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)

A number of cytochemical parameters of the hemocytes of larval Galleria mellonella, an insect frequently used as a model by comparative cellular immunologists, are described. Cytochemical methods were used to quantify hemocyte granule-associated components, the results are compared to those obtained for leukocytes from higher animals. Granulocytes contained a population of nonlysosomal granules rich in mucopolysaccharide not seen in plasmatocytes. The numbers and dimensions of these granules showed a positive correlation to cell size, probably reflecting a developmental sequence in granulocyte maturation. Both granulocytes and plasmatocytes had other granules containing the typical lysosomal enzymes, acid phosphatase, beta-glucuronidase, esterase, and lysozyme. The nonlysosomal enzyme alkaline phosphatase was not found in Galleria hemocytes; it is also absent from vertebrate monocytes, macrophages, and immature polymorphonuclear leukocytes. Insect hemocytes appear to lack certain components of antibacterial systems typical of mammalian blood cells, such as H2O2-generating systems, cationic proteins, and myeloperoxidase. The bactericidal mechanisms of hemocytes probably involve lysozyme, as well as other biologically active cellular and humoral factors unique to insects.
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PMID:Observations on the cytochemistry of the hemocytes of an insect, Galleria mellonella. 618 80

Human polymorphonuclear leukocytes (PMN) exposed to particulate and soluble stimuli secrete lysosomal enzymes. These stimuli cause prompt (less than 10 sec) changes in membrane potential followed 30--45 sec later by superoxide anion (O-2.) production. We describe a new technique utilizing flow dialysis apparatus which monitors the first stages of lysosomal enzyme release with a resolution of approximately 6 sec. Secretion of beta-glucuronidase from cytochalasin B-treated PMN could be detected 19+/-5 sec after exposure to the chemotactic peptide N-formylmethionylleucylphenylalanine (FMLP). The "lag" times for release of this enzyme were different for other stimuli: 35+/-8 sec (BSA/anti-BSA immune complex); 48+/-8 sec (serum-treated zymosan, "STZ"); 60+/-25 sec (calcium ionophore A23187). The lag times for lysozyme release were less dependent upon the stimulus presented (28+/-16 sec for FMLP, 28+/-8 sec fo BSA/anti-BSA, 32+/-10 sec for STZ, and 38+/-8 seconds for Con A); only A23187 had a long lag period: 74+/-27 sec. Lag periods for the onset of O-2. production (measured by the same mathematical criteria) were comparable to those for beta-glucuronidase release: 21+/-4 sec for FMLP, 43+/-14 sec for BSA/anti-BSA, 62+/-7 sec for Con A, and 50+/-13 sec for A23187. Changes in FMLP dose up to 100-fold affected the magnitudes of O-2. generation and beta-glucuronidase release, but did not alter the time required for the onset of these processes. A variety of agents, such as corticosteroids, colchicine, 2-deoxyglucose, and N-ethyl maleimide, also affected the magnitudes of the responses, but not the lag periods when FMLP was used as the stimulus. When BSA/anti-BSA immune complex was used as the stimulus, 2-deoxyglucose and N-ethyl maleimide increased the lag period for superoxide anion generation, but not for lysosomal enzyme release. This new flow dialysis technique has permitted us to demonstrate the O-2. production and lysosomal enzyme secretion are concurrent but dissociable processes which are subsequent to earlier responses of the granulocyte-to-ligand-receptor interactions as reflected by changes in membrane potential.
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PMID:Initial kinetics of lysosomal enzyme secretion and superoxide anion generation by human polymorphonuclear leukocytes. 624 64

Rhinovirus respiratory infections have been frequently associated with the precipitation of an asthma attack. As an explanation for virus-provoked asthma, it has been proposed that viruses or their products may alter beta-adrenergic responsiveness. Isolated human granulocytes have provided an in vitro study model for this problem. Granulocyte release of the lysosomal enzyme beta-glucuronidase (BG) occurred after incubation with complement-activated zymosan particles, and this release was inhibited by isoproterenol (ISO), histamine (HIS) acting via its H2 receptor, and prostaglandin E1 (PGE1). In asthma, the granulocyte response to HIS and ISO was impaired, and the ISO impairment was accentuated during virus-provoked asthma. After an in vitro incubation of polymorphonuclear leukocytes (PMN) with rhinovirus 16, the granulocyte response to ISO, HIS, and PGE1 was significantly reduced. This change in agonist response was proportional to the virus dosage, maximal at 37 degrees C and after a 60-min incubation period, and occurred with heat or UV-inactivated virus. It is possible that impaired beta-adrenergic responsiveness may also develop in other tissues, such as the airway smooth muscle, and thus explain, in part, wheezing during viral respiratory infections.
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PMID:Reduced granulocyte response to isoproterenol, histamine, and prostaglandin E1 after in vitro incubation with Rhinovirus 16. 625 14

