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)

D-penicillamine was introduced to treat neonatal hyperbilirubinaemia in 1973 and to prevent retinopathy of prematurity in 1980. In this study we investigated the renal and liver functions of neonates treated with DPA and the in vitro effect of the drug on superoxide anion generation and beta-glucuronidase release as well as on phagocytic and intracellular killing activation on human peripheral blood granulocytes. Our data concerning the renal and liver functions before and after 3 to 4 days DPA treatment reveal no pathological change during short-term administration in the neonatal period. Furthermore, none of the examined DPA concentrations influenced the phagocytic or killing activity of neutrophils.
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PMID:[D-penicillamine does not affect the liver and kidney function in newborn infants nor the in vitro function of phagocytes]. 194 83

Influence of D-Penicillamine (DPA) on metabolic and functional activities of neutrophil granulocytes was investigated in vitro by measuring superoxide anion production and beta-glucuronidase release as well as by determining phagocytic and intracellular killing activities of cells. Preincubation with DPA in the concentration range of 0.5-5.0 mM resulted in 28-53% increase in superoxide anion production by granulocytes stimulated with 10(-7) M FMLP. DPA in the same concentration range resulted in 145-371% rise in the FMLP-stimulated beta-glucuronidase release. However, uptake and subsequent killing of viable Staphylococcus aureus was not influenced by incubation of granulocytes with various concentrations of DPA (0.5-5.0 mM). From these results we conclude that DPA may influence the superoxide anion production and beta-glucuronidase release in granulocytes without altering the phagocytic and intracellular killing activities of these cells. We suppose that the unchanged antibacterial activity of neutrophil granulocytes is resulted by the two opposite DPA effects: acting extracellularly reduces free radical level while the direct membrane effect results in enhancing metabolic activity in granulocytes.
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PMID:Influence of D-penicillamine on metabolic and functional activities of neutrophil granulocytes. 196 71

D-Penicillamine (DPA) was introduced to treat neonatal hyperbilirubinemia in 1973 and to prevent retinopathy of prematurity in 1980. In this study we investigated the renal and liver functions of neonates treated with DPA and the in vitro effect of the drug on superoxide anion generation and beta-glucuronidase release as well as phagocytic and intracellular killing activation of human peripheral blood granulocytes. Our data concerning the renal and liver functions before and after 3 to 4 days DPA treatment reveal that the drug does not produce any pathological change during short-term administration in the neonatal period. Furthermore, it was found that superoxide anion generation was slightly increased, and beta-glucuronidase release markedly increased by preincubation with DPA at concentrations of 0.5-5 mM. The rise was directly proportional to the concentration in the examined range. On the other hand, none of the examined DPA concentrations influenced the phagocytic or killing activity of neutrophils.
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PMID:The effects of D-penicillamine on the renal and liver functions in neonates and the in vitro influence on granulocytes. 264 50

The effects of nonsteroidal anti-inflammatory agents on superoxide production and granule enzyme release by human polymorphonuclear leukocytes stimulated with either formyl-methionyl-leucyl-phenylalanine (fMet-Leu-Phe] or immune complexes were investigated. Cytochrome c reduction and the release of lysozyme, beta-glucuronidase, myeloperoxidase and gelatinase were measured. Auranofin, phenylbutazone, sulfasalazine and the phospholipase A2 inhibitor, 4-bromophenacyl bromide, strongly inhibited these responses in fMet-Leu-Phe stimulated cells, at concentrations below 50 microM. Indomethacin, piroxicam, mefenamic acid, primaquine and quinacrine at 50-250 microM were inhibitory. Up to 1 mM ibuprofen and chloroquine inhibited superoxide production but had little effect on degranulation. With cells stimulated by IgG aggregates (immune complexes), up to 1 mM ibuprofen, mefenamic acid and piroxicam did not inhibit either response. Indomethacin, phenylbutazone, sulfasalazine and primaquine inhibited, but considerably higher concentrations were required than with fMet-Leu-Phe. Quinacrine inhibited superoxide production equally well with both stimuli but inhibited enzyme release only with fMet-Leu-Phe. Only auranofin, 4-bromophenacyl bromide, and the weakly effective chloroquine exerted approximately the same effect with both stimuli. D-Penicillamine did not affect enzyme release with either stimulus and interfered in the superoxide assay. Gelatinase release induced by fMet-Leu-Phe was affected to the same extent, or slightly more, than release of the other granule enzymes. With immune complexes, there was only modest inhibition of gelatinase release by any of the drugs at 250-1000 microM. Our results reinforce previous observations that many anti-inflammatory drugs affect neutrophil functions, but their effects vary with stimulus. The relative insensitivity of immune complex-induced responses to most of the drugs must be taken into account when considering their mode of action.
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PMID:Inhibition by nonsteroidal anti-inflammatory drugs of superoxide production and granule enzyme release by polymorphonuclear leukocytes stimulated with immune complexes or formyl-methionyl-leucyl-phenylalanine. 303 27