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)

Antishock effect of N6, O2-dibutyryl cyclic AMP (DBcAMP) Was investigated in rats subjected to Noble-Collip drum trauma and compared with effects of hydrocortisone and Trasylol. Results obtained are as follows. 1)Hydrocortisone and Trasylol administered 1 hr before initiating drumming improved the survival rate from traumatic shock with concomitant reducton of levels of acid phosphatase and beta-glucuronidase in circulating blood. DBcAMP administered i.p. immediately after trauma also improved the survival rate to the same extent as did Traylol or hydrocortisone, while no inhibitory effects were observed on acid phosphatase and beta-glucuronidase. 2)The rectal temperature fell significantly after suffering trauma, and the rats with greater fall in rectal temperature had poorer chance for survival. The fall in rectal temperature was considerably prevented by DBcAMP in a dose of 0.5 mg/100 g body weight (b.w.). 3)DBcAMP induced a rise in plasma insulin level (IRI) and insulin/glucose ratio (I/G) in shock rats, and the elevation in blood lactate/pyruvate ratio (L/P) and excess lactate otherwise observed after trauma were satisfactorily prevented by DBcAMP administration. It is concluded that the antichock effects of DBcAMP primarily resulted from improvements of the intracellular metabolism induced by its easy passage through the cell membrane and its cAMP like action, while any preventive action was not observed against elevation of lysosomal enzymes in the circulating blood.
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PMID:Experimental study of dibutyryl cyclic AMP: its antishock effects observed in traumatic shock rats. 18 67

Androsterone, etiocholanolone, pregnanetriol, dehydroepiandrosterone, pregnanediol, tetrahydrocortisol, 5-pregnenolone and 11-beta-OH-androsterone were incubated with beta-glucuronidase preparations (Helix pomatia, bovine liver and E. coli) for 96 hrs at 37 degrees C. After extraction and silylation they were gas-chromatographed. The first 3 steroids were left practically intact. The least decomposition of the last 5 steroids occurred with the liver enzyme. Testosterone and 11-ketoandrosterone without the enzymes showed 74 and 35% recoveries. Cortisol and tetrahydrocortisol, incubated with the first two enzymes for 18 hrs at 37 degrees and 48 degrees C, showed nearly 100% recoveries. The recoveries of 17-OHCS in urines (pH 7.8-8.8), stored for 7 days, was 80% at 20 degrees-25 degrees C and 55% at 25 degrees-30 degrees C. The same samples, brought to pH 1.8-2.8 WITH NaHSO4 before the storage, showed a 100% recovery.
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PMID:[Decomposition of steroids during incubation with beta-glucuronidase and during storage of urine]. 76 25

Computerised gas chromatography-mass spectrometry was employed in the identification of polar corticosteroid metabolites excreted in the urine from the macaque monkey (Macaca fascicularis) and the baboon (Papio hamadryas). The following steroids were identified in significant amounts in the urine from both species: 3alpha,17alpha,20alpha, 21-tetrahydroxy-5beta-pregnan-11-one; 3alpha,17alpha,20beta,21-tetrahydroxy-5beta-pregnan-11-one; 5beta-pregnane-3alpha,11beta,17alpha,20alpha,21-pentol; 5beta-pregnane-3alpha,11beta,17alpha,20beta-pentol; 5alpha-pregnane-3beta,11beta,17alpha,20beta,21-pentol. 11beta,17alpha,21-Trihydroxy-4-pregnene-3,20-dione (cortisol), 11beta,17alpha,20beta,21-tetrahydroxy-4-pregnen-3-one and 11beta,17alpha,20beta,21-tetrahydroxy-5xi-pregnan-3-one were identified in macaque monkey urine. Two steroids, 17alpha,20beta,21-trihydroxy-4-pregnane-3,11-dione and 17alpha,20alpha,21-trihydroxy-4-pregnene-3,11-dione were excreted as major C21 metabolites in the baboon but were not identified in the urine from the macaque monkey. 3beta-Hydroxy-5alpha-pregnane metabolites were identified in the urine from both species. All these steroids were excreted conjugated to glucuronic acid, evidenced by their recovery after hydrolysis with beta-glucuronidase enzyme. An efficient 20beta-reduction of corticosteroids in both species is apparent, and the excretion pattern of polar steroid metabolites in the two species was shown to be similar.
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PMID:The characterization of polar corticosteroids in the urine of the macaque monkey (macaca fascicularis) and the baboon (papio hamadryas). 117 7

