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)

The effect of human peripheral blood polymorphonuclear leucocyte (PMN) extracts and PMN granule lysates on in vitro immunoglobulin (Ig) synthesis by autologous peripheral blood mononuclear cells was studied. The mononuclear cells were cultured for 3 days with or without autologous plasma. Newly synthesized Ig in the culture supernatants was measured using 14C-labelled amino acids by an immune coprecipitation method. Upon addition of a PMN extract to plasma-free cultures Ig synthesis was stimulated, the mean stimulation index (SI) of cultures from thirteen individuals, including nine normals, three patients with rheumatoid arthritis and one with psoriatic arthritis being 1-8 +/- 0-2 in comparison with control cultures (P less than 0-05). By contrast, in 10% fresh autologous plasma, PMN extracts yielded a mean SI of 0-9 +/- 0-1 indicating inactivation of the active extracts by plasma inhibitors. In experiments using PMN granule lysates containing high concentrations of beta-glucuronidase and cultured in RPMI 1640, the mean stimulation index was 3-2 +/- 0-7. Stimulation of Ig synthesis was also produced by trypsin. Stimulation of Ig synthesis was also produced by trypsin. Stimulating factors in PMN extracts were inhibited by Trasylol, a protease inhibitor. These results indicate that trypsin and proteolytic lysosomal enzymes in PMN increase Ig synthesis of human peripheral blood mononuclear cells. They suggest a possible new role of PMN in the potentiation of immunoglobulin synthesis.
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PMID:Enhancement of in vitro immunoglobulin synthesis of human lymphocytes by lysosomal enzymes from polymorphonuclear leucocytes. 30 Mar 11

Rats were injected with labeled Kunitz protease inhibitor and killed at various times thereafter. Radioactivity was measured in various fractions of kidney homogenates in order to study the time-dependent fixation to different cell organelles, expecially the transition from the brush border to lysosome fraction. With short survival periods (up to 5 min), the renal protease inhibitor is recovered nearly completely with the brush border fraction. With longer periods, a shift towards particles with higher densities and higher beta-glucuronidase activities takes place. Similar results have been achieved with insulin. Lysosomes were prepared and subfractionated following i. v. administration of the protease inhibitor or insulin. The radioactivity of the peptides was found in the lysosomal range of density. According to our present and previous results, the renal pathway of the protease inhibitor consists of 3 steps: binding to the brush border, reabsorption into micropinocytotic vesicles and phagosomes, and final enrichment in phagolysosomes with subsequent degradation. We suggest this type of transport to be representative for peptides in general.
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PMID:In vivo interaction of the Kunitz protease inhibitor and of insulin with subcellular structures from rat renal cortex. 107 84

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 evaluate the effects of acute pancreatitis on hepatic function and hepatic cellular and subcellular organellar fragility, we studied 1) the hepatic secretion of lysosomal enzymes (beta-glucuronidase, beta-galactosidase, and N-acetyl-beta-glucosaminidase) into bile in the isolated perfused rat liver model; 2) the aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT), and lysosomal enzyme levels in the effluent in an isolated liver model; 3) hepatic lysosomal fragility in an in vitro incubation study; and 4) protective effects of a new low molecular weight synthetic protease inhibitor, ONO 3307, against hepatic injury in doses of 2 and 5 mg/kg.h in acute pancreatitis induced by a supramaximal dose of cerulein in rats. Decreased hepatic secretion of lysosomal enzymes into bile and accelerated hepatic lysosomal fragility were observed in acute pancreatitis induced by cerulein. ONO 3307 showed a significant protective effect against this hepatic injury in acute pancreatitis, the dose of 5 mg/kg.h showing a more potent effect than the dose of 2 mg/kg.h. These results suggest that the impaired hepatic function, including depressed hepatic secretion of lysosomal enzymes, seems to be closely related to accelerated hepatic fragility and that some unknown protease, which is present in pancreatitis and is susceptible to inhibition by ONO 3307, plays a crucial pathologic role in the development of this liver injury during acute pancreatitis.
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PMID:Effects of acute pancreatitis on hepatic secretion of lysosomal enzymes into bile and hepatic lysosomal fragility: protective effects of a new synthetic protease inhibitor, ONO 3307. 150 86

