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)

Human gallbladder epithelium was homogenized with a view to maintaining the integrity of subcellular components. In such homogenates, N-acetyl-beta-glucosaminidase, beta-glucuronidase, beta-galactosidase, beta-glucosidase, beta-fucosidase, beta-xylosidase, and acid phosphatase were demonstrated together with phospholipase activity. All the enzymes exhibited structure-linked latency. After discarding cellular debris from the homogenate, remaining subcellular organelles were analytically separated by density gradient centrifugation. After 100,000 g for 1 hour, particles containing acid glycosidases were recovered at a sucrose density of 1.18-1.19, whereas the mitochondrial marker enzyme succinate-reductase accumulated at a density of 1.16. The bulk of sedimentable phospholipase activity was recovered with particles sedimenting at 1.18-1.19. The results are interpreted as indicating that phosphalipase is present in lysosomes of the human gallbladder epithelium. Release of acid hydrolases, in lysosomes of the human gallbladder epithelium. Release of acid hydrolases, in lysosomes of the human gallbladder epithelium. Release of acid hydrolases, particularly phospholipase A, from the gallbladder epithelium is discussed as mediation of an inflammatory reaction in the gallbladder, i.e. cholecystitis.
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PMID:On the mediation inflammatory reaction in the human gallbladder epithelium. 127 7

Clogging of endoscopic stents necessitates their replacement in many patients with malignant obstructive jaundice and limits their use in benign strictures. We studied the basic mechanism of clogging to find ways to prevent it. We did light and electron microscopy studies of blocked and functioning stents, which were prepared so that organic structures would be preserved. The material blocking the lumina was composed of a matrix of bacterial cells and their fibrillar anionic extracellular products. Crystals of calcium bilirubinate, calcium palmitate, and cholesterol were embedded within this matrix. Bacterial cells were attached to the stent surface by a fibrillar matrix, suggesting that the initial event in stent clogging is the development of an adherent bacterial biofilm. Bacterial enzyme activity (beta-glucuronidase and phospholipase) leads to the deposition of crystals. The use of antibacterial plastics in the manufacture of stents may reduce bacterial adhesion and stent clogging.
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PMID:Biliary stent blockage with bacterial biofilm. A light and electron microscopy study. 245 May 1

We have recently isolated a human phospholipase A2-activating protein (PLAP) that shares antigenic and biochemical similarities with melittin, a well characterized bee venom phospholipase-stimulatory peptide. To explore the potential mechanisms of action of PLAP that extend beyond its effects on eicosanoid synthesis, we examined its effects on the release of human neutrophil lysosomal enzymes and superoxide, and on RBC hemolysis. These results were compared to the effects of melittin, which has been reported to induce enzyme release and hemolysis. We also examined the effects of PLAP on neutrophil aggregation and chemotaxis. PLAP induced neutrophils to release beta-glucuronidase and metalloproteinase enzyme activities as well as produce superoxide ion in both a dose- and time-dependent manner. Eicosanoid synthesis inhibitors did not abrogate these responses. PLAP induced release of arachidonic acid metabolites, but this response could be abrogated by eicosanoid synthesis inhibitors. PLAP also induced neutrophil aggregation and chemokinesis, but not chemotaxis. Concentrations of PLAP that induced these responses did not induce cellular toxicity as determined by light and electron microscopy, lactic dehydrogenase release, trypan blue dye exclusion, and RBC hemolysis. In contrast, prolonged incubation with higher concentrations of PLAP induced cell death that was similar to that observed with melittin. These findings suggest that the mechanisms of action of PLAP extend beyond the eicosanoid synthetic pathway, and that disordered regulation of PLAP may be responsible, at least in part, for chronic immune and inflammatory states.
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PMID:A phospholipase A2-activating protein (PLAP) stimulates human neutrophil aggregation and release of lysosomal enzymes, superoxide, and eicosanoids. 254 Dec 2

This study was designed to clarify the role of phospholipase in the mechanism of plasmocid-induced mitochondrial dysfunction in the rat heart. Rats were divided into two groups: the control group, untreated; and the plasmocid group, in which plasmocid (30 mg/kg) was injected subcutaneously. In each group, the level of lipid peroxides and the phospholipase activity in heart homogenate were measured, and mitochondrial function (respiratory control index and the rate of oxygen consumption in State III) was determined polarographically. The activity of lysosomal enzymes (N-acetyl-beta-glucosaminidase and beta-glucuronidase) were also measured. The plasmocid group showed significant increases in lipid peroxide levels and phospholipase activity. Administration of plasmocid also caused mitochondrial dysfunction, while no significant changes were observed in the lysosomal enzyme activity of either group. These results suggested that plasmocid-induced mitochondrial dysfunction is based on the degrading of phospholipids by membrane bound phospholipase, and that lysosomal enzymes are unlikely to be involved in plasmocid-induced mitochondrial dysfunction.
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PMID:The role of phospholipase in plasmocid-induced mitochondrial dysfunction in rat hearts. 319 Apr 55