Flanagan, John F. (Duke University School of Medicine, Durham. N.C.). Hydrolytic enzymes in KB cells infected with poliovirus and herpes simplex virus. J. Bacteriol. 91:789-797. 1966.-The effect of poliovirus and herpes simplex virus infection on the activity of five hydrolytic enzymes was studied in tissue culture cells of KB type. During the course of poliovirus infection, the activity of beta-glucuronidase, acid protease, acid ribonuclease, acid deoxyribonuclease, and acid phosphatase in the cytoplasm rose to levels two- to fourfold greater than the activity present in the cytoplasm of uninfected cells. The rise in cytoplasmic activity was accompanied by a concomitant decrease in enzymatic activity bound to cell particles. Shift of enzymatic activity from the particulate to soluble state was first detected at 6 hr after poliovirus infection, coinciding with the appearance of new infectious particles and virus cytopathic effect. No net synthesis of these enzymes after poliovirus infection was found. Hydrocortisone added to the culture medium failed to affect either the titer of virus produced in the cells or the release of hydrolytic enzymes from the particulate state. Herpes simplex infection produced minimal alterations in the state of these enzymes in KB cells. It is hypothesized that the breakdown of lysosomes and release of hydrolytic enzymes accompanying poliovirus infection is produced by alterations in cell membrane permeability during the course of virus replication and by the consequent change in the ionic content of the cell sap.
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PMID:Hydrolytic enzymes in KB cells infected with poliovirus and herpes simplex virus. 428 87

Lysosomal membrane stabilization has been proposed as a mechanism for the anti-inflammatory action of corticosteroid hormones. This hypothesis was based on studies with liver organelles. We studied the action of steroids on intact lysosomes isolated from human peripheral blood polymorphonuclear (PMN) leukocytes. Both androstenedione and progesterone, 10(-3)-10(-5) M, caused leakage of acid hydrolase markers from these organelles, thus resembling their effects on liver lysosomes. But none of the anti-inflammatory steroids tested protected organelle membranes from either detergent lysis (Triton X-100) or heat incubation (37 degrees C, 90 min). Hydrocortisone (HC), HC sodium succinate, HC acetate, HC hemisuccinate, prednisone, and dexamethasone were without detectable stabilizing activity at concentrations of 10(-3)-5 x 10(-8) M. Release of the lysosomal marker, beta-glucuronidase, was not retarded by any of the compounds studied. In addition, PMN leukocyte lysosomes isolated from human volunteers receiving prednisolone were not more stable than control organelles, nor did serum from steroid-treated humans protect intact lysosomes from detergent lysis. Variations in cholesterol and phospholipid contents of liver and PMN leukocyte lysosome membranes could possibly account for the different reactivity to corticosteroids observed. We believe that the anti-inflammatory activity of adrenal corticosteroids can best be explained by their inhibitory effects on cellular metabolism rather than by their direct interaction with lysosomal membranes.
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PMID:Effects of steroid hormones on human polymorphonuclear leukocyte lysosomes. 443 Jul 21

Beta-glucuronidase activity was investigated during a 48-h period in which virus replication and changes in cell morphology occurred. Infection of an established line of chimpanzee liver cells with either nononcogenic adenovirus 5 or highly oncogenic adenovirus 12 under one-step growth conditions produced differing patterns of enzyme activity. There was an increase in total activity and also enhanced leakage of beta-glucuronidase from cells infected with adenovirus 12. In contrast, the enzymatic pattern of cells infected with adenovirus 5 was similar to that of uninfected cells. Hydrocortisone prevented the abnormal release of beta-glucuronidase from adenovirus 12-infected cells. The compound had no effect on total enzyme activity or on virus replication and the development of cytopathology.
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PMID:Beta-glucuronidase response of cells infected with Adenovirus types 5 and 12. 484 1

