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)

In vitro concentrations of chloroquine, amodiaquine, quinine, and mefloquine were assessed with respect to functional responses (chemotaxis, anion superoxide generation, and lysosomal enzyme release) of rat polymorphonuclear leukocytes (PMN) collected after induction of acute pleural inflammation. Chloroquine, amodiaquine, and mefloquine exhibited dose-dependent inhibition of: (1) random migration and oriented migration of PMN; and (2) opsonized zymosan- or phorbol myristate acetate-stimulated PMN O2- release. These effects were not stimulus-specific and were largely reversed by washing the cells before stimulation Mefloquine was the most effective drug. Quinine had no effect on PMN migration. Apart from quinine, the drugs induced similar dose-dependent increases in beta-glucuronidase release from unstimulated PMN. Only quinine inhibited the enzyme release from stimulated PMN. Our data show that the antimalarial derivatives affect PMN functions in various ways and suggest that their effects reflect nonspecific modifications of cellular membrane.
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PMID:Effects of some antimalarial drugs on rat inflammatory polymorphonuclear leukocyte function. 254 68

The effect of the antimalarial drug mefloquine on human neutrophil degranulation, chemiluminescence, superoxide production and viability was examined in vitro. Mefloquine was found to significantly stimulate the release of lysozyme, beta-glucuronidase and myeloperoxide at a concentration of 10 micrograms/ml (2.5 X 10(-5) M) without loss of cell viability. At 40 micrograms/ml mefloquine (1 X 10(-4) M) cell viability was significantly decreased. Mefloquine at 10 micrograms/ml also significantly increased the release of lysozyme and beta-glucuronidase but not myeloperoxidase when neutrophils were stimulated with opsonized zymosan. At a lower zymosan concentration myeloperoxidase release was also increased. Enzyme activity was not directly stimulated by mefloquine. Mefloquine at 10 micrograms/ml significantly increased luminol-dependent chemiluminescence but significantly inhibited lucigenin-dependent chemiluminescence when neutrophils were stimulated with opsonized zymosan. Under these conditions superoxide release, measured by cytochrome c reduction, was inhibited to a lesser degree. These results are discussed with reference to our previous report that mefloquine inhibits the neutrophil iodination reaction [Immunology 58: 125-130, 1986] and the use of mefloquine as an anti-inflammatory drug.
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PMID:Stimulation of human neutrophil degranulation by mefloquine. 284 64