Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

C3e is a leukocytosis-inducing peptide of degraded C3 that has the electrophoretic behavior of prealbumin and a MW of 10-12,000. Using a homogeneous preparation, the ability of C3e to promote lysosomal enzyme release from human polymorphonuclear leukocytes (PMNs) was examined by incubation of various concentrations of C3e with cytochalasin B-treated (5 micrograms/ml) human PMNs for 60 min at 37 degrees C. Amounts of extracellular beta-glucuronidase, myeloperoxidase, and lysozyme were determined in the cell-free supernatants and it was found that all three enzymes were released in significant amounts without concomitant release of the cytoplasmic enzyme lactate dehydrogenase (LDH). At a concentration of 25 micrograms/ml of C3e, 25 +/- 1.1% (SD) of lysozyme, 20 +/- 0.9% beta-glucuronidase, and 24.3 +/- 0.9% myeloperoxidase were released into the supernatant while the release of LDH remained within the 4-7% range throughout these studies. Furthermore the supernatants were found to contain a substance which was capable of a generating chemotactic fragment from isolated C5. The same range of C3e concentrations (5-25 micrograms/ml) was, however, incapable of effecting histamine release from basophils. These results suggest that generation of C3e in vivo may serve as a potent stimulus for the generation of the C5-cleaving enzyme from PMNs which in turn may function to recruit more neutrophils by a positive feedback mechanism.
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PMID:The release of lysosomal enzymes from human polymorphonuclear leukocytes by human C3e. 619 20

Protein-derived basic CD spectra for alpha-helical, beta-structural, beta-bends and irregular regions of the proteins have been determined from the experimental CD spectra of five reference proteins (myoglobin, lysozyme, ribonuclease A, papain, lactate dehydrogenase) with the knowledge of the fractions of the residues in the corresponding conformation. The alpha-helical and beta-structural regions of the reference proteins have been isolated from the X-ray data using the common "rigid" criteria for all the proteins, as proposed by Finkelstein and Ptitsyn. The residues in the beta-bend have been isolated using the data of Chou and Fasman and also three assumptions formulated in the present paper. The basic CD spectra thus obtained have been used for the analysis of secondary structures of 10 proteins (5 reference and 5 additional ones). There is a good agreement between the results of the X-ray data and those obtained from the CD spectra.
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PMID:[Determination of the secondary structure of proteins from their circular dichroism spectra. II. Estimation of the contribution of beta-pleated sheets]. 625 45

12-O-Tetradecanoylphorbol 13-acetate (TPA), phorbol 12,13-diacetate and phorbol 12,13-didecanoate were all potent inducers of thromboplastin activity in human monocytes in vitro, whereas 4 alpha-phorbol 12,13-didecanoate and 4 alpha-phorbol had no such effect. A concomitant increase in titrable apoprotein III antigen was found (apoprotein III is the protein component of thromboplastin). The increase was inhibited by cycloheximide and actinomycin D and partly by alpha-amanitin. The increase of thromboplastin activity was therefore most likely due to synthesis de novo of apoprotein III. The response was approximately halved in the absence of serum or Ca2+. Retinol had a weak inhibitory effect, and retinoic acid was inhibitory only at concentrations that also induced signs of cytotoxicity. TPA caused an initial rise in monocyte cyclic AMP concentration of about 90-120 min duration. No increase in 45Ca2+ influx was induced over 2 h. Good correlation exists between induction of apoprotein III synthesis in monocytes in vitro and mouse skin-tumour promotion in vivo by the various phorbol derivatives. Substances inactive in tumour promotion do not induce the synthesis of apoprotein III. General activating and cytotoxic effects of TPA were monitored by determining release of lysozyme, beta-glucuronidase and lactate dehydrogenase.
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PMID:Phorbol esters induce synthesis of thromboplastin activity in human monocytes. 627 36

The interaction of cytochalasin B-treated human neutrophils with the synthetic tripeptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP) results in a time- and concentration-dependent generation of superoxide anion (O2-) by an extracellular release of granule-associated beta-glucuronidase and lysozyme from these cells. Granule exocytosis was not accompanied by significant cytoplasmic lactate dehydrogenase extrusion. FMLP-stimulated O2- production occurs but is significantly curtailed in the absence of extracellular calcium. Nevertheless, incubation of neutrophils with EGTA in calcium-free medium had no effect on the O2- -generating system. Trifluoperazine (TFP), an inhibitor of calmodulin (a calcium-binding protein), caused a dose-related inhibition of FMLP-elicited degranulation and O2- production in the presence of absence of extracellular calcium. This effect TFP could be reversed by washing the cells before contact with FMLP. These data suggest that TFP represents a useful tool for defining the relevance of calmodulin and calcium to neutrophil function.
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PMID:Effects of trifluoperazine on human neutrophil function. 627 92

