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)

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

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

We studied the significance of urinary enzyme measurements in diagnosing proximal tubular damage in cirrhosis of the liver. Urinary excretion (u-enzyme) and fractional urinary excretion (FEenzyme) of gamma-glutamyltranspeptidase (GGT), leucine aminopeptidase (LAP), alkaline phosphatase (AP) and beta-glucuronidase (B-GLU) were quantified in 14 control subjects (group I), 12 cirrhotics with functional renal failure (group II), 13 cirrhotics with renal tubular damage (group III) and 7 non-liver patients with renal tubular damage (group IV). Urinary enzyme excretion and fractional enzyme excretion were significantly higher in the cirrhotics of group III than in the controls or group II. In group III, these tests usually reached values within the range of group IV. The sensitivity of urinary enzyme excretion was 0.92 and specificity ranged from 0.75 (u-LAP) to 1 (u-GGT; u-B-GLU). The sensitivity of fractional enzyme excretion was between 0.61 (FEB-GLU) and 0.84 (FEGGT; FELAP), while specificity was from 0.91 (FELAP; FEAP) to 1 (FEGGT; FEB-GLU). The results indicate that measurement of urinary enzymes may be very useful in diagnosing renal tubular damage in cirrhotic patients with impaired renal function.
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PMID:Urinary excretion of enzymes in cirrhotics with renal failure. 287 95

Histochemical techniques have been applied to the identification of cell types cultured from human endometrium. Previous work from this laboratory characterized two principal cell types found in cultures of endometrium: a mature epithelial cell and another cell which was classified as the endometrial stromal cell based on light and electron microscopy. In this report we compare the histochemical staining of endometrial tissue in frozen sections to that of cultured cells. These results confirm the epithelial and stromal nature of the respective cell types. Several markers were found that could distinguish between cells of epithelial and stromal origin. The enzymes alkaline phosphatase, gamma-glutamyltranspeptidase, peroxidase, and beta-glucuronidase were localized in glandular and surface epithelia in frozen sections and in colonies of epithelial cells in culture. Stroma in frozen sections and cultured stromal cells contained leucine aminopeptidase and fibronectin. Epithelia in sections and in culture could also be distinguished from cells of stromal origin by preferential binding of lotus and peanut lectin. Several other markers were found in both endometrial epithelium and stroma.
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PMID:Histochemical identification of cultured cells from human endometrium. 614 95

As measured by urinary D-glucaric acid excretion, an index of hepatic enzyme induction, glutethimide was the most powerful of six such inducers tested. In patients with tuberculosis, rifampicin, 450 mg daily, induced excretion rates of the lower dose range of anticonvulsants in epileptics. The effect was detectable in the first few days but the degree and rate of rise to maximum excretion were variable. This may be due either to disposition of rifampicin or to genetic susceptibility to enzyme induction. Plasma beta-glucuronidase, an essential enzyme of the glucuronic acid pathway, could be induced independently of an increase in D-glucaric acid excretion. Plasma gamma-glutamyltranspeptidase-levels, an index of hepatic microsomal enzyme induction, were elevated in only 20 of 83 subjects receiving rifampicin and isoniazid, and in all of them urinary D-glucaric acid excretion was normal. Neither of these indices, therefore, showed hepatic enzyme induction during combined therapy when other pathways such as oxidative metabolism continued to be induced. Different active sites of rifampicin and isoniazid on glucuronic acid and other biochemical pathways emphasize the complexity of final metabolic effects in patients on long-term therapy.
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PMID:Urinary D-glucaric acid excretion during rifampicin/isoniazid and anticonvulsant enzyme induction. 614 35

Renal tissue sections from 178 patients, whose kidneys were either normal or altered by various conditions such as hydronephrosis, interstitial nephropathies, chronic graft rejection, renal cancer etc., were investigated by computer-assisted histophotometry. We used enzyme histochemical and immunologic methods to measure kidneys suffering from various urological diseases quantitatively. Through this procedure, we were able to obtain information that allowed us to determine the degree of alteration in the metabolic state of tubular epithelial cells. The tissue activities of the following enzymes of the proximal tubule were investigated: alanine aminopeptidase (AAP), alkaline phosphatase (AP) and maltase (Ma) as membrane-bound markers, and beta-glucuronidase (beta-Gl) as a lysosomal marker. In addition, AAP and gamma-glutamyltranspeptidase (GGTP) were measured by immunofluorescent microscopy after having added specific anti-enzyme antibodies to the tissue sections. Compared to normal kidneys, quantitative enzyme histograms of diseased kidneys revealed a significant decrease in marker protein concentration of the tubule. The decline in tissue enzyme activities of AP, AAP, Ma and beta-Gl was accompanied by a significant decrease of enzyme concentrations as measured by the immuno histological method. This was especially true in cases with kidney cancer and in kidney tissues adjacent to infiltration adenocarcinoma. Morphological analyses of alterations were generally improved by enzymatic and/or immunologic histophotometry.
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PMID:Quantitative enzymatic and immunologic computer-assisted histophotometry of human kidney tissue following neoplastic and other clinically significant alterations. 687 27