We describe a patient whose peripheral blood neutrophils and bone marrow precursors (beyond promyelocytes) contained multiple large azurophilic granules. There were also giant granules in eosinophils, basophils, melanocytes, renal tubules, thyroid, and neurones, but not lymphocytes or monocytes. His clinical course included recurrent (ultimately fatal) infections and severe neurologic impairment. Immunofluorescent staining with fluoroscein- and rhodamine-conjugated antisera to primary and secondary granule markers showed virtually all of the granulocyte granules and rare monocyte granules to be fusion products containing both markers. Electron microscopy showed the granules to be large peroxidase-containing lysosomes. Only rare normal primary and secondary granules were present. Superoxide generation in response to opsonized zymosan was 7.3 nmole/min/10(6) cells (control 8.9); but in response to phorbol myristate acetate, only 2.2 (control 9.4). Nitroblue tetrazolium slides showed 3+ dye reduction in response to opsonized zymosan by 90% of granulocytes (control 91%) and to phorbol myristate acetate by 22% (control 99%), with 71% producing only a minimal 1+ response. Cellular contents of myeloperoxidase and beta-glucuronidase were elevated, but the percent release during exocytic degranulation was equivalent to control. Ingestion of complement-opsonized Staphylococcus aureus and zymosan was also normal. Killing of Staphylococcus aureus was 60% at 90-min incubation (control 92%). Granulocyte cyclic adenosine monophosphate (AMP) content was 4 pmole/10(7) cells (control 3.1). In order to determine whether these characteristics derived from the cells' genetic program or their environment, the patient's bone marrow was grown in long-term culture. Granulocytes produced in vitro demonstrated the same morphology, same defect in activation of nitroblue tetrazolium reduction, and same normal cyclic AMP level as those harvested from peripheral blood. These studies describe a new disorder of granulocytes; the structural similarity to, but biochemical differences from, Chediak-Higashi disease indicate the probable heterogeneity of mechanisms for the same morphological abnormality.
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PMID:Human neutrophil dysfunction with giant granules and defective activation of the respiratory burst. 630 85

When exposed to zymosan or latex particles or heat-inactivated staphylococci, freshly prepared human blood monocytes and granulocytes rapidly released a large fraction of their lysozyme content. Within 24 hours the total lysozyme activity in the monocyte suspensions tripled, while it doubled in the granulocyte suspensions, indicating synthesis of the enzyme following release. The monocytes in particular seemed to release and synthesize lysozyme without any other stimulus than contact with lymphocytes and the tube walls. Potassium caseinate in solution did not influence the lysozyme release. Myeloperoxidase and beta-glucuronidase, which in the granulocytes are kept in lysosomal fractions separate from most of the lysozyme, were neither released nor synthesized to a significant degree. Moreover, the minute amount of lactate dehydrogenase released indicated that the lysozyme release was not the result of cell lysis. Accordingly, the monocytes, which are not already stimulated by adherence to nonphagocytosable surfaces, are capable of selective enzyme release similar to that of the granulocytes.
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PMID:In vitro release of lysozyme from monocytes and granulocytes. 632 67

Histamine inhibits the in vitro release of granulocytic lysosomal beta-glucuronidase when incubated with complement activated zymosan particles and this is an H2-receptor response. The highly specific histamine H2-receptor agonist, dimaprit, also inhibits this secretory enzyme release but is less potent (-log molar ED50 6.71 with histamine vs. -log ED50 5.97 with dimaprit, p less than 0.05). No change in beta-glucuronidase release was found with the H1-agonst, 2-(2 pyridyl)-ethylamine. The antagonist activity of metiamide was similar with the two agonists (KB = 2.9 x 10(-8) M with histamine and KB = 3.6 x 10(-8) M with dimaprit). Diphenhydramine did not change the granulocyte response to either histamine or dimaprit.
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PMID:Dimaprit inhibition of zymosan-stimulated beta-glucuronidase release from human granulocytes. 644 28

Captopril, competitive inhibitor of angiotensin converting enzyme, is clinically employed for its antihypertensive activity and drug-dependent granulocytopenia or agranulocytosis have been seldom observed during treatment. In previous unpublished studies an activating effect of the drug on the complement alternate pathway has been demonstrated. In this paper we demonstrate that captopril-treated serum is able to "in vitro" induce granulocyte activation and aggregation. Granulocyte aggregation was shown by the turbidimetric method and cellular activation was confirmed by the release of the granule associated enzyme lysozyme and beta-glucuronidase. On this basis complement-mediated leukoaggregation and leukosequestration in vivo could be proposed as the effector mechanism of peripheral leukopenia.
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PMID:Captopril-induced granulocyte aggregation. A possible complement mediated mechanism of peripheral leukopenia. 676 21

