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)

A rat plasma salicylamide assay was developed using ring-labeled tritiated salicylamide, synthesized by reacting salicylamide with tritium oxide in the presence of heptafluorobutyric acid. The reaction yielded 3H-salicylamide of specific activity up to 8.41 mCi/mmole, 60% yield. Plasma containing 3H-salicylamide and its metabolites was extracted with a toluene-based scintillation fluid, which was subsequently counted. Specificity for free salicylamide was demonstrated by radio chemical and standard fluorescence plasma salicylamide level-time curves. Specificity resulted from nonextraction of the salicylamide sulfate and glucuronide metabolites. Sulfatase and beta-glucuronidase treatment allowed the analysis of plasma sulfate and glucuronide conjugates as free salicylamide. This procedure should be effective for the analysis of salicylamide and its metabolites in the presence of similar phenolic compounds.
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PMID:Radiochemical plasma salicylamide assay using ring-labeled tritiated salicylamide. 43 May 9

Oligosaccharides derived from chondroitin 4-sulfate (Ch4-S) and chondroitin were digested by canine liver lysosomes under acidic conditions. The degree of digestion of Ch4-S by hyaluronidase and beta-glucuronidase was examined on the basis of types of the digestion products. Tetradeca- and dodecasaccharides derived from Ch4-S and chondroitin were first digested by hyaluronidase, while the octasaccharide was hydrolyzed by beta-glucuronidase. Decasaccharide was degraded by both hyaluronidase and beta-glucuronidase. The results showed that decasaccharide from Ch4-S served as the largest-molecular-weight substrate for beta-glucuronidase in the degradation of Ch4-S by the enzymes of lysosomes in contrast to the results of the digestion studies of hyaluronic acid (HA). The contribution of beta-glucuronidase to the depolymerization of chondroitin and HA by hyaluronidase was examined in the presence of saccharo-1,4-lactone, a specific inhibitor of beta-glucuronidase, in the reaction mixture. The depolymerization of chondroitin by hyaluronidase was significantly reduced by the addition of saccharo-1,4-lactone. From the results, it is suggested that beta-glucuronidase contributes to the degradation of the even-numbered oligosaccharides which inhibit the action of hyaluronidase in the depolymerization of Ch4-S.
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PMID:Contribution of beta-glucuronidase to the degradation of chondroitin 4-sulfate by canine liver lysosomal enzymes. 44 79

Rabbit alveolar macrophages were exposed in culture medium to asbestos, beryllium sulfate, and beryllium oxide. The specific activities of the lysosomal hydrolases, acid phosphatase beta-N-acetylglucosaminidase and beta-glucuronidase plus the glycolytic enzyme, phosphohexose isomerase were determined in the medium, whole-cell homogenates, mitochondrial fractions, and supernatant. These hydrolases increased significantly in the medium but not in the mitochondrial fraction of cells exposed to dusts. Asbestos and beryllium sulfate were highly cytotoxic for alveolar macrophages in vitro and the data suggested that these agents were not associated with an increase in enzyme synthesis but rather a direct cytotoxic effect at the macrophage membrane level. For induction of enzyme release in vitro, a higher concentration of beryllium oxide was needed when compared with asbestos and beryllium sulfate. The cytotoxicity and enzyme release induced by these agents may represent an important nonspecific mechanism by which they induce inflammation and perhaps local proliferation of fibroblasts.
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PMID:Effects of asbestos and beryllium on release of alveolar macrophage enzymes. 45 20

Previous papers dealt with the discovery that hydrolysis of 17-hydroxycorticosteroid glucuronides in urine with beta-glucuronidase preparations from bovine liver is increased by adding sodium sulfate to the incubation medium. Here, we conclude that sodium sulfate not only increases the activity of bovine liver beta-glucuronidase on 17-hydroxycorticosteroid glucuronides and p-nitrophenyl glucuronides, but also removes the inhibitory activity of substances of high molecular weight in urine and, moreover, inhibits urine putrefaction during the hydrolysis. The net effect is an increased yield of urinary 17-hydroxycorticosteroids. In the incubation with sodium sulfate (Na2SO4, final concentration 80 g/liter, 500 Fishman units of beta-glucuronidase per milliliter of urine, pH 5.0, 48 degrees C, 18 h) the analytical recovery of 17-hydroxycorticosteroid glucuronides added to 12 urine samples proved to be 98 +/- 1.8% (95-100).
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PMID:Effect of sodium sulfate on the hydrolysis of 17-hydroxycorticosteroid- and p-nitrophenyl-glucuronides with beta-glucuronidase preparations from bovine liver. 55 62

A method is described for the preparation of pure beta-glucuronidase from bovine liver. The procedure includes ammonium sulfate, acetone and ethanol fractionation and a simple two-step ion exchange chromatography. The yield is acceptable and the method requires only standard laboratory equipment. The pure enzyme is easily crystallized from ammonium sulfate. Some practical applications of the pure beta-glucuronidase are discussed.
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PMID:Preparation of crystalline bovine liver beta-glucuronidase. 66 5

A mixture of [19-3H]hydroxyandrostenedione and [14C]androstenedione was administered intravenously to 3 women and urine was collected. Only negligible radioactivity could be extracted from the untreated urine. Most of the 14C but only 11% of the 3H was rendered solube in organic solvents by beta-glucuronidase. [3H-19]hydroxyandrostenedione was recovered from this fraction. The conjugates remaining in the urine were extracted into CHCl3 as their pyridinium salts. After solvolysis of the extract with HCLO4 in tetrahydrofuran, neutral metabolites were obtained. Substances extractable from water with organic solvents were obtained by solvolysis of the conjugates with perchloric acid in tetrahydrofuran. [3H-19]hydroxyandrostenedione was identified by isotopic dilution as the major product of solvolysis. Thus, 19-hydroxyandrostenedione undergoes conjugation with glucuronic acid and probably sulfuric acid, most likely at C-19. The major urinary metabolite is the sulfate-like conjugate. Reduction in ring A is less important than for other steroids.
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PMID:Metabolism of 19-hydroxyandrostenedione in human subjects. Urinary excretion of conjugates. 75 31

