) was studied in freshly isolated hepatocytes of the wild benthic fish, brown bullhead (Ictalurus nebulosus). Bullhead hepatocytes incubated with 40 microM [3H]BP for 1 h metabolized BP to water soluble metabolites which were separated on silica gel t.l.c. plates to reveal conjugates with glucuronic acid, glutathione, and sulfate (51%, 14% and 4% of total metabolites, respectively). Additional metabolites that were extractable with ethyl acetate were separated by reversed phase HPLC to reveal only two major metabolites: BP-9,10-dihydrodiol and BP-7,8-diol (13% and 2.6% of total metabolites, respectively). Hepatocytes isolated from individual fish displayed an 11-fold variability in the rates at which they metabolized BP (756 +/- 167 pmol x mg dry wt-1 x h-1), which correlated negatively (r = -0.7, P less than 0.01) with an 18-fold variability in the glycogen content of the cells. Hepatocytes isolated from the same fish, in parallel incubations under the same optimum conditions, metabolized BP-7,8-diol 4.5-fold faster than they metabolized BP. The variability in the rate of BP-7,8-diol metabolism was about 7-fold. Major metabolites included glutathione conjugates, glucuronides and sulfates (35%, 25% and 30% of total metabolites, respectively). These conjugates, like those formed from BP, were degradable with gamma-glutamyltransferase, beta-glucuronidase and arylsulfatase, respectively. Ethyl acetate extractable metabolites were predominantly isomeric benzo-ring tetrahydrotetrols (9% of total metabolites). In summary, this study indicates that during short-term incubations bull-head hepatocytes metabolize BP and BP-7,8-diol primarily to conjugated derivatives. The usefulness of thin-layer chromatography for the convenient determination of the rate of BP-7,8-diol metabolism is demonstrated.
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PMID:Metabolism of benzo[a]pyrene and (-)-trans-benzo[a]pyrene-7,8-dihydrodiol by freshly isolated hepatocytes of brown bullheads. 232 50

1. 3H-Dibenz[a,j]acridine (DBAJAC) metabolism occurred readily in vitro in incubations with hepatocytes from phenobarbital-pretreated, 3-methylcholanthrene-pretreated and untreated rats, with the formation of water-soluble conjugates and unconjugated metabolites. 2. For incubations of 3H-DBAJAC with hepatocytes the major organic solvent-soluble metabolites found with and without beta-glucuronidase/arylsulphatase hydrolysis were the phenols, 3-hydroxy-DBAJAC, and 4-hydroxy-DBAJAC, and the proposed proximate carcinogen, trans-3,4-dihydroxy-3,4-dihydro-DBAJAC. The latter comprised 34-66% of the total organic solvent-soluble metabolites. 3. In contrast to results previously reported for rat hepatic microsomes, the K-region 5,6-oxide, and its dihydrodiol were minor metabolites detected after hepatocyte incubations. 4. Faecal excretion accounted for the bulk of radioactivity after i.p. doses of 3H-DBAJAC (0.5 mg/kg), and i.v. doses (0.5 mg/kg) were rapidly excreted into the 6 h bile. The organic solvent-soluble fraction obtained after enzymic hydrolysis of bile (approximately 25% of excreted radioactivity) was subjected to h.p.l.c. It contained polar secondary oxidation products and virtually no 3,4-dihydrodiol. 5. Experiments conducted with greater hepatocyte densities (10(7) cells/ml) and longer incubation times showed increased extents of metabolism, DNA and protein binding of radioactivity which paralleled the extent of metabolism. Very considerable metabolism of the 3,4-dihydrodiol occurred by the end of the incubation period.
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PMID:The metabolism of the carcinogen dibenz[a,j]acridine in isolated rat hepatocytes and in vivo in rats. 234 5

Extensive studies of gene expression programs in carrot somatic embryos identified a gene, designated Dc3, that serves as a reliable molecular marker for the acquisition of embryogenic potential by carrot cells in culture. The complete sequence of a carrot genomic region, DcG3, encoding a Dc3-like mRNA, was determined. The DcG3 transcription unit contains a single intron and encodes mRNA that is expressed at high levels in embryonic tissue but is undetectable in somatic tissue of carrot. The predicted protein sequence of DcG3 is 163 amino acids and includes two approximately 50 amino acid direct repeats which in turn include additional repetitive elements with an unusual distribution of charged amino acids. Dc3 and Dc3-like mRNAs are encoded by a small divergent gene family. Furthermore, similarities of the Dc3 gene family with genes from other plant species that are expressed in response to environmental and developmental cues suggest a possible role in seed desiccation and possibly in more general water-stress responses in plants. Analysis of transgenic tobacco containing a beta-glucuronidase (GUS) reporter gene fused to a 1.7 kb 5' upstream element of DcG3 defined a promoter/enhancer complex that confers developmentally and environmentally regulated expression of GUS activity. Thus, DcG3 is phylogenetically conserved together with the trans-acting factors required for its regulated expression in transgenic tobacco.
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PMID:Molecular analysis of a phylogenetically conserved carrot gene: developmental and environmental regulation. 236 35

