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:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malotilate, a new hepatotrophic drug, improves serum transaminase levels and the markers of protein metabolism in the liver in chronic liver diseases. However, the effects of malotilate on alcoholic liver disease are not well known. In the present study, the effects of this drug on the recovery process of alcoholic liver disease after abstinence were analyzed. Many hepatic test values were significantly improved after abstinence from alcohol in both the malotilate-treated and nontreated control groups. However, the Normotest values improved significantly only in the malotilate group, and not in the control group. The improvement rates for choline esterase activity were significantly greater in the malotilate group than in the control group. Serum albumin levels significantly increased in the malotilate group but not in the control group. Changes in the serum markers of hepatic fibrogenesis were not different between the 2 groups. These results indicate that malotilate accelerates the recovery of impaired protein metabolism in alcoholic liver disease and that this drug may be useful for the treatment of alcoholic liver diseases.
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PMID:Effects of malotilate treatment on alcoholic liver disease. 254 9

Human plasma cholinesterase (acylcholine acylhydrolase, EC 3.1.1.8) consists of four main molecular forms designated as C1, C2, C3 and C4 according to their electrophoretic mobility on gels. The major component, C4, is the tetrameric form; C1 and C3 are the monomeric and dimeric forms, respectively. The C2 form, which has an apparent free electrophoretic mobility higher than that of the three size isomers, and, moreover, a higher isoelectric point, was found to be a covalent conjugate between the cholinesterase monomer and serum albumin. This result is supported by the following arguments: the non-catalytic subunit of C2 was found to be a carbohydrate-free protein of apparent molecular mass 65 kDa that could not be labelled by diisopropylfluorophosphonate in the labelling conditions of esterases. It possesses a high affinity for a long-chain aliphatic ligand (a substituted octadecylamine) and for Cibacron blue F3 GA, and could be adsorbed on an immunoadsorbent for albumin. The two subunits of C2 are disulfide bridge linked; the active center of the cholinesterase subunit is partly masked by the albumin molecule. The conjugation reaction very likely occurs in the hepatic cell and not in plasma.
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PMID:A naturally occurring molecular form of human plasma cholinesterase is an albumin conjugate. 255 23

We report here a case of pseudocholinesterase (E.C. 3.1.1.8) deficiency, silent type II. The proband was a 29-year-old healthy man. His parents were cousins. A family study revealed that 9 out of 17 members of family investigated (paternal side 6, maternal side 3) concentrations. Serum cholinesterase activity were correlated well with serum albumin concentrations in both healthy people and patients with chronic liver diseases. The ratio of cholinesterase activity to albumin concentrations in serum was found more useful to detect heterozygous pseudocholinesterase deficiency than the serum cholinesterase activity alone. Both the dibucaine number and the fluoride number were within normal range in all family who showed low cholinesterase activity in serum. The amount of immunoreactive substance in serum against anticholinesterase antibody was normal in the proband as well as his family, while it was about twice of the value expected from their activity in those who had low ratio of serum cholinesterase activity to albumin concentrations. These results altogether suggested that the proband was a case of homozygous pseudocholinesterase deficiency, silent type II.
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PMID:[A family of pseudocholinesterase deficiency (silent type II)]. 260 Oct 76

To examine the pathogenesis of thrombocytopenia associated with liver cirrhosis, the platelet count, spleen size and serum cholinesterase levels were measured together with plasma concentration of beta-thromboglobulin, fibrinopeptide A and serum albumin in 38 patients with histologically proven, severe but stable liver cirrhosis. The spleen size contributed most significantly to thrombocytopenia in this disorder and the serum cholinesterase level also correlated with the platelet count, both in decompensated and compensated liver cirrhosis. Plasma beta-thromboglobulin, serum fibrinopeptide A levels and serum albumin did not correlate with the platelet count. These findings indicate that disseminated intravascular coagulation is not likely to be the cause of thrombocytopenia in liver cirrhosis. Splenomegaly as well as the diminished protein synthetic activity of the liver participates in the pathogenesis of the thrombocytopenia in this disease.
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PMID:Thrombocytopenia in liver cirrhosis. 261 53

S-mercuric-N-dansylcysteine was investigated as a potential probe of protein sulphydryl groups using bovine serum albumin, S-carboxymethyl-bovine serum albumin, lysozyme, and partially reduced lysozyme as test proteins. Criteria used to assess covalent binding through mercury-bridged mercaptide linkages include a finite reaction time (minutes to hours), abolition of the characteristic fluorescence spectrum following addition of a reducing agent, and failure to separate probe and protein after chromatography or electrophoresis. By these criteria, both Torpedo californica acetylcholinesterase and human serum cholinesterase (butyrylcholinesterase) contain four free sulphydryl groups per tetrameric enzyme molecule whereas Electrophorus electricus acetylcholinesterase has none. Labeled acetylcholinesterase and butyrylcholinesterase remain active and responsive to the inactivator Zn2+. Zn2+ promotes an increase in the fluorescence of bound S-mercuric-N-dansylcysteine, whereas activators such as Mg2+ or gallamine promote a decrease, suggesting that the label may be a useful probe of ligand-induced conformational changes. With T. californica acetylcholinesterase, but not with human serum cholinesterase, Zn2+ also promotes access to two additional groups that are reactive towards the sulphydryl reagent.
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PMID:The reaction of S-mercuric-N-dansylcysteine with acetylcholinesterase and butyrylcholinesterase. 278 87

