Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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

Gallbladder tissue from patients with acute acalculous cholecystitis contains increased amounts of prostanoids when compared to normal gallbladder tissue. Platelet-activating factor (PAF) is a potent stimulus of eicosanoid formation. It has been implicated as a mediator of acute inflammatory processes and systemic responses to shock. In this study the role of PAF in acute acalculous cholecystitis was evaluated. Anesthetized cats underwent gallbladder perfusion with a physiologic buffer solution containing [14C]polyethylene glycol as a nonabsorbable tracer to quantitate mucosal water absorption. Platelet-activating factor was infused into the hepatic artery for 2 hours. Control experiments were performed when vehicle alone was infused. Experiments also were performed when indomethacin was administered intravenously and when indomethacin and PAF were administered. Gallbladder mucosal absorption/secretion and perfusate and tissue prostaglandin E (PGE) and 6 keto prostaglandin F1 alpha (6-keto PGF1 alpha) levels were evaluated. Gallbladder inflammation was evaluated by beta-glucuronidase and myeloperoxidase tissue concentrations and by a histologic scoring system. Platelet-activating factor eliminated gallbladder absorption and produced net fluid secretion associated with dose-related increases in perfusate PGE concentrations and gallbladder tissue PGE and 6 keto PGF1 alpha levels when compared to control values. Platelet-activating factor produced significant inflammation in the gallbladder with increases in the histologic score of inflammation and tissue lysosomal enzyme activities. Indomethacin significantly decreased the fluid secretion, prostanoid levels, and inflammation produced by PAF. The results suggest that PAF may induce acute gallbladder inflammation associated with systemic stress through a prostanoid-mediated mechanism.
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PMID:The role of prostanoids in the production of acute acalculous cholecystitis by platelet-activating factor. 217 43

Current information suggests that arachidonic acid metabolites are involved in the development of cholecystitis. The purpose of this study was to evaluate eicosanoid formation during the development of experimental cholecystitis in cats. Lysophosphatidylcholine is found in the gallbladders of patients with cholecystitis and is known to be a cytolytic, membrane-damaging substance. Anesthetized cats underwent gallbladder perfusion with and without 1.5 mmol/L lysophosphatidylcholine. Additional experiments were performed when calcium ionophore were added to the perfusates and experiments were performed when cats were treated with indomethacin and underwent perfusion with lysophosphatidylcholine. Changes in the gallbladder were determined by evaluating mucosal water transport as measured by determining the changes in concentration in a nonabsorbable marker, by protein secretion and by beta-glucuronidase accumulation in gallbladder tissue as an index of inflammation. Eicosanoid formation was evaluated by measuring perfusate concentrations and gallbladder homogenate concentrations by radioimmunoassay of prostaglandin E, 6 keto prostaglandin F1 alpha, leukotriene B4 and leukotriene C4. Lysophosphatidylcholine perfusion reversed the control patterns of absorption and produced water exsorption, produced an efflux of protein into the perfusate and increased beta-glucuronidase activity. These changes were accompanied by increased production of prostaglandin E and 6 keto prostaglandin F1 alpha in gallbladder perfusate and homogenate. The concentration of leukotriene C4 in gallbladder effusate was increased by lysophosphatidylcholine when compared with control values. Indomethacin inhibited the protein efflux, decreased beta-glucuronidase levels and decreased prostaglandin E and 6 keto prostaglandin F1 alpha formation when compared with values produced by lysophosphatidylcholine alone. Cyclooxygenase inhibition did not alter the secretion of water into the gallbladder or perfusate leukotriene C4 concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostanoids and leukotrienes in experimental feline cholecystitis. 236 79

The lysosomal enzymes beta-glucuronidase and acid phosphatase were studied in 112 patients with cholecystitis. Acid phosphatase activity was generally lower in patients with cholesterol stones compared with cases with pigment stones. beta-glucuronidase activity was higher in acalculous cholecystitis than in any other group, a fact compatible with the concept that in lithiasis the enzyme is secreted into the bile and therefore may participate in nidus formation. Histochemistry at light microscopical level clearly demonstrates the lysosomal distribution of these enzymes and their presence in the macrophages infiltrating lamina propria in cholesterolosis. Electron histochemistry in 45 patients showed acid phosphatase activity in lysosomes and some in mucous droplets. Thiamine pyrophosphatase activity, a marker for the Golgi system, showed a close association with these mucous droplets. The secretion of mucus will be accompanied by a secretion of acid phosphatase, and by implication other acid hydrolases, into the bile.
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PMID:Gallbladder epithelial acid hydrolases in human cholecystitis. 613 Nov 15

The development of experimental cholecystitis produced by lysophosphatidylcholine is associated with reversal of the normal absorptive characteristics of gallbladder mucosa, resulting in the intraluminal accumulation of water, glycoprotein, and protein. The purpose of the present study was to attempt to ascertain if the protein leaks into the lumen because of the cytolytic properties of lysophosphatidylcholine or if it is due to an active secretory process and to characterize the protein produced. Experiments were performed on anesthetized cats undergoing gallbladder perfusion with and without lysophosphatidylcholine. The amount of protein in the perfusate was measured and albumin clearance from blood to gallbladder lumen was calculated with and without the administration of vesicular transport inhibitors. In separate experiments, control and lysophosphatidylcholine (LPC) produced gallbladder perfusates were collected and the protein subjected to SDS-PAGE to ascertain the nature of the protein secreted. Inhibitors of both microtubular and microfilament activity decreased the protein accumulation and clearance produced by lysophosphatidylcholine. Gallbladder white blood cell accumulation and inflammation as evaluated by beta-glucuronidase and prostaglandin E levels were not significantly altered by cytochalasin or colchicine administration. Lysophosphatidylcholine also produced significant increases in perfusate LDH levels. The protein produced was primarily a 66-kDa protein. Transfer of the protein to a nitrocellulose membrane and immunoblotting with anti-albumin antibody demonstrated that the protein was albumin. The results suggest that during the development of cholecystitis, lysophosphatidylcholine produces albumin accumulation in the gallbladder primarily by inducing an active secretory process resulting in gallbladder distension.
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PMID:Gallbladder mucosal protein secretion during development of experimental cholecystitis. 772 80