Three lysosomal-type acid hydrolases were examined in subcellular fractions of the developing epidermis of fetal rats to assess the relationship of degradative enzymes to cornification. As the granular layer developed and cornified between 18 and 20 days (D) of gestation, epidermal acid phosphatase increased, acid phospholipase A remained constant, and beta-glucuronidase activity declined. The enzymes were present in 3,000, 17,000, and 100,000 g particulate fractions and soluble cytoplasm. However distribution differed: acid phosphatase and phospholipase A were more preferentially localized than was glucuronidase in the 17,000 g fraction which excluded mitochondria and ribosomes and was enriched in lamellar granules. The findings suggested that acid phosphatase and phospholipase were present in membrane-bound organelles (e.g., lamellar granules) in the granular layer. Particulate acid phosphatase increased with granular layers on days 19 and 20 while a 7-fold increase in soluble enzyme coincided with cornification on day 20. As shown by isoelectric focusing, the enzyme became more heterogeneous at day 20 than at day 18, suggesting increased glycosylation. The particulate fraction displayed lysosomal characteristics with respect to release of acid phosphatase, which was inhibited by hydrocortisone and enhanced by retinol. When fetal epidermis was allowed to cornify in organ cultures, similar increases in acid phosphatase occurred. The presence of hydrocortisone did not affect increase in total enzyme but a greater proportion remained in the particulate fraction. The findings suggest that particulate acid phosphatase and phospholipase are compartmentalized in organelles with lysosomal characteristics during development of granular cells and that release of phosphatase is coincident with cornification. This may reflect not only exocytosis of lamellar granules but also intracellular release of the hydrolytic enzyme.
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PMID:Acid hydrolases of the epidermis: subcellular localization and relationship to cornification. 618 89

The herpes simplex virus trans-activator Vmw65 interacts with the cellular factors Oct-1 and VCAF-1 to generate a multicomponent DNA binding complex that specifically recognizes conserved enhancer elements found upstream of the viral immediate-early genes, resulting in potent stimulation of their transcription. We have identified a HeLa cell factor, distinct from Oct-1 or VCAF-1, which significantly enhances the stability or formation of Vmw65-dependent complexes, as judged by mobility shift analysis using either nuclear extracts or bacterially expressed Oct-1 and Vmw65. This factor, designated SF (stimulatory factor), was partially purified from HeLa cell postnuclear extracts and has an apparent molecular weight of 1500-3000, based on ultrafiltration and size-exclusion chromatography. SF was shown to be resistant to inactivation by heat treatment, protease, nuclease, and phospholipase digestions, and extraction with organic solvents. Pretreatment of SF with beta-glucuronidase did not affect its ability to stimulate Vmw65-dependent complex formation but did reduce the electrophoretic mobility of the resulting complex. These data indicate that SF is probably a component of the Vmw65-induced complex and may be composed, at least partially, of carbohydrate.
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PMID:An unusual cellular factor potentiates protein-DNA complex assembly between Oct-1 and Vmw65. 838 Apr 10

A previous study demonstrated that the acute phase of silica-induced lung injury in rats can be attenuated by concomitant administration of amiodarone, a cationic amphiphilic drug that inhibits phospholipase activity in the lungs. The purpose of the present study was to determine whether continued amiodarone administration could inhibit subchronic silica-induced lung injury and fibrosis. Male Fischer-344 rats were administered amiodarone (150 mg/kg, p.o., 5 days/week) for 14 days and were then instilled with silica (100 mg/kg) intratracheally. Amiodarone treatment then continued for 60 days. Injury was evaluated by parameters in bronchoalveolar lavage fluid and fibrosis was assessed by lung hydroxyproline content and trichrome staining of collagen. Within the bronchoalveolar lavage fluid, amiodarone treatment resulted in significant decreases in silica-induced elevations in albumin levels, lactate dehydrogenase activity, beta-glucuronidase activity, and neutrophil influx. Amiodarone treatment resulted in significant reductions in silica-induced increases in lung weight and hydroxyproline levels; the diminution of fibrosis due to amiodarone treatment was confirmed histologically. These results indicate that subchronic pulmonary inflammation and fibrosis induced by silica in the rat can be attenuated by the concomitant administration of amiodarone.
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PMID:Subchronic pulmonary inflammation and fibrosis induced by silica in rats are attenuated by amiodarone. 883 39

