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)

We observed previously that allopurinol, which was used for the treatment of gout, had a life saving effect after experiment on traumatic shock rats and hemorrhagic shock rabbits. To evaluate the effect of allopurinol fifteen patients undergoing open heart surgery who were considered to have similar metabolic derangement in shock patient were examined. Allopurinol was given orally 2 mg per kg body weight twice before the start of nitrous oxide, oxygen and halothane anesthesia. In the control group of ten patients who were not treated with allopurinol, serum uric acid increased, the lactate/pyruvate ratio rose and beta-glucuronidase activity increased respectively after open heart surgery as in shock. But the metabolic changes of the fifteen patients pretreated with allopurinol were less significant, although same tendency was observed. The heart beat of all patients except one case in the allopurinol group, started spontaneously after extracorporeal circulation without using DC counter shock. In the control group all patients needed DC counter shock. We concluded that allopurinol was effective in preventing damage of cellular structures and derangements of metabolism of patients undergoing open heart surgery.
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PMID:Effect of allopurinol (zyloric) on patients undergoing open heart surgery. 47 98

The activity of some lysosomal enzymes has been investigated in venous and arterial blood collected from patients undergoing cardiopulmonary bypass. Before bypass, there is no arterio-venous difference in the activity of n-acetyl-beta glucosaminidase, beta-glucuronidase or lysozyme. After operation, the activity of n-acetyl-beta-glucosaminidase is greater in arterial than in superior caval blood within the first 24 h after bypass, and a small arterio-venous increment in the activity of beta-glucuronidase can also be detected towards the end of the first day. The site of enzyme release has not been identified with certainty but may lie within the pulmonary circulation.
Anaesthesia 1978 Mar
PMID:Lysosomal enzyme release from the lungs after cardiopulmonary bypass. 64 73

Lysosomal enzyme release occurs during cardiopulmonary bypass in man but the tissues from which these enzymes originate have not been identified. The activity of N-acetyl beta-glucosaminidase in plasma increases to a degree which is proportional to the duration of bypass and this enzyme may therefore be a better marker than beta-glucuronidase of tissue damage caused by cardiopulmonary bypass, as distinct from tissue damage solely to the operative procedure.
Anaesthesia 1977 Sep
PMID:Lysosomal enzyme release during cardiopulmonary bypass. 92 Sep 15

In 12 dogs, 70% hepatectomy was performed to investigate the changes in serum lysosomal enzyme beta-glucuronidase activities, and to compare them with other liver functions and with the restoration of liver mass. Three dogs died within 24 hours without recovering consciousness from anesthesia, and one died on the fourth postoperative day because of hepatic insufficiency. The other eight dogs were killed at various postoperative times up to eight weeks. Regeneration of the remaining liver occurred rapidly after operation. The peak elevation of serum glutamic oxaloacetic transaminase activity was found on the first postoperative day, with a steady return to normal within two or three weeks. To the contrary, the serum activity of beta-glucuronidase decreased during the first three days, but increased substantially between the seventh and 14th postoperative day, when regeneration was considered to be maximum. The results seem to indicate that serial determinations of lysosomal enzyme activities in the blood can be a beneficial biochemical index for detection of progressing liver regeneration following partial hepatectomy.
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PMID:Lysosomal enzyme beta-glucuronidase. Release from regenerating liver after partial hepatectomy. 94 7

14C-labelled 3,4-benzpyrene (14C-BP) in dose of 100 mug/animal was injected into female Sprague-Dawley rats under urethane anesthesia. The rats were cannulated at the duct and the output of metabolites in the bile was determined. Non-treated rats excreted 35.5% of the given dose within one hr. The main metabolites excreted in bile were fractionated chromatographically into three. One of these was a metabolite which was hydrolyzed by beta-glucuronidase, the other two were unknown substances. Unchanged BP was not detected. In rats pretreated with CCl4 (0.5 ml/kg, p.o.) 24 hr before experiment, the biliary excretion of BP-metabolites was found to be reduced, that is only 10% of the given dose was excreted within one hr. It was noted that the output within the first 90 min after injection of BP was significantly reduced. In the CCl4-treated rats, bile flow was found to be lowered. However, the reduced output of BP-metabolites was considered not as the result of lowered bile flow, but as the result of disturbance of BP-metabolism in the liver. Thus it is suggested that impaired hepatic junction as the result of CCl4 intoxication may last for more than two weeks, when the hepatic junction is evaluated in terms of biliary excretion of BP.
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PMID:[Effect of carbon tetrachloride on biliary excretion of 3,4-benzpyrene in rats]. 123 18