The time of appearance of a lysosomal enzyme, beta-glucuronidase, in the medium of cells infected with either measles virus or echovirus 6 varied with the host cell system. Replication and release of virus preceded leakage of beta-glucuronidase from green monkey kidney cells. In contrast, extracellular enzyme appeared before replication and release of virus in human amnion cells. Hydrocortisone depressed enzyme leakage but did not retard replication of measles virus or viral-induced cytopathology. The intracellular distribution of beta-glucuronidase in uninfected and measles virus-infected cells was also studied. Measles virus infection altered the position of particulate-bound beta-glucuronidase in linear sucrose gradients prior to substantial release of this enzyme intra- and extracellularly. At early stages in infection, most of the cell-associated virus banded with particulate-bound enzyme in the middle of the gradient. As infection progressed, separation of measles virus infectivity from enzyme activity occurred, and intracellular virus was recovered near the meniscus of sucrose gradients.
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PMID:Effect of host cell on distribution of a lysosomal enzyme during virus infection. 500 Jan 15

Homogenates of HeLa cells contain neuraminidase activity. This enzyme is particle-bound, and it has a pH optimum of 4.2. Hydrocortisone-regulated cells contain two to three times as much neuraminidase as the corresponding controls. The hydrocortisone treatment also causes an increase in the cell content of beta-glucuronidase and acid deoxyribonuclease.
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PMID:Neuraminidase activity in hela cells: effect of hydrocortisone. 547 38

The lysosomal enzymes, non-specific esterases, beta-glucuronidase, N-acetyl-beta-glucosaminidase and aryl sulphatases A and B, were examined histochemically in medial-edge epithelia (MEE) of single palatal shelves in vitro. Activities of most enzymes increased gradually in MEE with a peak at 24-26 h of culture. Aryl sulphatase B activities were lower than the others and aryl sulphatase A activities could not be detected in the palatal cells during the entire culture period. By 48 h, MEE cells degenerated and were lost. Cortisol suppressed increased activities of these hydrolytic enzymes and prevented programmed breakdown of the palatal epithelium.
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PMID:Cortisol inhibition of development of various lysosomal enzymes in cultured palatal shelves from mouse embryos. 658 15

The activity of prolylcarboxypeptidase (PCP), or angiotensinase C, was measured in lung tissues, leukocytes, and cultured human cells using Cbz-Pro-[14C]Ala as a substrate. A lysosomal fraction of homogenized rat or human lung contained most of the PCP activity in that tissue. Polymorphonuclear neutrophils, macrophages, and lymphocytes isolated from human blood had PCP activity. Fibroblasts cultured from human tissues had the highest activity (0.56-1.15 mumol/h per 10(6) cells), more than endothelial cells cultured from human pulmonary arteries. PCP of cultured human fibroblasts was similar to the human renal enzyme because it was resistant to moderate heating and was not inhibited by p-chloromercuriphenyl sulfonic acid. These properties and the substrate specificity distinguish PCP from cathepsin A, which is also in fibroblasts. Antibody to human renal PCP reacted with fibroblast PCP in immunofluorescence, indicating common antigenic determinants. Hydrocortisone changed PCP activity in fibroblasts in parallel with changes in beta-glucuronidase activity and cell-protein concentration; the activity was depressed at low concentration of the hormone. PCP activity was also found in synovial fluid from arthritic joints and in fibroblasts from the synovium. That PCP is found in both inflammatory exudates and in cells that appear at sites of inflammation indicates that, in addition to inactivating angiotensins, this enzyme may have a role in inflammation.
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PMID:Prolylcarboxypeptidase (angiotensinase C) in human lung and cultured cells. 745 50


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