Current information suggests that arachidonic acid metabolites are involved in the development of cholecystitis. The purpose of this study was to evaluate eicosanoid formation during the development of experimental cholecystitis in cats. Lysophosphatidylcholine is found in the gallbladders of patients with cholecystitis and is known to be a cytolytic, membrane-damaging substance. Anesthetized cats underwent gallbladder perfusion with and without 1.5 mmol/L lysophosphatidylcholine. Additional experiments were performed when calcium ionophore were added to the perfusates and experiments were performed when cats were treated with indomethacin and underwent perfusion with lysophosphatidylcholine. Changes in the gallbladder were determined by evaluating mucosal water transport as measured by determining the changes in concentration in a nonabsorbable marker, by protein secretion and by beta-glucuronidase accumulation in gallbladder tissue as an index of inflammation. Eicosanoid formation was evaluated by measuring perfusate concentrations and gallbladder homogenate concentrations by radioimmunoassay of prostaglandin E, 6 keto prostaglandin F1 alpha, leukotriene B4 and leukotriene C4. Lysophosphatidylcholine perfusion reversed the control patterns of absorption and produced water exsorption, produced an efflux of protein into the perfusate and increased beta-glucuronidase activity. These changes were accompanied by increased production of prostaglandin E and 6 keto prostaglandin F1 alpha in gallbladder perfusate and homogenate. The concentration of leukotriene C4 in gallbladder effusate was increased by lysophosphatidylcholine when compared with control values. Indomethacin inhibited the protein efflux, decreased beta-glucuronidase levels and decreased prostaglandin E and 6 keto prostaglandin F1 alpha formation when compared with values produced by lysophosphatidylcholine alone. Cyclooxygenase inhibition did not alter the secretion of water into the gallbladder or perfusate leukotriene C4 concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostanoids and leukotrienes in experimental feline cholecystitis. 236 79

Glycosaminoglycan (GAG) content in the kidney of homo (DI) Brattleboro rats was shown to be minimal whereas the activity of glycanohydrolases (GH) in the papilla of diabetic rats was comparatively high. Injection of the antidiuretic hormone (ADH) increased the GH in the renal papillae of both the DI and HZ (heterozygous) rats. Disappearance of the beta-glucuronidase staining occurred in the collecting tubule's epithelial cells under the effect of adiuretin--SD and water deprivation for 2 days. The activation and redistribution of the GH under the ADH influence and the role of GAG and GH in the mechanism of ADH action, were discussed.
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PMID:[The glycosaminoglycan-glycanohydrolase system in the renal tissue of Brattleboro rats with a hereditary defect in antidiuretic hormone synthesis]. 244 68

Protective effect of aprotinin pretreatment was assessed by functional, biochemical and morphological preservation in four hour global ischemia followed by one hour reperfusion in dogs. Cardioplegia was induced by intermittent infusion of cold Mg-lidocaine solution. Aprotinin 10,000 KIU/kg was given in low dose group (8 dogs), and 20,000 KIU/kg in high dose group (6 dogs); one half was given before ischemia and another half during ischemia. Betamethasone, coenzyme Q and nifedipine were also given equally in both groups before ischemia. Results were as follows: 1. Four (50%) of low dose group and all of high dose group were successfully taken off CPB and survived for one hour reperfusion. 2. High dose group showed significantly higher blood pressure and LVSWI than low dose group after one hour reperfusion (p less than 0.05). 3. Serum N-acetyl-beta-D-glucosaminidase and mitochondrial aspartate aminotransferase showed the significantly lower activity in high dose group than in low dose group after one hour reperfusion (p less than 0.05). There was no significant difference in the activities of serum beta-glucuronidase and MB-creatine kinase. 4. Myocardial tissues, excised after one hour reperfusion, contained significantly higher creatine phosphate in high dose group than in low dose group (p less than 0.05). There was no significant difference in the contents of adenosine triphosphate, calcium and water. 5. Severely injured mitochondrion were significantly lesser in high dose group than in low dose group. All lysosomes showed mild swelling or enlargement, but those membranous structures were well-preserved in both groups. In conclusion, aprotinin pretreatment might be effective in myocardial protection against prolonged global ischemia, by inhibiting the "leak out" of lysosomal enzymes.
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PMID:[Improved myocardial protection by aprotinin pretreatment in prolonged global ischemia]. 248 66

