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)

Leishmania mexicana mexicana (M379) amastigotes were found to contain much higher activities than cultured promastigotes of five putative lysosomal enzymes: cysteine proteinase; arylsulfatase (EC 3.1.6.1); beta-glucuronidase (EC 3.2.1.31); DNase (EC 3.1.22.1), and RNase (EC 3.1.27.1). The release profiles of the first three of these enzymes from digitonin-permeabilized amastigotes suggests that they are located within organelles. Cytochemical staining for cysteine proteinase, using gold labeled antibodies and arylsulfatase, showed that both were present in large organelles previously named "megasomes." Comparative studies with L. mexicana amazonensis (LV78), L. donovani donovani (LV9), and L. major (LV39) revealed that L. mexicana amazonensis was similar to L. mexicana mexicana in possessing both high amastigote cysteine proteinase activity and large numbers of megasome organelles in amastigotes, whereas the other two species lacked both these features. The results suggest that the presence of numerous lysosome-like organelles in the amastigote is a characteristic of the L. mexicana group of parasites.
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PMID:Leishmania mexicana: amastigote hydrolases in unusual lysosomes. 352 61

A previously unknown melatonin metabolite was isolated by chloroform extraction and reverse phase HPLC from human and rat urine after administration of synthetic melatonin and characterized by mass spectroscopy and proton magnetic resonance spectroscopy to 1-acetyl-1,2,3,3a,8,8a-hexahydro-8a-hydroxy-5-methoxypyrrolo[2,3-b ]indole, a cyclic isomer of 2-hydroxymelatonin. This isolation was based on the fact that our melatonin antibody (a-MT-K1) cross-reacted against this novel metabolite at a level of 0.1% (melatonin 100%). In our HPLC program for indoles the cyclic 2-hydroxymelatonin eluted at 25 min, separately from synthetic indoles, between 6-hydroxymelatonin (19 min) and melatonin (35 min). In [3H] melatonin studies it was found to be present (at 25 min in our HPLC), accounting for 5% of the urinary metabolites of melatonin in the rat. Since beta-glucuronidase-arylsulfatase treatment of rat urine did not liberate the cyclic 2-hydroxymelatonin this would appear to be excreted into urine as the free form.
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PMID:A cyclic isomer of 2-hydroxymelatonin: a novel metabolite of melatonin. 356 38

A comprehensive high-performance liquid chromatographic method was developed for quantitating propranolol and its known metabolites in serum, bile and urine. Analysis was performed before and after incubation of the samples with beta-glucuronidase-arylsulfatase to quantitate both free and conjugate forms of the oxidative metabolites. Fractionation of the basic, neutral and acidic metabolites was achieved by differential pH solvent extraction. The basic and neutral metabolites were extracted from the biological samples at pH 10.5 with 2% n-butanol in dichloromethane. Additional clean-up of the basic fraction by back-extraction into dilute acid was needed for those samples that were subjected to enzymatic hydrolysis. The original aqueous sample was titrated with acid to pH 1, followed by extraction of the remaining acidic metabolites into either n-butanol-dichloromethane (with unhydrolyzed serum) or carbon tetrachloride (with all other samples). Chromatographic separation of the metabolites in the different extracts was achieved on a reversed-phase C18 column, using a single isocratic mobile phase consisting of 0.044 M pH 2.7 phosphate buffer, tetrahydrofuran, methanol and acetonitrile, with the addition of n-butylamine as a competing base to control retention volume and peak shape. Detection and quantitation of propranolol and its metabolites in the low nanogram to sub-nanogram range was afforded by fluorescence at a low UV excitation wavelength. The coefficients of variation for replicate assay of spiked samples were uniformly less than 6% for all the analytes.
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PMID:Versatile isocratic high-performance liquid chromatographic assay for propranolol and its basic, neutral and acidic metabolites in biological fluids. 357 4