We have investigated extrahepatic metabolism of propofol in 10 patients undergoing orthotopic liver transplantation (group 1) (mean age 38 yr, mean weight 60 (SD 7) kg) and compared it with that in 10 patients without liver dysfunction undergoing extrahepatic abdominal surgery (group 2) (mean age 56 yr, mean weight 68 (11) kg). A single i.v. bolus dose of propofol 0.5 mg kg-1 was injected into a peripheral vein 5 min after the beginning of the anhepatic phase in group 1 and 60 min after the induction of anaesthesia in group 2. Arterial blood samples were obtained at 5, 10, 15, 20, 30, 40, 50 and 60 min after injection and urine samples were collected every 15 min. Propofol concentrations in whole blood and urine were measured by high performance liquid chromatography with fluorescence detection. Propofol glucuronide was measured in urine by incubation with a specific beta-glucuronidase. The area under the time-blood concentration curve from 0 to 60 min was found to be significantly greater in group 1 (13743 (2830) micrograms litre-1 h-1) than in group 2 (7992 (4895) micrograms litre-1 h-1) (P less than 0.05). Unchanged propofol was not detected in the urine of either group. No significant difference was found in the amount of propofol glucuronide excreted by patients in group 1 (457 (269) micrograms) and in group 2 (921 (672) micrograms). The presence of a propofol metabolite in urine when the liver was excluded from the circulation suggests that extrahepatic metabolism occurred.
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PMID:Extrahepatic metabolism of propofol in man during the anhepatic phase of orthotopic liver transplantation. 154 Apr 62

Cocaine and its derivatives blunted responses of neutrophils (cell/cell aggregation, up-regulation of the receptor for C3bi (CR3, CD11b/CD18), generation of superoxide anion (O2-) and degranulation to various stimuli. The order of potency of these agents was the same as that for local anesthesia: tetracaine greater than bupivacaine greater than cocaine greater than lidocaine. Neutrophil aggregation elicited by the chemoattractant FMLP (10(-7) M) was inhibited by cocaine (10 mM) to 13.6 +/- 6% of control (p less than 0.002); the IC50 was approximately 4 mM. Cocaine and the other local anesthetics not only inhibited the upregulation of CR3 and O2- generation, but also blocked degranulation of cytochalasin B-treated cells. Cocaine (10 mM) reduced beta-glucuronidase and lysozyme secretion to 4.3 +/- 0.7 and 13 +/- 2.2% controls, respectively; its IC50 was 4 mM. Local anesthetics added after ligand/receptor engagement (FMLP) interrupted aggregation and halted generation of O2-. Moreover, local anesthetics rapidly inhibited aggregation, O2- generation, and degranulation elicited by PMA (1 microgram/ml) or the Ca ionophore A23187 (10 microM): the effects of cocaine could therefore not be attributed to unique actions at the FMLP receptor. Peak levels of intracellular Ca2+ ([Ca]i) at 5 to 10 s, and levels of [Ca]i 120 s after FMLP in Fura 2-loaded cells were significantly lower in cells treated with lidocaine, findings that could be explained by enhanced 45Ca2+ efflux from neutrophils. In cells loaded with bis(carboxyethyl)carboxyfluorescine (pH indicator) local anesthetics failed to affect the initial FMLP-induced (0 to 15 s) drop of pHi but inhibited the later (120 s) realkalinization of the cytosol (lidocaine, bupivacaine). Most remarkably, autoradiographs of SDS gels prepared from stimulated, 32P-labeled neutrophils treated with local anesthetics showed no difference from resting cells, either with respect to patterns of phosphorylation and dephosphorylation or their kinetics. Labeling of a 47-kDa protein, a component of the reduced nicotinamide-adenine dinucleotide phosphate-oxidase system, was unchanged. The effects of local anesthetics, which blunt neutrophil responses without affecting protein phosphorylation, suggest that protein phosphorylation is an insufficient signal for neutrophil activation. Inasmuch as cocaine and its derivatives affect cell functions at sites distal to activation of protein kinase C, these agents should prove useful in uncoupling protein phosphorylation from functional responses.
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PMID:Cocaine and its derivatives blunt neutrophil functions without influencing phosphorylation of a 47-kilodalton component of the reduced nicotinamide-adenine dinucleotide phosphate oxidase. 216 79

