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)

Stimulation of polymorphonuclear leukocytes with kallikrein demonstrated that enzyme acts selectively on the release of lysosomal enzymes of these cells. The release of collagenase, similarly to the release of lysozyme into the incubation medium increased proportionally to kallikrein concentration and the duration of incubation. Kallikrein had a small effect on beta-glucuronidase secretion. No effect on cytoplasm lactate dehydrogenase release was detected. These results suggest that kallikrein, as a soluble stimulus, predominantly induces degranulation of specific granules containing collagenase capable of degrading the connective tissue. Secretion of lysozyme and collagenase requires the presence of active kallikrein. Soybean trypsin inhibitor diminished the enzyme release.
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PMID:Influence of human plasma kallikrein on lysosomal enzyme release from polymorphonuclear leukocytes. 165 May 20

Mediators released from injured human skin that initiate the inflammatory response have not been adequately identified. Organ culture of full-thickness skin explants enables us to do so, because injury to the skin can be made in vitro, eliminating the rapid leakage of serum and infiltration of leukocytes that occur in vivo. In our studies, the military vesicant sulfur mustard (SM) (10 microliters of a 0.01 to 1.0% dilution) was topically applied to injure the epidermis of the explant. Then, the explants were cultured in small Petri dishes, usually for 18 h at 36 degrees C, and the organ-culture fluids were assayed for various inflammatory mediators. We found that the culture fluids from SM-exposed and control explants contained similar amounts of angiotensin-converting enzyme, trypsin-like and chymotrypsin-like proteases, acid phosphatase, beta-glucuronidase, beta-galactosidase, lysozyme, deoxyribonuclease, ribonuclease, interleukin 1, and lactic dehydrogenase. However, the culture fluids from SM-exposed explants contained increased amounts of histamine and plasminogen-activating activity, and often prostaglandin E2, when compared to culture fluids from control explants. After 3 to 4 d in culture, full-thickness human skin explants, when exposed to 0.2% SM (but not when exposed to 1.0% SM), sometimes showed separation of the epidermis and increased collagenase activity (i.e., hydroxyproline release). Thus, histamine (from local mast cells), and prostaglandin E2 and plasminogen-activating activity (probably from both mast cells and epidermal cells) are apparently involved in early mediation of the inflammatory response.
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PMID:Mediators, initiating the inflammatory response, released in organ culture by full-thickness human skin explants exposed to the irritant, sulfur mustard. 171 Jun 39

During the past few years, a considerable number of studies have examined different aspects of the host response in gingival crevicular fluid (GCF), including the relationship of specific markers to the active phases of periodontal disease. Various indicators of the acute inflammatory response (the lysosomal enzymes beta-glucuronidase and collagenase, the cytoplasmic enzyme aspartate aminotransferase, and the arachidonic acid metabolite PGE2) have been shown to be associated with clinical attachment loss in chronic adult periodontitis in man and experimental periodontitis in animal models. In contrast, the relationship of indicators of the humoral immune response in GCF to active periodontal disease is equivocal. Furthermore, a number of indicators of the cellular immune response have been identified recently in GCF (i.e., Interleukin-1 alpha, IL-1 beta, tumor necrosis factor-alpha), but their relationship to active phases of periodontal disease have not been studied. The polymorphonuclear leukocyte (PMN) is the cellular hallmark of acute inflammation. Evidence from the GCF studies suggests that hyperreactivity of these cells plays a critical role in the active phases of some forms of periodontal disease. Metabolic activation of PMN can be associated with a number of potentially destructive reactions. The major effector mechanism for tissue destruction that can be specifically identified with the PMN is the synergistic effect of the release of PMN proteases and the generation of reactive oxygen metabolites by these cells. Priming of the PMN, where the PMN response is enhanced by agents that do not initiate the response, may be an important mechanism for PMN activation in the crevicular environment; for example, cytokines such as IL-1 beta and TNF-alpha, and lipopolysaccharides released from subgingival Gram-negative bacteria, can serve this function. The hypothesis proposed here argues that in addition to the severe forms of periodontal disease that have been associated with qualitative or quantitative PMN defects, tissue destruction in the periodontum can be observed with hyperreactivity of these cells. These differing conclusions do not create a dilemma, but may represent opposite ends of a balance that is no longer in equilibrium.
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PMID:Host mediators in gingival crevicular fluid: implications for the pathogenesis of periodontal disease. 173 70

