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)

Halofenate--free acid (HFA), the major metabolite of the hypolipidemic drug, halofenate, inhibited platelet aggregation induced by collagen and sodium arachidonate and blocked the second phase of aggregation caused by ADP, thrombin and epinephrine in human platelet-rich plasma. The aggregation of washed platelets by thrombin and collagen was also blocked. HFA also inhibited the release by thrombin and collagen of 5-hydroxytryptamine from dense granules of platelets and the release by thrombin of beta-glucuronidase from platelet alpha-granules. These inhibitory effects were concentration and time-dependent. HFA decreased platelet factor 3 activity by 31% and also inhibited the incorporation of 14C-acetate and U-14C-glucose into platelet lipids by 89% and 56% respectively. Thrombin-induced lipid peroxidation and prostaglandin formation was investigated by measuring the by-product malonyldialdehyde, and this was found to be inhibited by HFA. It is suggested that the effect of HFA on aggregation is attributable to inhibition of the release reaction which may in turn be a consequence of the effects of the drug on platelet lipid synthesis.
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PMID:The effect of halofenate--free acid on aggregation--the release reaction, coagulant activity, and lipid metabolism of human platelets. 57 7

The purpose of our investigation was to determine whether iopanoyl glucuronide, the major metabolite of iopanoic acid (Telepaque), undergoes hydrolysis by bacterial beta-glucuronidase in dogs. The conjugated compound was identified and quantitated by elemental analysis, fluorescent excitation analysis, thin-layer chromatography, and high pressure liquid chromatography. The experiments were performed before and after combined antibiotic treatment with neomycin and vancomycin. It was first determined that reabsorption and excretion of sodium iopanoate was only minimally diminished during antibiotic treatment. Known amounts of iopanoyl glucuronide were infused into the small bowel of 4 awake dogs with chronic bile fistula, and bile was collected for 5--8 hours. The excretion of the recirculated conjugated compound was 4--5 times lower during antibiotic treatment. Incubation of ileal fluid with bile containing iopanoyl glucuronide suggested that beta-glucuronidase hydrolyzes the conjugated compound. Hydrolysis was markedly decreased after pretreatment with antibiotics. These findings suggest that the beta-glucuronidase produced by bacteria may be a major mechanism in enterohepatic recirculation of iopanoyl glucuronide. Mechanisms and possible implications are discussed.
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PMID:Observation on the metabolism of iopanoyl (Telepaque) glucuronide in dogs treated with antibiotics. 71

By exploiting the unique characteristics of three ionophores, experimental conditions were found which permit the dissociation of respiratory stimulation from secretion in polymorphonuclear leucocytes. A marked stimulation of respiration was produced by ionophore X537A, which binds and transports both alkali-earth and alkali cations. The stimulatory activity of this ionophore was the same at either high or low Na+/K+ ratios in the medium and was virtually unaffected by extracellular Ca2+. A slight stimulation of oxygen consumption was also caused by the K+-selective ionophore valinomycin and by ionophore A23187, which complexes and transfers bivalent cations. Ionophore X537A and valinomycin were unable to stimulate selective release of granuleassociated beta-glucuronidase and gradually increased cell fragility, as monitored by increased leakage of lactate dehydrogenase. Ionophore A23187 slightly increased exocytosis of beta-glucuronidase. In a Mg2+-free medium, Ca2+, added simultaneously with ionophore A23187, greatly enhanced respiration and secretion of the granule enzyme. If Ca2+ was added a few minutes after the ionophore, exocytosis occurred, but no respiratory burst was observed. If the latter experiment was repeated in the presence of extracellular Mg2+, both secretion and respiration were stimulated. This effect was not produced by Mn2+ or Ba2+. It is proposed that Ca2+ is required for triggering selective secretion of granule enzymes from leucocytes is caused by an intracellular redistribution of cations, which may invovle Mg2+-dependent mechanisms.
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PMID:The dissociation of exocytosis and respiratory stimulation in leucocytes by ionophores. 78 49

