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:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study analyzed the neutrophils and sera of patients with rheumatoid arthritis and of normal controls. No significant differences were found in the activities of the granular enzymes beta-glucuronidase and lysozyme or the cytoplasmic enzyme lactic dehydrogenase (LDH). Normal neutrophils were found to release significant (P less than 0.05) amounts of the granular enzymes, but not of LDH in response to immunoglobulin G aggregates. There was no difference in the percent release exhibited by rheumatoid versus control neutrophils. Studies delineating the effects of rheumatoid factor sera and normal sera on aggregate-induced enzyme release revealed a significant negative correlation between the amount of rheumatoid factor in the sera and the percent release of beta-glucuronidase and lysozyme but not of LDH. These studies thus demonstrate no abnormalities in rheumatoid neutrophil or rheumatoid serum enzyme activities or in neutrophil response to immunoglobulin G aggregates. They suggest, however, that rheumatoid factor may partially inhibit the release of lysosomal enzymes, thus suppressing this important component of the rheumatoid inflammatory process.
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PMID:Neutrophil enzyme activities in rheumatoid inflammation. 47

Dogs were given gentamicin (10 mg/kg) intramuscularly every 8 hr for 10 days. Levels of serum creatinine rose by day 6 (0.91 +/- 0.08 vs. 0.75 +/- 0.02 mg/dl for controls, P less than 0.05) and of blood urea nitrogen by day 8 (24.3 +/- 4.80 vs. 16.1 +/- 0.90 mg/dl for controls, P less than 0.05). Gentamicin nephrotoxicity occurred earlier and was more marked when furosemide (2 mg/kg) was added: the level of serum creatinine by day 6 was 1.62 +/- 0.25 mg/dl (P less than 0.05), and the level of blood urea nitrogen by day 8 was 181 +/- 23.5 mg/dl (P less than 0.01). Elevations in the activities of the urinary enzymes beta-glucuronidase, N-acetyl-beta-glucosaminidase, and muramidase preceded rises in levels of serum creatinine and blood urea nitrogen. Examination of serial percutaneous renal biopsy specimens showed that gentamicin administration was associated with hyaline droplet degeneration, lysosomal changes, and, later, cell necrosis (primarily of the proximal tubules). Changes in renal morphology were more severe and occurred earlier when furosemide was administered concomitantly. In summary, furosemide enhanced gentamicin nephrotoxicity. Enzymuria was an early sign of gentamicin nephrotoxicity.
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PMID:Furosemide enhancement of experimental gentamicin nephrotoxicity: comparison of functional and morphological changes with activities of urinary enzymes. 50 Nov 48

Cartilaginous defects were created in the radiocarpal joints of 12 horses. Synovial fluid cytologic features, lysozyme activity, and beta-glucuronidase activity were monitored for 16 days. A comparison was made of plasma lysozyme and beta-glucuronidase activity and of synovial fluid lysozyme, beta-glucuronidase, and leukocyte concentrations. Plasma lysozyme was found to be independent of synovial fluid lysozyme activity. Synovial fluid lysozyme was significantly increased (P less than 0.001) in all joints with surgically induced defects (group I) compared with controls (arthrocentesis done; group III). However, there was no significant difference in lysozyme activity in group I joints and sham-operated controls (cartilage exposed only; group II). Increased lysozyme concentration was found to be positively correlated with increased numbers of leukocytes in the synovial fluid. Parallel changes were noted in synovial fluid beta-glucuronidase activity, indicating that much of the observed synovial fluid lysozyme activity was of lysosomal origin and not from cartilage destruction. Lysozyme activity in synovial fluid was found to be a very sensitive indicator of acute joint injury or inflammation (or both).
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PMID:Plasma and synovial fluid lysozyme activity in horses with experimental cartilage defects. 52 71

The effect of pyran copolymer, injected into mice bearing the M109 Madison lung carcinoma, on serum concentrations of lysozyme, beta-glucuronidase, and N-acetyl-beta, D-glucosaminidase was studied and compared with that of other immunoadjuvants. Increases in lysozyme levels ranging from 50 to 100% were observed after injection of pyran, BCG and Bru-Pel; increases in the levels of the other enzymes were less consistent. Other immunoadjuvants were less effective in raising serum concentrations of lysosomal enzymes. The findings were correlated with the results of previous studies on macrophage activation and antineoplastic action produced by these immunoadjuvants and suggest that serum levels of lysozyme can serve as indices of these effects.
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PMID:Effect of macrophage activation by immunoadjuvants on serum levels of lysosomal hydrolases in mice. 55 9