We used adult rat hepatocytes in primary culture (HPC) as a model system to study the hepatic phase II metabolism of the anticoagulant warfarin. Hepatocytes were isolated by a collagenase perfusion technique and maintained for 24 hr in Waymouth's medium containing 0.1 mM (R)-warfarin. When HPC medium was analyzed by reverse phase high performance liquid chromatography with diode-array detection, 4'-, 6-, and 7-hydroxywarfarin were identified. Several putative conjugates were observed eluting between 13 and 18 min. Treatment of hepatocyte medium with beta-glucuronidase and sulfatase resulted in the loss of five putative conjugates and concomitant increases in 4'-, 6-, and 7-hydroxywarfarin and warfarin, suggesting that these metabolites and warfarin were conjugated. Use of the beta-glucuronidase inhibitor saccharic acid 1,4-lactone enabled the determination of the relative extents of conjugation of each metabolite by glucuronic acid and sulfate. Glucuronidation was the predominant pathway for 4'-hydroxywarfarin, whereas 6-hydroxywarfarin and warfarin occurred mainly as sulfate conjugates. In contrast, 7-hydroxywarfarin was converted to both glucuronide and sulfate conjugates. Exposure of HPC to phenobarbital resulted in a decrease in cytochrome P-450-mediated production of hydroxylated warfarin metabolites; however, an increase in the production of 8-hydroxywarfarin was observed when HPC were exposed to beta-naphthoflavone. Unique conjugation patterns were found when hydroxylated warfarins were substituted for warfarin in HPC medium. Both 7- and 8-hydroxywarfarin were converted to one sulfate and two glucuronide conjugates, whereas 4'-hydroxywarfarin was converted to a single glucuronide conjugate. A spectral library of these conjugates was used to identify the major conjugates of warfarin formed by rat HPC.
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PMID:Phase II metabolism of warfarin in primary culture of adult rat hepatocytes. 173 19

Studies were conducted to assess the mitogenic effect of lysosomal hydrolases, enzymes known to have an association with allergen- or ozone-induced airway hyperreactivity, on bovine tracheal myocytes in culture. Addition of purified human placental beta-hexosaminidase and partially purified bovine liver beta-glucuronidase resulted in the doubling of cell count after 4 d of incubation in medium M199 with 0.4% FBS. Unstimulated cells remained quiescent without a significant increase of cell count. Lysosomal hydrolases also selectively enhanced 3H-thymidine incorporation four to seven times more than that in vehicle-treated cells or cells treated with endotoxin, a common contaminant of purified enzymes. Ovalbumin (glycoprotein control), pronase, and lysozyme caused a modest but statistically insignificant increase (up to twofold) in 3H-thymidine incorporation. Elastase, collagenase and dialyzed E. coli beta-glucuronidase had no effect. The mitogenic effect of hydrolases was equally seen in quiescent, serum-depleted cells as well as in those maintained in medium with 10% FBS, suggesting that it was independent of serum factors. The effect of lysosomal hydrolases was inhibited by exposure to yeast mannan, and mannosylated human serum albumin had a mitogenic effect, suggesting the involvement of a mannose receptor. We conclude that lysosomal hydrolases may play a role in the development of the hyperplasia/hypertrophy of respiratory smooth muscle.
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PMID:Mitogenic effect of lysosomal hydrolases on bovine tracheal myocytes in culture. 183 69

Two test teeth, anteriors with greater than or equal to 6 mm deep periodontal pockets from each of 10 patients with advancing periodontitis were included in this study. The clinical signs of advancing periodontitis, generalized moderate to deep pockets and to severe loss of alveolar bone, were observed in young adult. There have been several reports on factors, which reflect the conversion clinically from infection by highly pathogenic plaque bacteria to a from of periodontitis displaying relatively rapid loss of clinical attachment. The purpose of this investigation was to detect parameters in fluid, which could leak from the underlying inflamed connective tissue into the gingival crevice, and which could shown correlatively the progressive variations of periodontal disease by recurrent acute stage. In order to determine active disease sites and to monitor guantitatively response to therapy or to measure degree to susceptibility of future breakdown. Examinations on following parameters at pre- and post- periodontal treatment stages were carried out. Endotoxin, collagenase, alkaline phosphatase, beta-glucuronidase, interleukin-1 alpha, IgG antibody levels to Bacteroides gingivalis, Bacteroides intermedius were measured in gingival exudate samples, which were collected by the microtips technique from periodontal pockets. The following results were obtained: 1) Considering the effect of periodontal therapy, pathogenic responses on total colony forming unit (CFU), interleukin-1 alpha and changes of endotoxin and beta-glucuronidase levels after the treatment have indicated that specific changes in humoral responses. 2) There was not significant relation between alkaline phosphatase, collagenase, IgG antibodies level to Bacteroides gingivalis, Bacteroides intermedius and responses in active and also inactive disease sites. 3) This study has been resulted in the development of diagnostic techniques which requires strict criteria on the disease activity of the periodontal disease very specific in order to permit a more scientific approach to the care of periodontitis patients and to speculate the prognosis of the patients after the treatment.
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PMID:[Changes of factors on disease activity in advancing periodontitis]. 213 9