The activity of gold sodium thiomalate (GST) given i.m. to adjuvant-induced polyarthritic rats was studied alone or in combination with active doses of aspirin, indomethacin and hydrocortisone. In addition to paw volume and body weight changes, erythrocyte sedimentation rate, serum albumin/globulin and gold levels as well as plasma activities of beta-glucuronidase, acid phosphatase, lysozyme and lactic acid dehydrogenase were measured. In prophylactic studies the beneficial activity of GST was unaffected by aspirin, suggesting a positive drug interaction, but additive with indomethacin or hydrocortisone for the 1st but not 2nd lesion of the disease. These results were closely correlated with increased serum gold levels. Similar clinical findings were observed in therapeutic studies except that a positive drug interaction occurred between GST and hydrocortisone. Unlike in the prophylactic experiments, serum gold levels were unaffected by any of the agents tested in the therapeutic studies.
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PMID:Effect of concurrent administration of aspirin, indomethacin or hydrocortisone with gold sodium thiomalate against adjuvant-induced arthritis in the rat. 82

Glucocorticosteroids and mineralocorticosteroids were tested for their capacity to inhibit the nonphagocytic discharge of two lysosomal enzymes--a cartilage matrix-degrading neutral protease and beta-glucuronidase--from highly purified human neutrophils. Lysosomal enzyme discharge from neutrophils adherent to nonphagocytizable, immobilized, heat-aggregated IgG was inhibited by the four glucocorticosteroids--methylprednisolone sodium succinate, triamcinolone acetonide hemisuccinate, para methasone acetate, and hydrocortisone sodium succinate. These glucocorticoids also inhibited zymosan-induced release of beta-glucuronidase from neutrophils that had been pretreated with cytochalasin B in order to completely prevent the onset of phagocytosis. Inhibition by the glucocorticoids of lysosomal enzyme discharge provoked by a soluble divalent cation ionophore was also observed. Neither desoxycorticosterone acetate nor aldosterone hemisuccinate, two mineralocorticosteroids, inhibited lysosomal enzyme release. Similarly, the salt moieties of some of the steroids tested, such as sodium succinate and sodium acetate, failed to elicit an effect on enzyme release. Therefore interference with lysosomal enzyme discharge was restricted to the glucocorticosteroid ring structure. Because interference either with the adherence of neutrophils to immune reactants or with the activities of the discharged lysosomal enzymes by the glucocorticoids could be interpreted as inhibition of lysosomal enzyme release, steroidal effects on these parameters were examined. None of the glucocorticoids tested elicited any significant effects on neutrophil adherence or lysosomal enzyme activity. Thus it appears that glucocorticosteroids are capable of inhibiting directly the nonphagocytic discharge of lysosomal enzymes from human neutrophils.
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PMID:Glucocorticosteroid inhibition of nonphagocytic discharge of lysosomal enzymes from human neutrophils. 83 39

Changes in intracellular water content appear to be common abnormalities induced by a wide variety of pathogenic mechanisms. Such changes in cell water produce changes in the water in various subcellular organelles bound by semipermeable membranes. Cell and subcell functions then alter in their turn. In isolated alveolar macrophages (rabbit), intracellular and intramitochondrial oedema reduces mitochondrial O2 utilization. Metabolic control is maintained because lactate production reverses (Pasteur effect). On reconstitution, O2 utilization and lactate production return towards normal, indicating reversibility. Cellular and intramitochondrial dehydration also reduces mitochondrial O2 utilization but metabolic control is lost because lactate production also decreases. Osmotic reconstitution does not reverse the abnormality. Exposure to hypotonic media leads to release of lysosomal enzymes (beta-glucuronidase, EC 3.2.1.31) to the extracellular phase of isolated alveolar macrophages. Some of this release is caused by exocytosis although, at low osmotic concentrations, intralysosomal oedema ultimately ruptures lysosomes, with extensive discharge of enzyme. In turn, lysosomal enzymes may injure more normal cells. Impairment of energy metabolism caused by hypoxia leads to intracellular oedema, because Na+ accumulates in the cells when ATP is no longer available for the sodium pump. Continued studies of the disorders in cell physiology caused by changes in cell and subcell water should provide important new insights into a wide variety of disease states (including pulmonary oedema).
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PMID:Intracellular and subcellular oedema and dehydration. 104 40