Gingival crevicular fluid was collected from multiple sites in patients with chronic adult periodontitis, and analysed for the lysosomal enzymes beta-glucuronidase and arylsulphatase, the cytoplasmic enzyme lactate dehydrogenase, total IgA, IgG and IgM and the protease inhibitor alpha 2-macroglobulin. The within-mouth (intraclass) correlation coefficients were calculated to describe the relationship between samples collected from individual patients. Data collected at baseline and 3 months after root planing and scaling were analysed, as was the change between examinations. Volume of crevicular fluid demonstrated the smallest intraclass correlation coefficient (0.16 at baseline, 0.12 at 3 months; 0.11 change), while probing depth and enzyme activity had moderate intraclass correlations (i.e. 0.36, 0.36, 0.26 for beta-glucuronidase). Immunoglobulin and alpha 2-macroglobulin activity in the fluid had the strongest correlations (i.e. 0.64, 0.57, 0.65 for IgG). The correlations for anatomically related teeth within a quadrant (molar, non-molar) were equivalent to or greater than the correlation for all samples within a mouth. Examined by tooth type, the intraclass correlations for volume of crevicular fluid, probing depth, beta-glucuronidase, arylsulphatase and lactate dehydrogenase were higher for non-molar teeth. In contrast, intraclass correlations for IgA, IgG, IgM and alpha 2-macroglobulin in samples from molar teeth were either equivalent to or greater than the correlations for non-molar samples. Calculation of intraclass correlation coefficients for such data can (1) indicate the degree of variability present in multiple samples of crevicular fluid collected from individual patients, (2) provide information about the source of host mediators in the fluid, and (3) help identify appropriate sampling strategies for the fluid.
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PMID:Within-mouth correlations for indicators of the host response in gingival crevicular fluid. 170 87

The causes of organ failure following cardiopulmonary bypass (CPB) were multi-factorial. Damage was initiated by elastase which was released from activated granulocytes under conditions of significant reduction in the protease inhibitor level (p less than 0.01). Platelet aggregation, initiated by the CPB, altered the eicosanoid metabolism. As a result, the level of thromboxane A2 increased and became dominant in relation to prostaglandin I2. The increase in endothelin excretion observed during and after the CPB induced a further vasoconstrictive response in the microvasculature and accelerated ischemic cellular damage. Upon completion of the CPB, the elevation of the lysosomal enzyme beta-glucuronidase was influenced by the concentration of elastase (r = 0.78). The endothelin level correlated slightly with the elastase level (r = 0.4) during the CPB. This might indicate that there was an interaction between the activated granulocytes and endothelin production. The increase in the alveolar-arterial oxygen tension difference (Aa-DO2) only correlated with the elastase concentration (r = 0.55). Renal damage, which was detected by an increase in renal tubular enzymes (N-acetyl-beta-D-glucosaminidase and gamma-glutamyltranspeptidase), was affected by endothelin (r = 0.68, 0.58) and elastase (r = 0.61, 0.51) respectively, but not by thromboxane B2. Even after the CPB, damage was thought to be perpetuated by the continuous elevation of elastase and endothelin. Since thromboxane A2 dominance subsided immediately after the cardiopulmonary bypass, the effect of thromboxane A2 on the development of organ failure was possibly only influential during the CPB. The cardiac index demonstrated a negative correlation with endothelin (r = -0.69) and a positive correlation with the ratio of TxB2/PGF1 (r = 0.51).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mechanisms of organ failure following cardiopulmonary bypass--preventive effects of ulinastatin]. 177 3

