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 potency of the calcium ionophore A23187 in inducing three activities of human leukocytes (histamine secretion from basophils, enzyme secretion from PMNs, and proliferation of lymphocytes) was markedly dependent on the solvent (DMSO versus ethanol versus aqueous buffer) used for its initial sonication. While 0.1 micrograms/ml of DMSO- and ethanol-solubilized A23187 induced maximal histamine release from basophils and histaminase release from PMNs, concentrations of aqueous buffer-sonicated ionophore of greater than or equal to 1 microgram/ml were required for an equivalent response. Ionophore sonicated in organic solvents caused a maximum release of 40% of PMN beta-glucuronidase, at an optimal concentration tenfold higher than that required for maximal histaminase release; ionophore sonicated in aqueous buffers, even at high concentrations, effected a release of less than 5% of cellular beta-glucuronidase. A23187 also induced lymphocyte proliferation over a narrow concentration range; 0.05 micrograms/l of DMSO-sonicated ionophore induced optimal proliferation and concentrations greater than or equal to 0.2 micrograms/ml were toxic. Twofold higher concentrations of ethanol-sonicated ionophore and fourfold higher concentrations of aqueous-sonicated ionophore were necessary for maximal proliferation, and the magnitude of the maximal response with aqueous-sonicated A23187 was only one-half that of DMSO-solubilized agent. Ionophore-induced release of histamine from basophils and enzymes from PMNs was not cytotoxic, since ionophore induced neither LDH nor histamine release from heat-treated (47 degrees C) cells. These results explain several previous, discordant reports on the presence or absence of an effect of A23187 on cellular secretory events, on differing dose-response relationships, and on cytotoxic versus noncytotoxic mechanisms of action.
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PMID:Effect of solvent on the histamine-releasing, enzyme-releasing, and mitogenic properties of the calcium ionophore A23187. 9 71

The role of particle-bound complement proteins in the induction of noncytotoxic enzyme release from human granulocytes was investigated with the use of sera genetically deficient in complement and highly purified complement components. Release of histaminase, one of two important histamine catabolizing enzymes, and beta-glucuronidase from polymorphonuclear leukocytes was solely dependent on particle-bound C3b (the larger cleavage product of the third component of complement) when fluid-phase complement was excluded. The extent of enzyme release was a function of particle-bound C3b input, was reduced by exposing the particles to C3b inactivator, and was blocked by fluid-phase C3b. Phagocytosis of the C3b-coated particles was not required for enzyme release from neutrophils. In contrast, phagocytosis of "opsonized" particles was required for noncytotoxic release of histaminase and arylsulfatase from eosinophils; other proteins, as well as C3b, were able to opsonize particles for induction of enzyme release from eosinophils. These studies suggest a dual role for complement (particularly C3) in modulating vascular permeability phenomena, i.e., release of vasoactive mediators by the action of C3a and C5a, and release of the corresponding enzymes that inactivate the mediators by C3b.
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PMID:Complement-dependent histaminase release from human granulocytes. 10 69

Phagocytosis of opsonized zymosan by human eosinophils results in a dose-dependent noncytotoxic release of histaminase as well as arylsulfatase and beta-glucuronidase. The calcium ionophore A23187 also stimulates release of eosinophil histaminase at concentrations of ionophore which barely release arylsulfatase and beta-glucuronidase. Zymosan-induced histaminase release from eosinophils but not from neutrophils was abolished or markedly reduced in the presence of cytochalasin B, suggesting a difference in the mechanisms of histaminase release from the two granulocyte cell types.
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PMID:Histaminase release from human eosinophils. 40 20