The possibility of minimizing organ damage following cardiopulmonary bypass (CPB) was examined. In the control group, n = 21, upon completion of CPB, elevation of the lysosomal enzyme beta-glucuronidase, which is a sensitive indicator of cellular damage, was affected by the concentration of granulocyte elastase (r = 0.59) or the endothelial-derived constricting factor, endothelin, (r = 0.8). Renal damage, which was detected by an increase in renal tubular enzymes (N-acetyl-beta-D-glucosaminidase and gamma-glutamyltranspeptidase) in urine, was also affected by endothelin (r = 0.79, r = 0.56), elastase (r = 0.6, r = 0.71), and by free hemoglobin levels (r = 0.76, r = 0.82). Next, the efficacy of pharmacological intervention for the prevention of renal damage was evaluated. During CPB, the administration of an elastase inhibitor (ulinastatin, 3 x 10(5) IU), n = 8, or a calcium antagonist (nicaldipine HCl, elastase release inhibitor; 5 gamma/kg per min), n = 8, significantly reduced the elevation of beta-glucuronidase and renal tubular enzymes (p < 0.05). Although the ulinastatin and nicardipine groups demonstrated low values of elastase in the Intensive Care Unit (ICU), only the values of the nicardipine group reached statistical significance (p < 0.05). A reduction in endothelin levels compared to the control group was observed in the nicardipine group. However, preventive and counteractive effects of nicardipine against vasoconstriction caused by endothelin were also considered to play an important role in the prevention of renal damage. The addition of haptoglobin (4,000 IU) to the priming solution of the CPB also reduced levels of renal tubular enzymes (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacological intervention for renal protection during cardiopulmonary bypass. 830

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 < 0.01). 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 elastase and endothelin concentrations (r = 0.8 and r = 0.67 respectively). 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 = 0.61, 0.75) and elastase concentrations (r = 0.74, 0.75) respectively. In the group treated with nicardipine during the CPB, an increase in beta-glucuronidase was significantly low (p < 0.01) and renal tubular damage was significantly reduced. Moreover, lesser elevation of the elastase level on arrival in the ICU was evidenced (p < 0.05). Thus we concluded that nicardipine inhibited the release of elastase from the activated neutrophils and prevented the vasoconstriction caused by the endothelin secretion.
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PMID:[Mechanisms of organ failure following cardiopulmonary bypass--preventive effects of Ca2+ blocker (nicardipine)]. 847 80

The bisecting N-acetylglucosamine residue is formed by UDP-N-acetylglucosamine:beta-D-mannoside-beta-1, 4-N-acetylglucosaminyltransferase III (GnT-III), a key branching enzyme for N-glycans. We found that forskolin, an adenylyl cyclase activator, markedly enhanced GnT-III at the transcriptional level in various hepatoma cells and hepatocytes, resulting in an increase of bisecting GlcNAc residues in various glycoproteins, as judged from the lectin binding to erythroagglutinating phytohemagglutinin (E-PHA). In whole cell lysates, the E-PHA binding was increased, and leukoagglutinating phytohemagglutinin (L-PHA) binding was decreased at 12 h after forskolin treatment, by time, both GnT-III activity and mRNA had reached the maximum levels. In contrast, the binding capacity as to E-PHA, determined by fluorescence-activated cell sorting on the cell surface, was decreased, suggesting that bisecting GlcNAc structures in certain glycoproteins changed the expression levels of glycoproteins and decreased their sorting on the cell surface. Fractionated organelles of M31 cells showed that the binding capacity as to E-PHA was mainly localized in Golgi membranes and lysosomes. This was also supported by a fluorescence microscopy. In order to determine whether or not the bisecting GlcNAc residue acts as a sorting signal for glycoproteins, N-oligosaccharide structures of lysosomal-associated membrane glycoprotein 1 and beta-glucuronidase, gamma-glutamyltranspeptidase, and secretory glycoproteins such as ceruloplasmin and alpha-fetoprotein were measured by E-PHA and L-PHA blotting after immunoprecipitation. The expression levels of lysosomal membrane glycoprotein 1 and gamma-glutamyltranspeptidase on the cell surface were decreased at 12 h after forskolin treatment, indicating that the bisecting GlcNAc structure may act as a negative sorting signal for the cell surface glycoproteins and may alter the characteristics of hepatoma cells. This is the first report on glycoprotein sorting related to a specific structure of oligosaccharides, bisecting GlcNAc.
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PMID:Bisecting GlcNAc structures act as negative sorting signals for cell surface glycoproteins in forskolin-treated rat hepatoma cells. 900 30

In 30 patients with mononucleosis-like syndrome (MLS) caused by cytomegalovirus (CMV), diagnosed on the basis of clinical symptoms, haematological & serological changes (after excluding Epstein-Barr virus, HAV, HBV and HCV infections), the following measurements were done weekly during consecutive two months': bilirubin concentration, aspartate & alanine aminotransferases (AST & ALT), alkaline phosphatase (ALP), beta-glucuronidase (B-GR), and gamma-glutamyltranspeptidase (GGTP) activity. Increase in bilirubin concentration was found in 6% of patients, increase of AST and ALT activity--in 70%, GGTP--in 50%, ALP--in 25%, and of B-GR--in 16% of the subjects. The highest bilirubin concentration, and high levels of AST, ALT, and B-GR were noted in the 2nd week of infection, whereas the peak activity of ALP and GGTP was found in the 3rd week of the disease. In all patients normalization of bilirubin concentration was earliest (5th week of infection); followed by decrease of AST, ALT, B-GR, and ALP activity (7th week), and subsequently--that of GGTP (8th week of the disease). The results of the investigations have shown that in the course of MLS the changes of hepatic activity are limited and transient; they return to normal synchronously with the withdrawal of clinical symptoms (4th-6th week of the disease), without permanent measurable consequences. In patients with MLS and increase AST & ALT activity (400-600 iu) as well as slight increased of bilirubin concentrations hepatitis C,A and B should be excluded. In has not been established so far whether the changes of hepatic function during MLS are the consequence of direct infection by CMV, reactivation of the primary occult infection (asymptomatic), or re-infection by a different serotype.
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PMID:[Biochemical changes of liver damage factors in the course of mononucleosis like syndrome caused by cytomegalovirus]. 1134 95


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