Rabbit polymorphonuclear leukocytes were incubated with a sonically treated suspension of pooled dental plaque to determine if the plaque would induce release of lysosomal enzymes from the polymorphonuclear leukocytes. Cells incubated with plaque at 37 degrees C released significantly greater amounts of the lysosomal enzymes, beta-glucuronidase and lysozyme, than did cells incubated with plaque at 0 degrees C or without plaque at 37 degrees C. This response was both dose and time dependent. Release of the cytoplasmic enzyme lactate dehydrogenase was minimal, and there were no significant differences in lactate dehydrogenase release between cells at 0 and 37 degrees C, or without plaque. These results indicate that dental plaque can induce the selective release of lysosomal enzymes, which could be involved in the periodontal injury produced by dental plaque.
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PMID:Exocytosis of polymorphonuclear leukocyte lysosomal contents induced by dental plaque. 56 Oct 32

The dose-response effects of phorbol myristate acetate and cytochalasin B on secretion of azurophil and specific granule enzymes from viable human polymorphonuclear leukocytes have been examined. Secretion of the azurophil granule enzymes elastase and beta-glucuronidase from cells exposed to 50 ng/ml of phorbol myristate acetate is dependent on prior exposure of the cells to greater than 0.5 mg/ml of cytochalasin B. In contrast, the secretion of the specific granule enzyme lysozyme is not dependent on pretreatment with cytochalasin B. The concentration of phorbol myristate acetate needed to elicit maximal secretion of specific versus azurophil granule enzymes differs, being 5.0 ng/ml and 50 ng/ml, respectively. The results suggest that cytochalasin B-sensitive cellular components, possibly microfilaments, may selectively modulate some step in the exocytosis of azurophil granule enzymes from human polymorphonuclear leukocytes exposed to phorbol myristate acetate.
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PMID:Cytochalasin B-dependent release of azurophil granule enzymes from human polymorphonuclear leukocytes. 61 56

The activity of some lysosomal enzymes has been investigated in venous and arterial blood collected from patients undergoing cardiopulmonary bypass. Before bypass, there is no arterio-venous difference in the activity of n-acetyl-beta glucosaminidase, beta-glucuronidase or lysozyme. After operation, the activity of n-acetyl-beta-glucosaminidase is greater in arterial than in superior caval blood within the first 24 h after bypass, and a small arterio-venous increment in the activity of beta-glucuronidase can also be detected towards the end of the first day. The site of enzyme release has not been identified with certainty but may lie within the pulmonary circulation.
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PMID:Lysosomal enzyme release from the lungs after cardiopulmonary bypass. 64 73

N-acetyl-beta-glucosaminidase (EC 3.2.1.30, recommended name beta-N-Acetylglucosaminidase) was found to be a constituent of human cardiac lysosomes. beta-glucuronidase was also found in this tissue, while lysozyme, an enzyme present in leucocyte lysosomes, was not detectable in the heart. The activities of both N-acetyl-beta-glucosaminidase and beta-glucuronidase were elevated in plasma during the first 24 h after the onset of chest pain in patients with acute myocardial infarction and the peak levels of N-acetyl-beta-glucosaminidase correlated well with those of creatine kinase. N-acetyl-beta-glucosaminidase showed a further rise in plasma activity which gave a peak at 72 h after the onset of chest pain and this was accompanied by a rise in lysozyme activity. It is suggested that lysosome disruption caused by myocardial cell necrosis was responsible for the initial rise in plasma lysosomal enzyme activity and that the subsequent inflammatory reaction gave rise to the second peak.
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PMID:Plasma lysosomal enzyme activity in acute myocardial infarction. 64 16

The ability of highly purified human leukocytic pyrogen (LP) to induce neutrophil lysosomal protein release is described. Human peripheral blood neutrophils isolated by Ficoll-Hypaque and dextran sedimentation were exposed to purified human LP. The specific granule-associated proteins, lysozyme and lactoferrin were selectively released, whereas primary granule (beta-glucuronidase) and cytoplasmic (lactic dehydrogenase) enzyme markers were not. Optimum release was observed after 45 min in the presence of Ca++ and Mg++. Cytochalasin B (5 microgram/ml) had no effect on LP-induced lysosomal enzyme release. Since the pyrogenicity of LP is dependent on prostaglandin synthesis, the effect of two potent inhibitors of prostaglandin synthesis on lysozyme release was studied. Both indomethacin and naproxen failed to inhibit specific granule protein release. These observations suggest that the concommitance of fever, elevated serum or urine lysozyme and hypoferremia may, in part, be explained by the interaction of LP and peripheral blood neutrophils.
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PMID:Human leukocytic pyrogen induces release of specific granule contents from human neutrophils. 65 95

On the basis of experimental research results a method to assess the functional state of pulmonary alveolar macrophages in rabbits and rats has been proposed as a criterion of the biological effect of chemical atmospheric pollutants. The test involves a cytological assay, determination of the viable cells quantity and of the phagocytic competence, and also the biochemical study of alveolar macrophages enzymes activity (acid phosphatase, beta-glucuronidase, lysozyme, beta-galactosidase, beta-glucosidase, N-acetyl-beta-D-glucosaminidase). It has been shown that this method is informative and reliably reproducible, and that it was reasonable to use it in environmental health and other branches of experimental biology and medicine.
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PMID:[Method of studying the functional state of pulmonary alveolar macrophages during exposure to atmospheric pollutants]. 71 64


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