Patients with juxtapapillary duodenal diverticula have an increased occurrence of calcium bilirubinate gallstones. One possible hypothesis to explain this observation is enzymatic deconjugation of bilirubin conjugates in the bile. Beta-glucuronidase of human or bacterial origin may lead to deconjugation of the bilirubin glucuronides in bile. This, in turn, may increase the amounts of unconjugated, water-insoluble bilirubin which can precipitate as calcium bilirubinate, the main component of brown pigment stones. In this study we compared gallstone patients with and without duodenal diverticula treated with endoscopic papillotomy. Increased occurrence of bacteria producing beta-glucuronidase (p less than 0.01) and increased activity of bacterial beta-glucuronidase (pH 7.0) in the bile itself (p less than 0.01) were found in patients with duodenal diverticula. When the activity of the enzyme at pH 4.5, the optimum of the human enzyme, was measured, no such difference was found. The results support the hypothesis of bacterial glucuronidase as an etiologic factor in pigment gallstone disease in patients with duodenal diverticula. The high activity of bacterial enzyme found in the bile in some patients without diverticula suggests bacteria as an etiologic factor, independent of the presence of diverticula.
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PMID:Beta-glucuronidase activity in the bile of gallstone patients both with and without duodenal diverticula. 249 96

The metabolism of 14C-labelled 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ) was studied in suspensions of hepatocytes isolated from PCB-pretreated rats. The metabolites found after incubation of IQ/MeIQ (0.1 mM) with PCB-pretreated hepatocytes for 3 h were separated into three principal groups: ethyl acetate-extractable metabolites (2-4%), water soluble metabolites (94-98%) and covalently bound metabolites (0.4-0.5%). The water soluble metabolites were separated by HPLC. The metabolites were evaluated by beta-glucuronidase lability, sulphate incorporation and compared with glucuronides formed by microsomes. Mass spectroscopy and proton NMR were also run. The major metabolites formed were a N2-sulphamate, an O-sulphate in position 5 for IQ and 5 for MeIQ and an O-glucuronide in the same position. The MeIQ N2-sulphamate was much less abundant than the IQ N2-sulphamate. When compared with hepatocytes from uninduced rats, it was found that primarily the formation of ring-hydroxylated conjugates increased after PCB-pretreatment. The major ethyl acetate-extractable metabolites were the N2-acetyl derivatives and an unidentified metabolite. A small peak representing the 5-hydroxy-IQ or 5-hydroxy-MeIQ could also be seen in the HPLC chromatogram of the ethyl acetate extractable metabolites. All major water soluble products described in hepatocytes were also found in urine and bile of uninduced rats exposed to IQ/MeIQ in vivo.
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PMID:Characterisation of metabolites of the food mutagens 2-amino-3-methylimidazo[4,5-f]quinoline and 2-amino-3,4-dimethylimidazo[4,5-f]quinoline formed after incubation with isolated rat liver cells. 251 Sep 46

Progesterone -6,7-3H (P*) was incubated in minces of human secretory and proliferative endometrium in absence as well as in presence of 10 and 100 micrograms/ml of unlabelled progesterone (P), in Eagle's Culture Medium throughout 72h. The following metabolites of P* were found in culture media: 1. C-21 derivatives of P* reduced at C-5, and C-20 positions. Also, a 3 beta-hydroxy-5 alpha pregnane-20-One conjugated to a glucuronic acid moiety was identified. 2. Concentrations of water-soluble derivative accounted for 21% and 29% of the recovered radioactivity in proliferative and secretory endometria, respectively. 3. After beta-glucuronidase cleavage, 80% to 95% of the water soluble derivatives were released as free steroids. 4. Approximately 60% corresponded to 3 beta -hydroxy- 5 alpha pregnane-20-one of the pooled water extracts. 5. Alson, 17% and 13% as well as 9% and 8% recoveries under 10 and 100 micrograms/P were observed in proliferative and secretory endometria, respectively. Glucuronidation seems to be a compensatory route to metabolize P and P* in human endometrium as might also occur in other species.
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PMID:Steroid conjugate formed by human endometrium. 251 89

1. The in vitro incubation of mussel digestive gland with 1 mM aminofluorene resulted in the formation of glucuronides that (a) became mutagenic with carp liver S9, and (b) liberated S9-dependent mutagenic aglucones after beta-glucuronidase treatment. 2. Natural populations of mussels from unpolluted and polluted sites, as well as mussels exposed to 3 ppm of aminofluorene or to used engine oil, did not accumulate detectable amounts of premutagens, mutagens, or mutagenic glucuronides/aglucones either in digestive gland tissue or in shell-cavity water. 3. The mutagenicity testing of mussel's glucuronides/aglucones does not seem to be useful as a biomonitor of environmental carcinogens.
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PMID:Glucuronides in mussel Mytilus galloprovincialis as a possible biomonitor of environmental carcinogens. 256 91


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