Defiency of beta-glucuronidase was demonstrated in serum, leukocytes, and cultured skin fibroblasts of two unrelated patients. One patient died at 2 9/12 years with a phenotype consistent with severe mucopolysaccharidosis; the other is 14 years of age and well, except for hypertension and obstructive lesions of large blood vessels. Analysis of urinary mucopolysaccharides revealed impaired degradation of dermatan sulfate and, to a lesser extent, of heparan sulfate. Cultured skin fibroblasts accumulated excess glycosaminoglycans (the term glycosaminoglycans is synonymous with acid mucopolysaccharides) as indicated by 35-SO-4 uptake.
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PMID:Variation in the phenotypic expression of beta-glucuronidase deficiency. 80 60

The ability to form androgen conjugates and the hormone dependency of the conjugating enzymes have been studied in the rat epididymis. Following the in vitro incubation of 3H-testosterone with epididymal slices from intact and castrated rats, the radioactivity recovered was partitioned between water and ether. Examination of the water soluble radioactivity demonstrated the presence of glucuronides and sulfates. The total radioactivity in the conjugate fraction was the same for both intact and castrated animals. However, castrated rats showed a 3-fold increase in the glucuronide fraction with a corresponding decrease in the formation of sulfates. Characterization of the ether soluble radioactivity after solvolysis of the conjugate fraction from castrated animals, showed DHT (17beta-hydroxy-5alpha-androstan-3-one) and 3alpha-diol (5alpha-andro-stane-3alpha, 17beta-diol) to be the main metabolites. After beta-glucuronidase hydrolysis of the same, only 3alpha-diol could be demonstrated at a significant level, although traces of DHT and delta16 compounds were present. Corresponding hydrolysis of the water phase from incubation of epididymis from intact rats, demonstrated a marked quantitative difference. Here approximately 40% of the conjugated aglycones consisted of delta16 compounds, whilst only about 12% was comprised of 3alpha-diol. The preferential conjugation of DHT and 3alpha-diol to a sulfate radical was demonstrated in both intact and castrated rats. Since the conjugated delta16 compounds were detected only in the epididymis from intact animals, it is possible that these are formed by the spermatozoa.
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PMID:Androgen metabolism by rat epididymis. 4. The formation of conjugates. 94 Nov 82

Anti-ulcer effects of cetraxate, a new compound possessing anti-plasmin, anti-casein and anti-trypsin actions were investigated by using experimental gastric ulcer models in rats. Cetraxate, 300 mg/kg p.o. showed significant inhibitory effects of 65.3%, 70.0%, 30.2%, and 67.1% against aucte types of ulcers producing by aspirin, phenylbutazone, indomethacin, and pyloric ligature (Shay's ulcer), respectively. These effects were greater than those obtained by gefarnate and aluminum sucrose sulfate may be mainly attributed to the protecting action of this drug on gastric mucosa. Ctraxate further revealed remarkable inhibitory effects on chronic types of ulcers produced by acetic acid, clamping, and clamping-cortisone. In acetic acid ulcer in particular, cetraxate was found to have a dose-dependent inhibitory effect at doses over 50 mg/kg. Of test drugs including L-glutamine and methylmethionine sulfonium chloride, cetraxate showed the most remarkable inhibitory effect on beta-glucuronidase activity in ulcer tissue of these three types of ulcers. These findings suggest that cetraxate may prevent the connective tissue in the ulcer location from decomposition due to lysosomal enzymes such as beta-glucuronidase, thereby accelerating the recovery from ulcer.
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PMID:Anti-ulcer effects of 4'-(2-carboxyetyl) phenyl trans-4-aminomethyl cyclohexanecarboxylate hydrochloride (cetraxate) on various experimental gastric ulcers in rats. 100 3

The metabolism of iv-administered 14C-cortisol (F) by pregnant baboons (107, 124 and 150 days gestation) was compared with that previously reported for nonpregnant animals and with that of animals examined 6-18 h after spontaneous vaginal delivery (178 plus or minus 4 days). Unconjugated, glucuronoside (beta-glucuronidase) and sulfate (H2SO4-ethyl acetate) fractions were extracted with ethyl acetate from urine containing more than 80% of injected 14C. Metabolites of interest were isolated by paper partition chromatography and purified by crystallization and derivative formation. Compared with nonpregnant animals, the following changes (P less than 0.05) were observed in pregnancy: (1) an increase in the percent urinary 14C in the unconjugated fraction and a decrease in the proportion of 14C appearing in the glucuronoside fraction; (2) an increase in excretion of metabolites more polar than the cortols; (3) a decrease in excretion of metabolites less polar than cortisone in the glucuronoside fraction; (4) an increase in unconjugated F excretion. Production rate of F (11.9 plus or minus 0.7 mg/day) estimated by isotope dilution and percent urinary 14C in tetrahydrocortisol and tetrahydrocortisone from the glucuronoside fraction were as in nonpregnant animals. With the exception of an increase in F production (22.7 plus or minus 0.8 mg/day), presumably the result of the stress of labor, F metabolism in the immediate postpartum period was strikingly similar to timals indicates that changes in the mother alone can account for the altered metabolic disposition of F in pregnancy and suggests that the fetus takes little part in metabolism of maternal circulating F.
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PMID:Cortisol metabolism in the baboon during pregnancy and the postpartum period. 109 Apr 36


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