In order to obtain sufficient quantities of beta-glucuronidase for use in structural studies, the enzyme was purified from its richest known source, the female rat preputial gland, by a method similar to that of Ohtsuka and Wakabayashi (1969) (Enzymologia 12, 109). The purified enzyme has an S-o20, w of 12.5 S and a D-o20, w of 4.3 times 10- minus 7 cm-2 S-minus 1. Sedimentation diffusion and sedimentation equilibrium yielded molecular weights of 267,000 and 283,000, respectively. The limiting viscosity (3.6 ml/g) and the f/fo (1.08 at sigma equals to 0.2 g of H2O/g of protein) indicate that the enzyme is a typical globular protein possessing little asymmetry. The circular dichroism spectrum indicates approximately 14% alpha-helix and a far greater amount of random coli than beta structure. The enzyme is acidic, having an isoelectric point of 6.15. In electrophoresis on polyacrylamide gels containing sodium dodecyl sulfate the enzyme exhibits a single band at molecular weight 72,000, a result indicating that the enzyme consists of four subunits of similar molecular weight. Tryptic peptide mapping suggests that the subunits are identical.
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PMID:Physical and chemical properties of beta-glucuronidase from the preputial gland of the female rat. 114 Dec 28

The turnover of rat liver lysosomal proteins was studied by a double isotope-labeling technique. The cellular fractions investigated included soluble lysosomal proteins, lysosomal membrane proteins, highly purified lysosomal beta-glucuronidase, and for comparison, microsomal proteins and soluble cytoplasmic proteins. Both "normal" lysosomes and Triton WR-1339-filled lysosomes (tritosomes) were studied, with similar results. It was found that (a) the turnover rate of lysosomal proteins, of both the soluble and membranous compartments, was very similar to that of the proteins of the microsomal and soluble cytoplasmic fractions, and (b) the turnover rate of lysosomal proteins was asynchronous. The latter conclusion was based on two lines of evidence: (a) lysosomal beta-glucuronidase had a distinctly slower turnover rate than the average rate of the soluble lysosomal proteins, and (b) subunits of the proteins of the soluble lysosomal fraction as separated by sodium dodecyl sulfate. Sephadex G-200 gel filtration showed different rates of degradation.
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PMID:Turnover studies on proteins of rat liver lysosomes. 115 Jun 46

In the determination of urinary 17-hydroxycorticosteroids, the urine is saturated with NaHSO3 after hydrolysis with beta-glucuronidase and then extracted with methylene chloride. Sodium bisfulfite removes almost all non-steroidal impurities in the urines from patients medicated with acetylspiramycin, leucomycin, erythromycin, triacetylolenadomycin, rifampicin and tranquilizers such as chlorpromazine, which interfere with the absorption at 410 nm. in the subsquent Porter-Silber reaction. In order to increase the specificity of a routine method, a procedure conducted by Allen has been often employed: The sum of 370- and 450-nm. absorbances is subtracted from twice absorbance at 410 nm. However, the procedure could not be used in the medicated urines mentioned above, because the spectral absorption curve of these drugs and their metabolites in the Porter-Silber reaction was not a straight but a strongly convex or concave line in the 370-450-nm. range. Using the present method, interference with the Porter-Silber reaction was not found in the urines from patients medicated with chloramphenicol, minocycline, chlordiazepoxide, meprobamate, methyprylon, nitrazepam, synthetic penicillins such as hetacillin, oxacillin and cloxacillin, or cephalosporins such as cephalexin and cephalothin. However, to obtain correct values in urines from patients medicated with spironolactone, it was necessary to subject the urines to treatment with methylene chloride before enzyme hydrolysis.
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PMID:The effect of sodium bisulfite on the removal of drugs and their metabolites interfering with the Porter-Silber reaction in the determination of urinary 17-hydroxycorticosteroids. 116 83

Massive doses of methylprednisolone were given to dogs prior to severe, lethal, hemorrhagic shock. An untreated group of dogs subjected to hemorrhagic shock served as controls. No persistent significant differences were seen in cardiac output, mean arterial blood pressure, superior mesenteric artery flow, and survival. Calculated total peripheral resistance tended to be lower in the treated dogs and was significantly lower after reinfusion of shed blood. Pretreatment with methylprednisolone did not prevent plasma elevations of the lysosomal enzymes, cathepsin D and beta-glucuronidase. Stabilization of hepatic lysosomes in treated dogs subjected to hemorrhagic shock was not evident. The results failed to indicate significant salutary effects of methylprednisolone sodium succinate in this lethal hemorrhagic shock model.
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PMID:Inadequacy of steroids in the treatment of severe hemorrhagic shock. 116 20


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