Carbamazepine 10,11-oxide (1a,10b-dihydro-6H-dibenzo[b,f]oxireno[d]azepine-6-carboxamide), a key intermediate in carbamazepine metabolism, was found to be unusually resistant to enzymatic hydrolysis when incubated with microsomal and cytosolic fractions from rabbit, rat, and guinea pig livers. However, its hydrolysis product, trans-10,11-dihydro-10,11-dihydroxy-5H-dibenzo[b,f]azepine-5-carboxamide , was excreted, as previously reported, both in the free and in conjugated forms, as the main metabolite in the urine of humans under carbamazepine treatment. The free diol and that obtained after treatment with beta-glucuronidase/arylsulfatase were both found by Mosher's method to be formed in an enantiomeric excess of 80%, the prevalent enantiomer having the (-)-10S,11S absolute configuration, as determined by applying the CD exciton coupling method to its bis[p-(dimethylamino)benzoyl] ester. This finding confirms the pronounced enantioselectivity of the microsomal epoxide hydrolase toward meso and racemic substrates, but is in contrast with the prevalent formation of (R,R)-diols in most other known cases of enzymatic hydrolysis of epoxides. Preparatively useful syntheses of the racemic trans-10,11-dihydro-10,11-diol and of 9-(hydroxymethyl)-10-carbamoylacridan, another carbamazepine metabolite, are reported for the first time.
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PMID:The metabolism of carbamazepine in humans: steric course of the enzymatic hydrolysis of the 10,11-epoxide. 357 65

The disposition of 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), a highly toxic environmental contaminant which accumulates in human tissues, was examined in the male Fischer rat after iv and oral exposure. Greater than 70% of an oral dose of 0.1, 0.5, or 1.0 mumol PeCDF/kg body wt was absorbed by the gastrointestinal system. After either oral or iv administration of 0.1 mumol/kg, the dibenzofuran was rapidly removed from the blood and accumulated in the liver and adipose tissue and to a lesser extent in the skin and muscle. Three days after administration, 70% of the iv dose of PeCDF was found in the liver, 7% in the fat, 1% in the skin, and 0.5% in the muscle. Route of exposure had little effect on tissue distribution. TLC analyses indicated that greater than 99% of the [14C]-PeCDF-derived radioactivity which had accumulated in the liver and adipose tissue was unmetabolized PeCDF which was eliminated very slowly (t1/2 = 193 and 69 days, respectively). The whole body half-life calculated from the daily fecal excretion rate was approximately 64 days. Excretion occurred primarily via the feces. No radioactivity was detected in expired air and less than 0.02% was detected in the urine. TLC analysis of fecal extracts indicated greater than 90% of the [14C]PeCDF-derived radioactivity in the feces was polar metabolites of the parent compound. Pretreatment with 500 micrograms PeCDF/kg body wt caused biliary excretion to nearly double. Treatment of bile with beta-glucuronidase or arylsulfatase had little effect on the chromatographic profile. Therefore, PeCDF was readily absorbed from the gastrointestinal tract, concentrated primarily in the liver, and was slowly eliminated from the body as polar metabolites. The long half-life and high body burden of PeCDF suggest that the toxicity of this chemical may be enhanced due to bioaccumulation upon chronic low-level exposure.
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PMID:Disposition and excretion of 2,3,4,7,8-pentachlorodibenzofuran in the rat. 362

The influence of the peptide hormone relaxin on the glycosaminoglycan (GAG) metabolism was investigated in the pubic ligament of the symphysis pubis and in serum of the virgin mouse. Fresh weight DNA and GAG content per 1 ligament is significantly increased, the level of water soluble protein is not affected. A shift in the electrophoretic GAG pattern by an increasing amount of hyaluronic acid and a decreasing amount of chondroitin sulfate and dermatan sulfate can be observed. Concerning GAG-splitting enzymes (N-acetylglucosaminidase, arylsulfatase, beta-glucuronidase) the N-acetylglucosaminidase reveals a significant increase of its activity in the interpubic ligament and in the serum. The data demonstrate that relaxin treatment induces some changes in the GAG metabolism.
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PMID:Effects of the hormone relaxin on the metabolism of the glycosaminoglycans in the mouse symphysis pubis. 369 38