The concentrations of Mg, Zn, Cu and albumin, and pseudocholinesterase activity were measured in the sera of 31 AIDS patients, 27 belonging to group IVC1 and 4 to group IVC2. Mean values for all patients were within the normal ranges. Only two patients showed hypozincaemia. A correlation was found between the concentrations of serum zinc and albumin. The serum albumin concentration was correlated with the serum pseudocholinesterase activity.
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PMID:Concentrations of magnesium, zinc and copper in serum of patients with acquired immuno-deficiency syndrome. 280 13

Malotilate, a hepatotropic agent, was given to 39 cirrhotic patients for more than 32 weeks. The serial changes in the serum levels of hepatic fibrogenesis markers, such as procollagen type III N-terminal peptides (P-III-N-P) and immunoreactive prolyl hydroxylase beta-subunit (IR-BPH) were analyzed. Serum albumin levels, transaminase and choline esterase activities and the Normotest values were found to be significantly improved by malotilate treatment. The levels of both serum markers of hepatic fibrogenesis were also significantly reduced by malotilate. The prognoses of the decompensated liver cirrhosis patients treated with malotilate were significantly better than those who did not receive malotilate. These results indicate that the effects of malotilate on chronic liver diseases are not simply biocosmetic, but rather are related to an improvement in the basal changes of the liver, including a decrease in the fibrogenetic stimulus. These effects of malotilate improved the prognosis of liver cirrhosis.
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PMID:Effects of malotilate treatment on the serum markers of hepatic fibrogenesis in liver cirrhosis. 285 77

The blood esterase mediating the hydrolysis of esmolol was characterized in several different species including man. In contrast to most ester-containing drugs, hydrolysis of esmolol was mediated by an esterase in the cytosol of red blood cells (RBC) in man and dogs and not in plasma or RBC membrane. Species differences in the esterase activity existed. Guinea pig and rat blood esterase activities were much greater than those in the dog followed by those in man. In addition, the esterase activity in rat and guinea pig blood was localized in plasma and not in RBC. Purified human serum cholinesterase, human RBC membrane acetylcholinesterase, human hemoglobin, human carbonic anhydrases A and B, and human and dog serum albumin were all inactive against esmolol. Esmolol esterase activity in human and dog blood was inhibited by sodium fluoride, EDTA, and p-hydroxymercuribenzoate, but not by echothiophate, eserine, and acetazolamide. In contrast, echothiophate and sodium fluoride, but not eserine, inhibited the esterase activity in rat and guinea pig plasma. Metabolic interaction studies indicated that acetylcholine, succinylcholine, procaine, and chloroprocaine did not interfere with the metabolism of esmolol by human and dog blood. Based on the results, it appeared that an arylesterase in human and dog RBC cytosol mediated the hydrolysis of esmolol while an aliphatic esterase mediated the hydrolysis of esmolol in guinea pig and rat plasma.
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PMID:Biochemical properties of blood esmolol esterase. 286 4

Biochemical and hemodynamic changes were assessed in 13 dogs subjected to sub-coronary valvular aortic stenosis and chronic protein-calorie malnutrition (PCM). Red blood cell, hemoglobin, serum albumin, free fatty acids, blood glucose, cholinesterase and blood amino acid levels were measured. The dynamic geometry of the left ventricle (LV) was assessed with chronically implanted sonomicrometric piezoelectric crystals. Cardiac function was evaluated by mean velocity of circumferential fiber shortening (mean VcF) and the relationship between LV end-systolic pressure (LVESP) or LV wall stress (LVWst) and LV end-systolic diameter (LVESD). The following results were obtained: A decrease in body weight and increases in free fatty acids and 3-Methylhistidine were observed following long-term PCM. Mean VcF was not depressed in dogs subjected to PCM. The relationship between LVESP or LVWst and LVESD shifted downward and to the right after PCM, indicating reduced myocardial contractility. These findings suggest that the left ventricle in hypertrophied dog hearts subjected to PCM retains normal pump function, despite a low state in the myocardium.
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PMID:Biochemical and hemodynamic changes in the hypertrophied dog heart subjected to chronic protein-calorie malnutrition. 295 29

Thyroid function was studied in 40 patients with chronic heart failure. Thyroid antibodies and microsome antibodies were negative in all cases. Serum T4, and T3 concentrations showed significant inverse correlation with cardiothoracic ratio, mean right atrial pressure, pulmonary artery systolic pressure, and peripheral venous pressure. Serum T4, T3 concentrations showed significant correlation with PaO2, serum albumin, and serum cholinesterase. Serum TSH concentrations increased with increasing cardiothoracic ratio. Histological examinations showed fibrosis and atrophy of the thyroid gland in 2 cases. These findings suggest the possible development of primary hypothyroidism as a result of chronic heart failure.
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PMID:Primary hypothyroidism in severe chronic heart failure. 296 70


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