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)

In this study the causes of organ damage after cardiopulmonary bypass were multifactorial. The concentration of the proteolytic enzyme elastase, which was released from activated granulocytes in the milieu of significantly reduced levels of alpha 1-protease inhibitor (p less than 0.01), increased during cardiopulmonary bypass (p less than 0.01). In addition, bypass initiated platelet aggregation, which both altered the eicosanoid metabolism and caused the level of thromboxane A2 to increase and surpass the level of prostaglandin I2. Because thromboxane A2 dominance subsided immediately after cardiopulmonary bypass, the effect of thromboxane A2 (vasoconstriction) on the development of organ damage may have been influential only during bypass. Both during and after bypass, the increase in endothelin excretion (p less than 0.01 to 0.05) was believed to induce a further vasoconstriction in the microvasculature. On completion of the cardiopulmonary bypass, the elevation of the lysosomal enzyme beta-glucuronidase, which is a sensitive indicator of cellular damage, was influenced by the concentrations of elastase (r = 0.8) and endothelin (r = 0.52). As evidenced by leuko-sequestration in the lung after cardiopulmonary bypass, the increase in the alveolar-arterial oxygen tension difference correlated with the elastase concentration (r = 0.68). Renal damage, which was detected by an increase in renal tubular enzymes (N-acetyl-beta-D-glucosaminidase and gamma-glutamyltranspeptidase) was affected by the endothelin (r = 0.68, 0.56) and elastase levels (r = 0.58, 0.68), respectively, but not by the ratio of thromboxane B2 to prostaglandin F1 alpha. The elastase level influenced the pulmonary vascular resistance (r = 0.56). However, neither the cardiac index nor the systemic and pulmonary vascular resistances were influenced by the endothelin level and the ratio of thromboxane B2 to prostaglandin F1 alpha.
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PMID:Evidence of organ damage after cardiopulmonary bypass. The role of elastase and vasoactive mediators. 135 50

To determine if alloxan-induced lung injury could be prevented by an antiprotease, ulinastatin, we used three groups of five anesthetized, ventilated dogs. They were given saline (20 ml/kg/hr) infusion alone (saline group), alloxan (75 mg/kg) + saline infusion (alloxan group), or ulinastatin (50,000 U/kg) + alloxan + saline infusion (ulinastatin group). The course of all dogs was followed for three hours. In the saline group, extravascular lung water to blood-free dry weight (Qwl/dQl) was 3.22 +/- 0.31 g/g (mean +/- SE). The alloxan group presented the following significant findings: a decrease in white blood cell and platelet counts (44.2% and 68.2% of control, respectively) at five minutes; an increase in thromboxane B2 and 6-keto-prostaglandin F1 alpha (731.6% and 476.6% of control, respectively) at 15 minutes; an increase in beta-glucuronidase (124.8% of control) at 30 minutes; and an increase in Qwl/dQl (8.84 +/- 1.82 g/g) at the end of experiment. The addition of ulinastatin significantly reduced most alloxan-induced effects: differences in white blood cell counts, thromboxane B2, 6-keto-prostaglandin F1 alpha, and Qwl/dQl between the saline and ulinastatin groups were small. We conclude that ulinastatin significantly reduces the extent of lung water accumulation in alloxan-induced lung injury.
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PMID:Effects of ulinastatin, an antiprotease, on alloxan-induced lung injury in dogs. 163 81

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

Mouse calvaria were maintained in organ culture without serum additives. The effects of Cu2+ on bone resorption and on the synthesis and action of prostaglandins were studied. Non-toxic concentrations of copper sulphate (5 microM) were found to decrease active resorption, measured by 45Ca release, to 54% control values (p less than 0.001), while prostaglandin F (PGF), prostaglandin E2 (PGE2), and 6-keto-prostaglandin F1 alpha, (6-keto-PGF1 alpha), determined by radioimmunoassay, were increased above controls (p less than 0.05). These effects of Cu2+ on prostaglandin synthesis were confirmed by the isolation and quantitation of [3H]-labelled metabolites released from calvaria which had been pre-labelled with [3H]-arachidonic acid. PGE2, PGF2 alpha, 6-keto-PGF1 alpha, and thromboxane B2 (TxB2) were all higher in copper-exposed calvaria, but their relative amounts remained unchanged. There was no evidence that Cu2+ influenced the mobilisation of [3H]-arachidonic acid from prelabelled calvaria. The stimulation of bone resorption by exogenous prostaglandins was decreased in the presence of Cu2+ (p less than 0.005), while parathormone-mediated bone resorption was virtually unaffected. Cu2+ also increased the inhibition of bone resorption seen with indomethacin (p less than 0.05). In addition to the effects of the metal on prostaglandin action Cu2+ also decreased beta-glucuronidase activity in the media to 86% of the control values (p less than 0.001). The action of Cu2+ in inhibiting bone resorption in vitro appears complex but does not involve inhibition of prostaglandin synthesis. It is likely that Cu2+ has more than one inhibitory locus.
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PMID:Inhibition of prostaglandin action and bone resorption by copper. 644 29