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)

Zymosan coated with complement (Zc) was observed to induce a transient elevation of the intracellular cyclic AMP in human polymorphonuclear cells: a two- to three-fold increase was observed within 1 min after stimulation and approached prestimulation levels by 2 min incubation. These changes in cyclic AMP were not associated with significant changes in cyclic GMP levels. Zymosan caused the release of PAF and beta-glucuronidase and particle uptake, which was initiated about 5 min after stimulation. These results suggest that the transient increase in cyclic AMP content might regulate an early event during mediator release. In an attempt to study further the significance of this rise in cyclic AMP, cells were preincubated with various phosphodiesterase inhibitors. Preincubation of the cells with methylisobutylxanthine (MIX, 10(-6) M to 5 X 10(-5) M), theophylline (3 X 10(-5) to 3 X 10(-3) M) or dipyridamole (10(-6) M to 10(-4) M) enhanced the increase in cyclic AMP levels, but resulted in dose-dependent inhibition of Zc-induced mediator release. Particle uptake and beta-glucuronidase release were less sensitive than PAF release to phosphodiesterase inhibitors, which argues in favour of the independence of both phenomena. Synergistic experiments with MIX and cyclic AMP indicate that the effect of this drug is through its action on cyclic AMP levels. These results suggest that while Zc-induced cyclic AMP elevation might occur in an intracellular place critical to its effect; phosphodiesterase inhibitors may elevate cyclic AMP levels throughout the cell and therefore inhibit the biological response.
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PMID:Modulatory role of cyclic AMP in the release of platelet-activating factor from human polymorphonuclear leucocytes. 627 75

We compared levels of (+)-catechin, (-)-epicatechin, and their metabolites in rat plasma and urine after oral administration. Rats were divided into four groups and given (+)-catechin (CA group), (-)-epicatechin (EC group), a mixture of the two (MIX group) or deionized water. Blood samples were collected before administration and at designated time intervals thereafter. Urine samples were collected 0-24 h postadministration. (+)-Catechin, (-)-epicatechin and their metabolites in plasma and urine were analyzed by HPLC-mass spectrometry after treatment with beta-glucuronidase and/or sulfatase. After administration, absorbed (+)-catechin and (-)-epicatechin were mainly present in plasma as metabolites, such as nonmethylated or 3'-O-methylated conjugates. In the CA and MIX groups, the primary metabolite of (+)-catechin in plasma was glucuronide in the nonmethylated form. In the EC and MIX groups, in contrast, the primary metabolites of (-)-epicatechin in plasma were glucuronide and sulfoglucuronide in nonmethylated forms, and sulfate in the 3'-O-methylated forms. Urinary excretion of the total amount of (-)-epicatechin metabolites in the EC group was significantly higher than the amount of (+)-catechin metabolites in the CA group. The sum of (+)-catechin metabolites in the urine was significantly lower in the MIX group than in the CA group, and the sum of (-)-epicatechin metabolites in the MIX group was also significantly lower than in the EC group. These results suggest that the bioavailability of (-)-epicatechin is higher than that of (+)-catechin in rats, and that, in combination, (+)-catechin and (-)-epicatechin might be absorbed competitively in the gastrointestinal tract of rats.
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PMID:In vivo comparison of the bioavailability of (+)-catechin, (-)-epicatechin and their mixture in orally administered rats. 1169 13