Protein-derived basic CD spectra for alpha-helix, antiparallel and parallel beta-structures, beta-bends and irregular form of proteins have been determined from the experimental CD spectra of six (myoglobin, lysozyme, ribonuclease A, papain, lactate dehydrogenase, subtilisin BPN') or seven (glyceraldehyde-3-phosphate dehydrogenase added) reference proteins and the analysis of the X-ray data. The secondary structures of thirteen proteins (seven reference and six additional ones) have been analysed using the basic CD spectra thus obtained. The data obtained have been compared with the results of the X-ray data analysis. It is shown that the accuracy of determination of the beta-structure and beta-bends contents using our basic CD spectra is about 2-3 times better than using the basic spectra reported by Chang et al. (Analyt. Biochem. 91, 13-31, 1978).
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PMID:[Determination of protein secondary structure from circular dichroism spectra. III. Protein-derived base spectra of circular dichroism for antiparallel and parallel beta-structures]. 627 89

The anti-inflammatory effects of gold compounds include suppression of PMN lysosomal enzyme release. Since lysosomal products can provoke PMN aggregation, we assessed the effect of two gold compounds, auranofin and GST, on suppressing aggregation, degranulation, and metabolic functions of the cells. Aggregation of 1 x 10(7) cytochalasin B-treated PMNs in response to 2 x 10(-7)M FMLP, as assessed by light scattering, was inhibited in a dose-dependent fashion by both drugs. Concentrations of auranofin ranging from 5 to 20 microM caused 30.8% to 89% inhibition, whereas 200 microM GST reduced aggregation by only 32%. FCS or BSA added to suspensions of normal PMNs considerably reduced the gold compound inhibitory effect on PMN aggregation. Cell viability assessed by dye exclusion and lactate dehydrogenase release was unaffected by the drugs. The suppressive activities of the drugs could not be removed by washing the PMNs. Correspondingly, the drugs suppressed lysosomal enzyme release induced by FMLP of PMNs rendered secretory with cytochalasin B. Concentrations of 20 microM auranofin and 200 microM GST resulted, respectively, in a 61.5% and 19.3% reduction of release of lysozyme, 61.7% and 27.1% reduction of beta-glucuronidase, 84.8% and 33.7%s reduction of myeloperoxidase, and 50.0% and 25.0% reduction of lactoferrin. Furthermore, auranofin inhibited 14C-1-glucose oxidation through the hexose monophosphate shunt in response to stimulation by either PMA or methylene blue. The in vivo studies suggested that auranofin could prevent neither neutropenia induced by zymosan-activated serum nor a corresponding rise in plasma lactoferrin levels. These findings suggest that the beneficial effect of gold compounds in rheumatoid arthritis are unlikely to be related to their ability to dampen PMN activation in vivo.
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PMID:Correlation of in vitro and in vivo effects of gold compounds on leukocyte function: possible mechanisms of action. 628 1

Leukotriene D4 (LTD4), the most active spasmogenic leukotriene constituent of the slow reacting substance of anaphylaxis was converted by suspended human polymorphonuclear leucocytes (PMNs) to a single, less polar metabolite which was not further catabolized. This product was identified as leukotriene E4 (LTE4) by its retention time during reverse phase-high performance liquid chromatography (RP-HPLC) and subsequent bioassay on the guinea-pig ileum. LTD4 with a retention time of 21 +/- 1.6 min (mean +/- SD) and a contractile activity of 5.0 +/- 0.4 u./pmol (mean +/- SD) was quantitatively converted extracellularly by PMNs to LTE4 with a retention time of 26 +/- 1.8 min and a contractile activity of 1.2 +/- 0.3 u./pmol. Subcellular fractionations of PMNs revealed the recovered LTD4-to-LTE4 converting activity, termed LTD4 dipeptidase, to be localized only in he granule fraction. There was a time- and calcium-dependent extracellular release of LTD4 dipeptidase in association with lysozyme (r = 0.97, n = 16, P less than 0.001), a constituent of both specific and azurophilic granules, in the absence of release of cytoplasmic lactate dehydrogenase (LDH) and of beta-glucuronidase from the azurophilic granule. Phorbol myristate acetate (PMA), which selectively induces secretion of specific granules, released lysozyme and the LTD4 dipeptidase in a constant dose-dependent manner from PMNs (r = 0.96, n = 8, P less than 0.001). Calcium ionophore A23187 at concentrations less than 10(-7) M stimulated the parallel secretion of LTD4 dipeptidase and lysozyme (r = 0.91, n = 9, P less than 0.005), dipeptidase and lysozyme (r = 0.91, n = 9, P less than 0.005), whereas higher concentrations resulted in secretion of beta-glucuronidase and additional lysozyme without further release of dipeptidase. Thus, human PMNs can convert LTD4 to LTE4, a less vasoactive and spasmogenic leukotriene, via the secretion of a dipeptidase associated with the specific granules.
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PMID:Conversion of leukotriene D4 to leukotriene E4 by a dipeptidase released from the specific granule of human polymorphonuclear leucocytes. 629 69