Biochemical and functional measurements of rat pulmonary alveolar macrophages were measured 4 h after 1 10-s, 26 to 28% total body surface area, full-thickness scald burn induced under ether anesthesia. Both phagocytic activity and capacity were significantly decreased to a comparable extent, whereas microbicidal activity was increased almost twofold in macrophages from the burned animals. Concurrent with the decreased phagocytic function was a marked impairment in chemotaxis and random migration of these cells when zymosan-activated serum was used as the chemoattractant. When biochemical parameters were examined, it was demonstrated that, on a per-cell but not total-protein basis, alveolar macrophages from burned animals had elevated levels of RNA, total protein beta-glucuronidase, acid phosphatase, and 5'-nucleotidase. These results raise the possibility that the increased pneumonitis in burned individuals may be due to more complex macrophage dysfunctions than impaired microbicidal activity, as was once thought. Alternatively, the biochemical and functional changes observed may be a reflection of a new population of macrophages appearing in the lungs after thermal injury.
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PMID:Biochemical and functional alterations in macrophages after thermal injury. 620 38

An experimental model of haemorrhagic hypotension was standardized using rabbits to investigate the shock lung syndrome over a period of 120 minutes. Acute hypovolaemia was induced by withdrawal of blood under anaesthesia to a mean arterial pressure of 30 +/- 5 mmHg within 10 minutes. The mean leucocyte counts and the release of lysosomal enzymes (acid phosphatase and beta-glucuronidase) in the blood and in lung tissue, as well as the metabolic capacities of lung tissue in terms of protein and lipid biosynthesis, were investigated at set intervals after 30, 60, 90 and 120 minutes. The results indicate a progressive decline in leucocyte numbers over 120 minutes to about 40% of the original. An immediate granulocytopenia was observed with a relative lymphocytosis within 30 minutes. The beta-glucuronidase and acid phosphatase contents of the plasma increased with time; beta-glucuronidase activity increased progressively as leucocytes disappeared from the circulation. Concomitantly, the capacity of the lung tissue to synthesize protein and lipids was retarded with time, becoming significantly lower than baseline values after 60 minutes of hypovolaemia. The decline in leucocyte numbers in the circulation correlated well with the increase in beta-glucuronidase activity and the retarded metabolic capacity of the lung tissue.
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PMID:Shock lung--experimental studies on a haemorrhagic hypovolaemic rabbit model. 661 40

A method was developed for the hydrolysis of conjugated iodothyronines in bile with the aid of beta-glucuronidase/arylsulfatase and for subsequent direct estimation of total and free iodothyronines with the aid of specific radioimmunoassay. The amount of conjugated fraction could then be calculated from the difference. Thus, basal biliary excretion of several iodothyronines was measured in 31 normal, fed rats in which the bile duct was drained with polyethylene tubing under pentobarbiturate anesthesia and the bile was collected for 2 h. The free fraction of thyroxine, 3,5,3'-triiodothyronine and 3,3'-diiodothyronine was approx. 30% of total content, while that of 3,3',5'-triiodothyronine and 3,5-diiodothyronine was approx. 20% and that of 3',5'-diiodothyronine was less than 10%. This suggests some considerable differences in the conjugation of individual iodothyronines in the liver. The concentration of T4 in bile was about the same as in plasma, while that of other iodothyronines was about 3-8 times higher than in plasma. This shows close interrelations between the iodothyronine deiodinating pathway in liver cells in vivo and the spectrum of iodothyronine in bile. The average ratio of T3/rT3 as found in bile was about 4.
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PMID:Direct quantitative estimation of several iodothyronines in rat bile by radioimmunoassay and basal data on their biliary excretion. 711 59


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