In order to investigate the availability and release of enzymes from eosinophilic granulocytes in response to a variety of stimuli, guinea pig peritoneal eosinophils were obtained after repeated intraperitoneal injections of freeze-dried Trichinella spiralis larvae. The activities of the enzymes peroxidase, arylsulfatase B, beta-glucuronidase, aminopeptidase, histaminase, cytochrome c oxidase, acid phosphatase, adenosine triphosphatase and glucose 6-phosphatase, and the major basic protein (MBP) were studied histochemically and, in part, also biochemically. Eosinophils were incubated with the following substances: histamine, platelet activating factor, calcium ionophore, compound 48/80, leukotriene B4, prostaglandins E1, and E2, heparin, and eosinophil-chemotactic factors from neutrophils and lymphocytes. Eosinophils displayed a selective and stimulus-dependent enzyme and MBP reaction. Calcium ionophore and compound 48/80 provoked a release of cytotoxic major basic protein, partly associated with peroxidase release, while leukotriene B4 and eosinophil chemotactic factors caused histaminase and peroxidase release and activated leucinaminopeptidase. Heparin and calcium ionophore induced release of both MBP and histaminase. These data support the concept that eosinophils exhibit either inflammatory or cytotoxic, or antiinflammatory properties upon stimulation by various agents.
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PMID:Activation and release of enzymes and major basic protein from guinea pig eosinophil granulocytes induced by different inflammatory stimuli and other substances. A histochemical, biochemical, and electron microscopic study. 275 82

Because imidazole acetic acid (IAA), a product of histamine catabolism was shown to inhibit histaminase release from human polymorphonuclear leukocytes (PMNs), the effect of this compound on other neutrophil functions was investigated. IAA at concentrations of 10(-10) or more inhibited histaminase release induced by particle-bound C3b, the larger fragment of the activated form of the third component of complement. Release of histaminase induced by aggregated IgG, phorbal myristate acetate (PMA), formyl-methionyl-leucyl-phenylalanine (FMLP) and calcium ionophore was not affected by IAA. In addition IAA had no effect on release of beta-glucuronidase, myeloperoxidase, and lysozyme or on phagocytosis and superoxide generation. IAA did modestly inhibit neutrophil chemotaxis. These findings suggest a highly specific modulating effect of the histamine catabolite IAA on complement-mediated PMN function.
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PMID:Specific modulation of complement-dependent human granulocyte function by imidazole acetic acid. 625 58

Biochemical analysis of 328 human prostatic fluid samples were performed. The urea concentration of 69 samples was similar to that of serum and not indicative of significant contamination with urine. The pH of normal fluids was acidic (mean pH = 6.7). The interrelationships between zinc, citrate, acid phosphatase aminopeptidase, beta-glucuronidase, diamine oxidase and pH were investigated by factor analysis. Two significant factors were extracted, the first accounted for 89% of their common variance and the second for 11%. Zinc, citrate, acid phosphatase and aminopeptidase were positively and pH was negatively related to factor one. Beta-glucuronidase was positively related to factor two and diamine oxidase was largely independent of both factors. It was concluded that variables related to factor one share a common secretory control and mechanism, that some other mechanism operates in the case of beta-glucuronidase and that diamine oxidase may not be a true secretory product of the prostate.
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PMID:The interrelationships between acid phosphatase, aminopeptidase, diamine oxidase, citric acid, beta-glucuronidase, pH and zinc in human prostatic fluid. 681 44

282 human prostatic fluid samples have been investigated for their pH value, zinc, and citrate concentration and their acid phosphatase, leucine aminopeptidase, diamine oxidase, and beta-glucuronidase activities. The results have been analysed in terms of the clinical status of the patients. Significant differences between patient categories were found with all but diamine oxidase and beta-glucuronidase. These differences were mainly found between men with apparently healthy prostates and prostatitis patients; the pH being raised and the acid phosphatase, leucine aminopeptidase, zinc and citrate being reduced. The diagnostic value of these parameters was evaluated, each could be used to classify correctly 90% of patients from these 2 groups. Zinc, citrate and leucine aminopeptidase showed no age relationship and were better than acid phosphatase and pH in discriminating between BPH and prostatitis. Evidence was also found for a return of normal secretory function sometime after an episode of prostatitis. Zinc and citrate are likely to be the most useful parameters for clinical evaluation.
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PMID:The response of seven prostatic fluid components to prostatic disease. 717 28