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

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

Aprotinin, a proteinase inhibitor, was evaluated as a pharmacologic aid in dogs subjected to lethal hemorrhagic shock. Survival time, hemodynamic changes, and plasma enzyme analysis were measured as criteria for drug effects. Mixed-breed dogs (n = 14) were divided into 2 groups of 7 each: nontreated dogs in shock (group 1) and aprotinin-treated dogs in shock (group 2). One of 7 dogs in group 1 and 2 of 7 dogs in group 2 survived. Survival time, for the remaining dogs in group 1 (190 min, n = 6) and group 2 (188 min, n = 5) were not significantly different. There was no significant difference in mean arterial pressure, mean pulmonary arterial pressure, cardiac output, or left ventricle systolic pressure associated with aprotinin treatment at any time after hemorrhagic shock. There was no significant difference in plasma lactic acid, aspartate aminotransferase, alanine aminotransferase, creatine phosphokinase, alpha-amylase, and beta-glucuronidase associated with treatment at any time; however, there were significant (P less than 0.05) increases with time. The gastrointestinal tract was the site of most obvious lesions found at necropsy. Lesions varied considerably in extent and severity without apparent correlation to the treatment regimen. These experiments did not show beneficial effects of aprotinin in dogs subjected to hemorrhagic shock, but neither did they completely rule out some valuable actions that may have been obscured by the type of model used.
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PMID:Effect of the proteinase inhibitor aprotinin in the management of hemorrhagic shock in the dog. 30 50

Myocardial contractility was evaluated in 8 out of 14 anaesthetized mongrel dogs during haemorrhagic shock and after volume replacement with Dextran 60 using the force-velocity relation of the contractile elements at zero load (Vmax). 7 animals received 50,000 or 20,000 KIE respectively of a proteinase inhibitor after bleeding and immediately before and one hour after the infusion of Dextran 60. The release of the lysosomal enzymes acid phosphatase and beta-glucuronidase was inhibited significantly (p less than 0.05) in the animals treated with Trasylol. However, the inhibition of the lysosomal enzymes seems not to have a decisive influence on the dynamic of the macro- and microcirculation and the myocardial contractility.
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PMID:[Myocardial contractility in dogs in hemorrhagic shock and after volumn replacement (author's transl)]. 108 72

The effects of human urinary trypsin inhibitor (UTI) were studied in experimental shock models. Administration of 50,000 U/kg, i.v., of UTI protected against mortality from shock induced by burn, endotoxin or trauma. Aprotinin at a dose of 50,000 U/kg improved only endotoxin shock and showed a moderate but not significant effect on burn and traumatic shock. Administration of 50,000 U/kg, i.v., of UTI protected against the aggravation in systemic hemodynamics in canine hemorrhagic shock. Furthermore, in rat traumatic shock, 50,000 U/kg, i.v., administration of UTI significantly reversed the increased serum beta-glucuronidase and trypsin activities and the decreased hepatic ATP level, and it moderately suppressed the increased serum uric acid level. Aprotinin failed to affect all these biochemical changes induced by drum trauma. These results suggest that the protective effect of UTI against experimental shock is possibly exerted through lowering the elevated enzyme activities in the serum during shock.
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PMID:Protective effects of urinary trypsin inhibitor in experimental shock. 241 41

Protective effect of aprotinin pretreatment was assessed by functional, biochemical and morphological preservation in four hour global ischemia followed by one hour reperfusion in dogs. Cardioplegia was induced by intermittent infusion of cold Mg-lidocaine solution. Aprotinin 10,000 KIU/kg was given in low dose group (8 dogs), and 20,000 KIU/kg in high dose group (6 dogs); one half was given before ischemia and another half during ischemia. Betamethasone, coenzyme Q and nifedipine were also given equally in both groups before ischemia. Results were as follows: 1. Four (50%) of low dose group and all of high dose group were successfully taken off CPB and survived for one hour reperfusion. 2. High dose group showed significantly higher blood pressure and LVSWI than low dose group after one hour reperfusion (p less than 0.05). 3. Serum N-acetyl-beta-D-glucosaminidase and mitochondrial aspartate aminotransferase showed the significantly lower activity in high dose group than in low dose group after one hour reperfusion (p less than 0.05). There was no significant difference in the activities of serum beta-glucuronidase and MB-creatine kinase. 4. Myocardial tissues, excised after one hour reperfusion, contained significantly higher creatine phosphate in high dose group than in low dose group (p less than 0.05). There was no significant difference in the contents of adenosine triphosphate, calcium and water. 5. Severely injured mitochondrion were significantly lesser in high dose group than in low dose group. All lysosomes showed mild swelling or enlargement, but those membranous structures were well-preserved in both groups. In conclusion, aprotinin pretreatment might be effective in myocardial protection against prolonged global ischemia, by inhibiting the "leak out" of lysosomal enzymes.
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PMID:[Improved myocardial protection by aprotinin pretreatment in prolonged global ischemia]. 248 66

We report on a 26-yr-old patient with an 11-yr history of insulin-dependent diabetes mellitus who exhibited insulin resistance with a requirement of up to 15,000 U of intravenous (i.v.) insulin/day. Attempts to diminish her insulin requirement by administration of sulfated insulin or Trasylol were unsuccessful, with the patient remaining resistant to subcutaneous (s.c.) and i.v. administration of pure pork insulin. Chloroquine phosphate therapy (500 mg twice a day) resulted in a decreased requirement for i.v. insulin (700 U/day as compared with the pretreatment requirement of 8400 U/day). Accelerated insulin degradation in s.c. fat tissue of the patient before treatment with chloroquine was demonstrated. This activity was decreased by 64% during chloroquine therapy. Inhibition of insulin degrading activity (IDA) during chloroquine therapy was associated with reductions in the leukocyte lysosomal enzymes alpha-galactosidase and hexosaminidase-A but not hexosaminidase-B and beta-glucuronidase. This study constitutes the first reported use of chloroquine for treatment of insulin resistance as a result of accelerated insulin degradation, and it provides evidence of the effectiveness of this agent in this rare condition.
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PMID:In vivo chloroquine-induced inhibition of insulin degradation in a diabetic patient with severe insulin resistance. 609 90