To elucidate heterologous promoter function in gymnosperms, we introduced the bean phenylalanine ammonia-lyase-beta-glucuronidase (PAL2-GUS) gene fusion into white pine (Pinus strobus L.). Over 15 lines were produced and integration of Agrobacterium T-DNA was confirmed by Southern analysis. Induction of the reporter gene was detected in all of the lines tested following UV illumination. In contrast, a weak but constant induction was seen in only a few lines following treatment with salicylic acid (SA) or jasmonic acid (JA). However, pretreatment of suspension cultures with SA or JA enhanced the induction of PAL2-GUS expression by UV irradiation. This specific enhancement or potentiation was reduced by 50% by treating the cells with indomethacin, an inhibitor of phospholipase activity, suggesting that the observed potentiation of UV induction involves the octadecanoid pathway. The UV induction was completely abolished by treating the cells with okadaic acid, an inhibitor of phosphatase activity. Thus, the induction of the heterologous PAL2 promoter from bean is consistent with the induction of phenylalanine ammonia-lyase (PAL) in angiosperms. Furthermore, our findings suggest that conifers, although phylogenetically distant to angiosperms, share some conserved promoter elements and some signal transduction mechanisms for UV-light perception.
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PMID:Inducible expression of the heterologous PAL2 promoter from bean in white pine (Pinus strobus) transgenic cells. 1144 95

Bacteria are traditionally accorded a greater role in pigment gallstone formation in Eastern populations. Stone color is thought to predict the presence of bacteria; that is, black stones (Western predominant) are supposedly sterile and brown stones (Eastern predominant) contain bacteria. We previously reported that, regardless of appearance, most pigment gallstones contain bacteria. This study examined, in a large Western population (370 patients), the incidence, appearance, and chemical composition of pigment stones, and the characteristics of gallstone bacteria. One hundred eighty-six pigment stones were obtained aseptically. Bacteria were detected by means of scanning electron microscopy and gallstone culture. Chemical composition was determined by infrared spectroscopy. Bacteria were tested for slime and beta-glucuronidase production. Seventy-three percent of pigment stones contained bacteria. Choledocholithiasis was associated with gallstone bacteria. Ca-bilirubinate was present in all pigment stones. Ca-palmitate was characteristic of infected stones, and more than 75% Ca-carbonate was characteristic of sterile stones. Neither chemical composition nor stone appearance predicted the presence of bacteria. Ninety-five percent and 67% of infected pigment stones contained bacteria that produced slime and beta-glucuronidase, respectively. Most pigment stones contained bacteria that produced beta-glucuronidase, slime, and phospholipase, factors that facilitate stone formation. Thus bacteria have a major role in Western pigment gallstone formation. Furthermore, gallstone color did not predict composition or bacterial presence.
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PMID:Pathogenesis of pigment gallstones in Western societies: the central role of bacteria. 1250 29

Clostridium perfringens is the cause of several human diseases, including gas gangrene (clostridial myonecrosis), enteritis necroticans, antibiotic-associated diarrhea, and acute food poisoning. The symptoms of antibiotic-associated diarrhea and acute food poisoning are due to sporulation-dependent production of C. perfringens enterotoxin encoded by the cpe gene. Glucose is a catabolite repressor of sporulation by C. perfringens. In order to identify the mechanism of catabolite repression by glucose, a mutation was introduced into the ccpA gene of C. perfringens by conjugational transfer of a nonreplicating plasmid into C. perfringens, which led to inactivation of the ccpA gene by homologous recombination. CcpA is a transcriptional regulator known to mediate catabolite repression in a number of low-G+C-content gram-positive bacteria, of which C. perfringens is a member. The ccpA mutant strain sporulated at a 60-fold lower efficiency than the wild-type strain in the absence of glucose. In the presence of 5 mM glucose, sporulation was repressed about 2,000-fold in the wild-type strain and 800-fold in the ccpA mutant strain compared to sporulation levels for the same strains grown in the absence of glucose. Therefore, while CcpA is necessary for efficient sporulation in C. perfringens, glucose-mediated catabolite repression of sporulation is not due to the activity of CcpA. Transcription of the cpe gene was measured in the wild-type and ccpA mutant strains grown in sporulation medium by using a cpe-gusA fusion (gusA is an Escherichia coli gene encoding the enzyme beta-glucuronidase). In the exponential growth phase, cpe transcription was two times higher in the ccpA mutant strain than in the wild-type strain. Transcription of cpe was highly induced during the entry into stationary phase in wild-type cells but was not induced in the ccpA mutant strain. Glucose repressed cpe transcription in both the wild-type and ccpA mutant strain. Therefore, CcpA appears to act as a repressor of cpe transcription in exponential growth but is required for efficient sporulation and cpe transcription upon entry into stationary phase. CcpA was also required for maximum synthesis of collagenase (kappa toxin) and acted as a repressor of polysaccharide capsule synthesis in the presence of glucose, but it did not regulate synthesis of the phospholipase PLC (alpha toxin).
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PMID:The CcpA protein is necessary for efficient sporulation and enterotoxin gene (cpe) regulation in Clostridium perfringens. 1529 23


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