A quantitative cytochemical study has been made, using scanning-integrating microdensitometry, of 1000 toxic granulation blood neutrophils from 20 infected patients, in comparison with 1250 normal blood neutrophils. Myeloid precursor cells in 10 normal marrows were also studied. Normal bone marrow granulocyte maturation was associated with a progressive decrease in azurophilic granule enzymes (myeloperoxidase, beta-glucuronidase, acid phosphatase, chloroacetate esterase), and also Alcian blue staining from acid mucosubstance, but an increase in the specific granule marker lactoferrin. Toxic granulation blood neutrophils showed minor changes in the enzyme content of their azurophilic and specific granules, consistent with cell immaturity, and an increase in acid mucosubstance in azurophilic granules. Abnormal maturation of azurophilic granules, with persistence of acid mucosubstance, is the likely explanation for the intense Romanowsky dye staining of the toxic granulation neutrophil.
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PMID:Quantitative cytochemistry of the toxic granulation blood neutrophil. 684 17

The reaction of FMLP with granulocytes causes aggregation and degranulation and enhances adherence to endothelium. To evaluate whether prevention of granule extrusion could impair these granulocyte activities, granulocytes were treated with either dexamethasone or hydrocortisone prior to treatment with FMLP. Dexamethasone was added to suspensions of cytochalasin B-treated granulocytes; it markedly impaired the aggregation response of the granulocytes of FMLP. When cytochalasin-B was not used, granulocyte aggregation in response to FMLP or PMA was inhibited by dexamethasone. Although dexamethasone prevented aggregation of cells following stimulation with FMLP or PMA, it failed to prevent the aggregation of granulocytes induced by rabbit lactoferrin. Adherence of granulocytes to human endothelial monolayers was enhanced by FMLP; dexamethasone inhibited the enhancement. However, with the addition of human lactoferrin to the granulocytes exposed to dexamethasone, the cells were able to adhere as well to endothelium as the cells exposed to FMLP but free of dexamethasone. When cytochalasin-B-treated granulocytes were incubated with dexamethasone or hydrocortisone prior to the addition of FMLP, the subsequent release of lactoferrin was substantially blocked, whereas the release of the primary granule products, lysozyme and beta-glucuronidase, was attenuated but not completely blocked. Thus, corticosteroids might block chemotactic-factor-induced granulocyte aggregation by selectively preventing release of specific granule products that contribute to and sustain aggregation.
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PMID:Mechanism of dexamethasone inhibition of chemotactic factor induced granulocyte aggregation. 705 39

The effect of corticosteroid therapy on the broncho-alveolar cell response, the changes in activity of some lysosomal enzymes and the protein and lipid biosynthesis rates in lung tissue of normal rabbits and of rabbits after induction of an acute inflammation by the intravenous injection of complete Freund's adjuvant (CFA) 0,2 ml/kg body weight was investigated. Three intramuscular injections of methylprednisolone acetate (Depo-Medrol) 1,2 mg/kg over a period of 8 days reduced the mean total broncho-alveolar free cell yields significantly. The percentages of lymphocytes and granulocytes were decreased. The increase in the macrophage percentage was associated with a significant increase in the acid phosphatase activity of the broncho-alveolar cells. The beta-glucuronidase activity, on the other hand, was lowered in alveolar cells and even significantly suppressed in lung tissue. Protein and lipid biosynthesis was significantly retarded in lung tissue 8 days after the start of therapy. Administration of a single dose of CFA 0,2 ml/kg evoked an acute lung inflammation and a significant increase in total alveolar free cell yields. The macrophage percentage was reduced and the lymphocyte numbers doubled, whereas the granulocyte percentage increased more than sevenfold. The change in the percentage distribution of granulocytes may be associated with the marked increase in beta-glucuronidase activity of the cells as well as of the lung tissue. In the inflammatory phase, protein biosynthesis was significantly increased but lipid synthesis was not affected. Corticosteroid therapy in animals treated with adjuvant reversed all the effects of CFA. It has very pronounced anti-inflammatory action and a catabolic effect on protein and lipid metabolism.
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PMID:The effect of corticosteroid therapy on lysosomal enzymes and protein and lipid metabolism in rabbit lung after administration of Freund's adjuvant. 713 14


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