During the course of carrageenan-induced inflammation in rats major changes were observed in the activities of neutrophil granule enzymes. The activities of three enzymes--gelatinase, collagenase and beta-glucuronidase, the markers of three different types of granules, have been measured and compared to those of a control group of animals. Total collagenase and gelatinase activities of control rats were 59.4 +/- 3.6 (mean +/- SD) and 23.0 +/- 2.9 units/mg protein, respectively. Significantly reduced levels of both collagenase (35.6 +/- 2.5 units) (p less than 0.05) and gelatinase (7.1 +/- 0.7 units) (p less than 0.001) were measured in the blood neutrophils of inflamed rats; and the collagenase activity of neutrophils derived from inflamed pleural exudate was also significantly decreased to a level of 19.7 +/- 1.8 units/mg protein (p less than 0.01). However, the gelatinase activity of exudate neutrophils did not differ from that of blood cells of inflamed rats. In contrast, no change was found for the beta-glucuronidase activity in blood neutrophils of control and inflamed rats. These observations support the concept that during the inflammatory response in rats, neutrophils in the circulation may become activated as judged by the extracellular secretion of collagenase and gelatinase. Therefore, neutrophils accumulating in acute inflammatory lesions contain decreased levels of collagenolytic enzymes and the significance of this observation is discussed.
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PMID:Neutrophil enzyme activities in carrageenan-induced inflammation in rats. 255 Nov 53

The susceptibility of a number of human neutrophil granule enzymes to oxidative inactivation was investigated. Addition of H2O2 to the cell-free medium from stimulated neutrophils resulted in inactivation of all enzymes tested. This was inhibited by azide and methionine, indicating that inactivation was due to myeloperoxidase-derived oxidants. Lysozyme was more than 50% inactivated by one addition of 100 nmol of H2O2/ml, whereas myeloperoxidase, beta-glucuronidase, gelatinase and collagenase were almost completely inactivated by three additions. Cathepsin G was slightly less susceptible, whereas elastase was extremely resistant to oxidative attack. Myeloperoxidase-dependent enzyme inactivation may be a means whereby the neutrophil can terminate the activity of its granule enzymes and control the release of degradative enzymes into the tissues.
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PMID:Myeloperoxidase-dependent oxidative inactivation of neutrophil neutral proteinases and microbicidal enzymes. 282 16

These experiments were designed to determine whether hypercholesterolemia and the accumulation of cholesterol or cholesteryl esters in rabbit carrageenan granuloma macrophages might influence selected markers of macrophage activation. Granulomas induced by subcutaneous injection of carrageenan into rabbits were harvested after 4, 14, and 28 days. Macrophages were isolated from granuloma tissues by collagenase digestion and cultured overnight. Secretion of lysosomal beta-glucuronidase, membrane 5'-nucleotidase, cellular plasminogen activator, and superoxide anion generation were measured as markers of activation. beta-Glucuronidase activity secreted into the media by granuloma macrophages from normocholesterolemic (NC) and hypercholesterolemic (HC) rabbits showed a trend toward an increase with time between 4 and 14 days in both groups. This was confirmed in a separate experiment with a significant increase by 14 days, together with a significantly greater secretion by NC macrophages and a significantly elevated level of cellular beta-glucuronidase activity in NC relative to HC macrophages. Activity of the membrane ectoenzyme 5'-nucleotidase was minimal in lysates of NC or HC macrophages, in contrast to freshly isolated human monocytes, indicating that both NC and HC granuloma macrophages were highly activated. Cellular plasminogen activator activity was significantly increased between 4 and 14 days, and was significantly greater in HC than in NC macrophages at 14 days. Stimulation of macrophages with phorbol myristate acetate increased superoxide anion generation by both NC and HC macrophages; however, no difference in superoxide anion generation was observed between macrophages from NC and HC rabbits. On the basis of the 5'-nucleotidase findings, it is concluded that both the NC and HC granuloma macrophages are highly activated, and further that hypercholesterolemia does not enhance macrophage generation of superoxide anion, either spontaneously or as the result of phorbol myristate acetate stimulation. Although hypercholesterolemia results in macrophage activation in terms of an increased cellular plasminogen activator activity, the secretion of the lysosomal enzyme beta-glucuronidase is diminished. Thus, hypercholesterolemia associated with macrophage cholesterol and cholesteryl ester accumulation has no consistent overall influence on activation, a finding of potential importance in the context of atherogenesis.
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PMID:Influence of hypercholesterolemia and cholesterol accumulation on rabbit carrageenan granuloma macrophage activation. 283 4

When added to cultures of parathyroid hormone (PTH)-stimulated bones, dichloromethylenebisphosphonate (C12MBP) and 3-amino-1-hydroxypropydilene-1,1-bisphosphonate (AHPrBP) inhibit completely and in a parallel manner the development of resorption lacunae, the loss of calcium by the explants and their PTH-induced excretion of lysosomal hydrolases (beta-glucuronidase and N-acetyl-beta-glucosaminidase). The loss of collagen (hydroxyproline) by the bones is usually less inhibited than their loss of calcium and their heparin-induced excretion of collagenase is unaffected. To interpret these data, it is proposed that these bisphosphonates act more on the activity of osteoclasts, suppressing simultaneously their excretion of lysosomal enzymes and their erosion of mineralized bone matrix, than on that of other cell types (osteoblasts ?) responsible for collagenase production and the removal of uncalcified collagen.
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PMID:Bisphosphonates and bone resorption: effects on collagenase and lysosomal enzyme excretion. 299 48


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