Metabolism of benzo(a)pyrene (BaP) in vivo and in vitro was studied using two benthic fish species, English sole (Parophrys vetulus) and starry flounder (Platichthys stellatus), and Sprague-Dawley rats. At 24 h after administration of BaP (7.9 mumol/kg of body weight) to fish either p.o. (Experiment 1) or i.p. (Experiment 2), the specific activity of binding of BaP metabolites to hepatic DNA (pmol of BaP equivalent per mg of DNA) was higher in sole [2.1 in Experiment 1; 28 +/- 5 (SE) in Experiment 2] than in flounder (0.5 in Experiment 1; 14 +/- 4 in Experiment 2). Treatment of bile with beta-glucuronidase and arylsulfatase released a significantly higher proportion of 7,8-dihydroxy-7,8-dihydro-BaP (BaP 7,8-diol) from sole bile than from flounder bile in both experiments. However, the rate of BaP metabolism and rate of formation of BaP 7,8-diol by hepatic microsomes were comparable for both fish species. Thus, the differences in both the level of DNA binding and the concentration of BaP 7,8-diol in bile of BaP-exposed sole and flounder were apparently due to differences in detoxication, rather than formation, of BaP 7,8-oxide and BaP 7,8-diol-9,10-epoxide. The rate of formation of BaP 7,8-diol by rat liver microsomes (28 +/- 1 pmol of BaP 7,8-diol formed per min per mg of protein) was comparable to that by hepatic microsomes from both fish species (50 +/- 10 for sole and 33 +/- 6 for flounder), although the rate of BaP metabolism (600 +/- 200) was approximately 3 times greater than that by the fish species (190 +/- 60 for sole and 180 +/- 40 for flounder). Thus, greater proportion of BaP was converted to BaP 7,8-diol by liver microsomes of fish species than rat. These differences in BaP metabolism in vitro help explain, in part, the substantially lower binding (0.3 +/- 0.1; Experiment 2) for hepatic DNA in BaP-exposed rat than that in either sole or flounder.
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PMID:Comparative metabolism of benzo(a)pyrene and covalent binding to hepatic DNA in English sole, starry flounder, and rat. 373 Oct 58

The activities of acid phosphatase, N-acetyl-beta-D-glucosaminidase, alpha-mannosidase, alpha-fucosidase, beta-glucuronidase, arylsulfatase, and cathepsin D were biochemically investigated in the bovine cornea by separating the tissue into two layers, epithelium and stroma-endothelium. Acid phosphatase, alpha-mannosidase, alpha-fucosidase, and arylsulfatase disclosed much higher activities in the epithelial layer than in the stroma-endothelial layer. The other enzymes showed little difference in enzyme activity between the two layers.
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PMID:Acid hydrolases in the bovine corneal epithelium. 375 93

Experimental gingivitis provides a useful model for studying the initiation of periodontal disease in man. This study evaluated over a 4-week period the Plaque Index (PLI), Gingival Bleeding Time Index (GBTI), and gingival crevicular fluid (GCF) for resting and flow volume as well as the concentration and total activity of three enzymes in the GCF (lactate dehydrogenase--LDH, beta-glucuronidase--BG and arylsulfatase--AS) from the maxillary right quadrant of eight subjects with healthy gingiva. After rising sharply during the 1st week, the PLI continued to increase during the 2nd week but remained constant during the 3rd and 4th weeks. The GBTI, and the resting and flow GCF volumes, increased steadily throughout the study. LDH concentration in GCF varied minimally during the experiment, while total LDH activity rose slightly over the 4-week period. BG concentration and total activity in GCF rose steadily from baseline to the 3rd week and then either fell or leveled off during the 4th week. AS concentration in GCF rose from baseline to the 2nd or 3rd week and then fell. AS total activity in GCF rose from baseline to the 2nd week and then remained constant. These data suggest that while clinical signs of inflammation increased over the 4 weeks of the experiment, a homeostatic mechanism in the crevicular environment may control ground substance-degrading enzyme activity during experimental gingivitis in man.
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PMID:Lactate dehydrogenase, beta-glucuronidase and arylsulfatase activity in gingival crevicular fluid associated with experimental gingivitis in man. 388 71

The kinetics of the formation of mutagenic metabolites of benzo[a]pyrene (BP) in an isolated perfused rat-liver system have been studied. No genotoxic activity was detected in the perfusate using either the Ames test or the new bioluminescence test for genotoxic agents (BLT). The bile excretion showed strong genotoxic activity especially in the presence of the deconjugation enzymes beta-glucuronidase and arylsulfatase. The BLT was 1000-fold more sensitive than the Ames test in detecting the genotoxic activity in the bile excretion.
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PMID:The formation of genotoxic metabolites of benzo[a]pyrene by the isolated perfused rat liver, as detected by the bioluminescence test. 400 Jan 52


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