The possible sources of biochemical changes in the lung, including changes in activities of lactate dehydrogenase (LDH), beta-glucuronidase (beta-GLU), choline kinase (CHK), and protease inhibitor (PI), as well as protein content, were evaluated following exposure to NO2. Hydroxyurea-induced granulocytopenia attenuated the LDH and beta-GLU responses (46% and 61%, respectively) following acute, but not subacute, exposure to NO2. Increases in PI activity and pulmonary protein content following exposure to NO2 were not altered by inhibition of protein synthesis by cycloheximide. The observed increase in PI activity appears to result from an activation process, whereas a major source of increased pulmonary protein content following exposure appears to occur from leakage into the lung. The response of the lung to irritant insult is thus dynamic, and the contribution from various sources to the biochemical makeup of the lung following irritant insult may depend on the phase of the pulmonary response.
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PMID:Pharmacologic manipulation of the murine pulmonary biochemical response to NO2. 226 87

When rat hepatocytes were cultured in the presence of various specific protease inhibitors, lysosomal acid phospholipase A1 activity decreased progressively. Exposure of the cultured cells to 0.1 micrograms/ml of pepstatin, E 64, leupeptin or chymostatin also reduced the catalytic activities of several lysosomal marker enzymes. Irrespective of the protease inhibitor type employed, acid phospholipase A1 activity reacted most sensitively, followed by acid phosphatase, acid beta-N-acetyl-D-hexosaminidase and acid beta-glucuronidase. Of the protease inhibitors studied, pepstatin appeared to be most potent in reducing lysosomal enzyme activities in cultured hepatocytes. These findings suggest that proteolytic processes at as yet unknown, possibly extralysosomal sites play an important role in the turnover rates of lysosomal enzymes.
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PMID:Protease inhibitors reduce lysosomal acid phospholipase A1 activity in cultured rat hepatocytes. 231 14

Circulating concentrations of digestive enzymes, certain lysosomal hydrolases and protease inhibitors were measured in 19 heavy smokers and 13 non-smokers before (basal) and at 15, 30, and 60 minutes after a single intravenous injection of secretin (75 CU). In smokers, basal serum amylase and immunoreactive pancreatic elastase 2 (IRE2) concentrations were about 100% and 25% higher respectively, than in the non-smokers, whereas, no differences were observed in basal immunoreactive cationic trypsinogen (IRCT) concentrations and in acid phosphatase and beta-glucuronidase activities between the two groups. Furthermore, a single injection of secretin to cigarette smokers significantly increased serum amylase, IRCT and IRE2 by 155%, 200%, and 100%, respectively when compared with their corresponding basal levels. No such increment was observed in the non-smokers. In addition, there were no significant differences in serum trypsin or elastase inhibitory capacity or immunoreactive alpha 1-protease inhibitor and alpha 2-macroglobulin levels between smokers and non-smokers. The levels and inhibitory capacity of these protease inhibitors was also not affected by secretin injection. These data suggest that cigarette smoking enhances the responsiveness of the exocrine pancreas to a physiological stimulus such as secretin, with resultant substantial increase in the concentrations of pancreatic hydrolases in blood.
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PMID:Raised serum concentrations of pancreatic enzymes in cigarette smokers. 243 81

The biochemical and histopathological response of the lung following acute and repeated (subacute) exposure to nitrogen oxide (NO2) was examined. Activities of lactate dehydrogenase, beta-glucuronidase, choline kinase, and protease inhibitor were measured in murine pulmonary tissue immediately and two days following exposure. Nonenzymatic parameters, pulmonary protein content, and wet lung weight were also monitored. Immediately following acute exposure to NO2, only the nonenzymatic parameters were elevated. By two days following acute exposure, following subacute exposure; however, the nonenzymatic parameters were attenuated with respect to the enzymatic activities. The lung exhibits a dynamic response following damage by oxidants such as NO2. This response is divided into three distinct phases (exudative, proliferative, and tolerant), which can be characterized both biochemically and histopathologically.
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PMID:Phase-dependent response of the lung to NO2 irritant insult. 263 69


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