UICC, other well-defined asbestos samples and different man-made mineral fibers (MMM) such as glass fiber and synthetic amphibole asbestos were studied in vitro by using rat and guinea pig lung macrophages. These samples had relatively narrow length and diameter spectra. Most of the fiber samples were added to the cultures on a gravimetric basis, although some were added on a numerical basis. Electrocorundum and DQ12 (Dorentruper Quartz) were used as controls at comparable gravimetrical concentrations. The assays used were the release of lactate dehydrogenase (to demonstrate plasma membrane permeability) and the release of beta-glucuronidase (to indicate lysosomal permeability). Carbohydrate metabolism was monitored by the measurement of lactic acid production and, as one of the tests for macrophage function, the production of lysozyme was determined. The phagocytic ability of the cells was measured, after the addition of opsonized zymosan, by bioluminescence following luminol enhancement. Only some results could be evaluated, however, due to technical difficulties. A length- and dose-dependent cytotoxicity of the fibers was found in this system which was similar to that previously described with permanent cell lines. No great differences were found between fibers having different physicochemical compositions if their geometric dimensions were similar. Long, very thin fibers of glass, chrysotile, crocidolite and synthetic fluoroamphiboles were all toxic in the test system.
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PMID:Macrophage functions after exposure to mineral fibers. 631 84

We have found that pretreatment of human neutrophils with phenytoin (0.05 to 0.8 mM) results in concentration-dependent, reversible inhibition of both superoxide anion generation and release of lysosomal enzymes (myeloperoxidase, lysozyme, beta-glucuronidase) provoked by either the synthetic peptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP) or the complement fragment C5a. In contrast, phenytoin did not inhibit either enzyme release or superoxide anion generation by neutrophils stimulated with phorbol myristate acetate or serum-opsonized zymosan particles. Phenytoin did not provoke leakage from neutrophils of the cytoplasmic enzyme, lactate dehydrogenase, and did not inhibit directed migration (chemotaxis) of neutrophils toward either FMLP or C5a. Specific binding of 3H-FMLP to neutrophil membrane receptors was not altered significantly by pretreatment of the cells with a wide range of concentrations of phenytoin. With flow microfluorometry and the fluorochrome, 3,3'-dipentyloxacarbocyanine, phenytoin was shown to prevent FMLP-induced changes in fluorescence intensity (i.e., apparent neutrophil membrane depolarization). These data indicate that various neutrophil functions may be regulated independently at other than the receptor level and that neutrophil chemotactic responses to FMLP and C5a do not appear to be dependent on membrane events registered by 3,3'-dipentyloxacarbocyanine.
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PMID:Selective inhibition by phenytoin of chemotactic factor - stimulated neutrophil functions. 631 77

Sodium benzoate is widely used as a food preservative and reputed to be a scavenger of hydroxyl radical (.OH). The effects of sodium benzoate on the function of polymorphonuclear leukocytes (PMN) stimulated by S. aureus or the chemical agent, phorbol myristate acetate (PMA) were examined in vitro using assays of chemiluminescence (CL), total bactericidal activity, intracellular recovery of bacteria, as well as release of lactate dehydrogenase (LDH), lysozyme and superoxide anion (O2(-)). Sodium benzoate decreased chemiluminescence, superoxide anion and lysozyme release by PMN stimulated with S. aureus but did not similarly affect these responses of PMN to the chemical agent, PMA. The ability of PMN to kill S. aureus was also impaired by sodium benzoate and associated with a reduced number of intracellular bacteria recovered after 90 minutes incubation. LDH release from PMN was not demonstrable at concentrations of sodium benzoate below 100 mM indicating that damage can not account for these findings. The underlying mechanism of the altered bactericidal function of PMN treated with sodium benzoate appears to be a result of decreased uptake of S. aureus.
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PMID:Effect of sodium benzoate on polymorphonuclear leukocyte function. 632 35


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