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)

Acetylcholinesterase (AchE: EC 3.1.1.7) was identified and purified from the hemolymph of the scorpion Heterometrus bengalensis. The purity of the enzyme was determined by polyacrylamide gel electrophoresis (PAGE). The molecular weight of the enzyme, determined by sodium dodecyl sulfate-PAGE, was 80,000. The purified AchE hydrolysed acetylthiocholine iodide, but it did not react with butyrylthiocholine iodide. BW284C51, a specific inhibitor of AchE, strongly inhibited the enzyme. The known inhibitor (tetramonoisopropylpyrophosphortetramide) of pseudocholinesterase did not produce any inhibition of the enzyme activity. The purified AchE of scorpion hemolymph was vulnerable to high substrate concentration. The presence of Cu2+ and Ni2+ reduced the enzyme activity, whereas the metal ion, Sn2+, enhanced AchE activity. Ca2+ produced neither inhibition nor activation. (Na+, K+)-ATPase and Mg2+-ATPase activities were greatly enhanced by the purified AchE.
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PMID:Acetylcholinesterase (EC 3.1.1.7), a neurotransmitter enzyme in scorpion hemolymph. 296 37

In a prospective study involving 25 consecutive adult orthotopic liver transplantation (OLT) patients, of whom 23 had cirrhosis, we have related pretransplantation recipient parameters to blood loss during transplantation. In phase 1 (explantation of diseased liver) blood loss was 0.1-7.2 1, in phase 3 (following restoration of the portal blood flow after implantation) 0.1-39.7 1, and total blood loss was 1.6-47.2, median 9.2 1. Five patients (20%) died from causes directly related to defective haemostasis during the operation. Pretransplantation cholinesterase, antithrombin III and albumin correlated most strongly with blood loss in phase 1; a history of ascites, antithrombin III and cholinesterase levels correlated with blood loss in phase 3, and a history of ascites, urinary sodium and antithrombin III with total blood loss. Cholestasis did not influence blood loss. Portal hypertension per se presumably played only a restricted role. A pretransplant 24-h urinary sodium excretion of 10 mmol or less and a serum sodium of 132 mmol/l or less were highly predictive of blood loss exceeding 10 1 during OLT. Urinary sodium determination under test conditions and serum sodium measurement should already be part of the assessment of potential OLT candidates by the referring hospital.
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PMID:Liver disease and its effect on haemostasis during liver transplantation. 299 51

It is demonstrated by experiments with rabbits that the Ca2+-ATP-ase activity is stabilized when using combined anesthetics (diacetylcholine + halothane + N2O) as distinct from application of halothane. A decrease in the cholinesterase activity is less pronounced than under the halothane action but more than with the diacetylcholine application. A decrease in the Na+, K+-ATP-ase activity is observed with all types of anesthesia. A considerable inhibition of creatine kinase under the action of combined anesthesia and halothane and an increase of the lactate dehydrogenase activity under diacetylcholine application in mitochondria are shown. Reliable differences in the succinic dehydrogenase activity are not detected.
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PMID:[Effect of combined anesthetics on the activity of various myocardium enzymes]. 303 46

1. Using a K+-sensitive extracellular electrode, we attempted to determine whether cholinergic stimulation of the simian palm eccrine sweat gland is associated with transient net K+ efflux as in other exocrine glands. 2. When isolated secretory coils placed in a glass capillary were continuously superfused (method A), 32% of total cellular K+ was lost during 3 min of stimulation with methacholine (MCh) followed by K+ reuptake when stimulation was stopped. 3. When secretory coils were stimulated in a small chamber (without continuous superfusion, method C), MCh (5 x 10(-6) M)-induced maximal K+ efflux as determined by the peak level of extracellular K+ concentrations was dose dependent, inhibited by atropine but not altered by a cholinesterase inhibitor, physostigmine (1.3 x 10(-5) M). Thus the peak K+ level was used as a measure of K+ efflux throughout the study. 4. Phenylephrine (10(-4) M) and A23187 (5 x 10(-6) M) also induced K+ efflux but to a lesser extent than did MCh. 5. Ouabain (10(-3) M)-induced K+ loss was 2.4-fold higher than the peak level of MCh-induced K+ efflux. 6. In a Ca2+-free medium with added EGTA, inhibition of K+ efflux was only partial in the first MCh stimulation but progressively increased on repeated stimulation, suggesting that cytoplasmic or membrane Ca2+ not readily accessible to EGTA may be important for K+ efflux. Inhibition of K+ efflux in the Ca2+-free medium was completely reversed on subsequent addition of Ca2+. 7. Five millimolar Ba2+ partially inhibited MCh-induced K+ efflux. 8. 10(-4) M-bumetanide itself caused a small K+ loss and strongly inhibited the subsequent MCh-induced K+ loss. 9. MCh-induced K+ loss was drastically inhibited in the low-Cl- (by replacing with gluconate- or methylsulphate-) or low-Na+ (by replacing with Tris+) medium. 10. K+ efflux occurs predominantly across the basolateral membrane. 11. Vinblastine at 10(-4) M, which completely inhibits sweat secretion (our unpublished results), however, showed no effect on MCh-induced K+ efflux. 12. We conclude that the transient net K+ efflux associated with MCh stimulation constitutes a crucial primary ionic event in cholinergic eccrine sweat secretion as in other exocrine secretory cells.
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PMID:K+ efflux from the monkey eccrine secretory coil during the transient of stimulation with agonists. 315 70

To elucidate the mechanism underlying temperature-induced changes in airway cholinergic contractility, the effects of organ bath cooling were evaluated in isolated rabbit airway smooth muscle (ASM) segments isometrically contracted with methacholine (METH) (10(-8)-10(-3) M) and electrical field stimulation (ES), wherein the ES stimulus frequency was varied between 1 and 100 Hz. Cooling from 37 to 25 degrees C produced systematic increases (P less than 0.01) in isometric tension at various administered doses of METH and at different levels of ES. Since the potentiated contractions to ES significantly exceeded (P less than 0.001) the corresponding increases in METH-induced contractility, we evaluated whether the latter was attributed to temperature-mediated changes in intrinsic airway neuronal acetylcholine (ACh) release. Accordingly, the effects of ASM cooling were independently determined before and after inhibition of the Na+-K+ electrogenic pump with ouabain (10(-5) M), and depletion of intrinsic neuronal ACh stores with hemicholinium-3 (HC-3) (10(-3) M). In the presence of either ouabain or HC-3 the above responses to temperature reduction were reversed, and airway cooling was associated with abrupt relaxation of ASM segments precontracted with METH. In contrast, neither inhibition of cyclooxygenase products with indomethacin (10(-6) M) nor cholinesterase inhibition with neostigmine (10(-3) M) notably influenced the ASM responses to organ bath cooling. Thus these findings demonstrate that 1) both METH-induced and neurally mediated cholinergic contractility are augmented during airway cooling; 2) the potentiated cholinergic responses are attributed to enhanced presynaptic release of ACh at the airway neuromuscular junction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of temperature on cholinergic contractility of rabbit airway muscle. 332 12

The aim of the study is to follow up the changes in auditory and vestibular systems, common interactions between the sensory systems and the changes in some biochemical indices after vestibular loading in drivers. Several groups of drivers of heavy freight trucks were studied, aged from 25-60 and a length of service from 5 to 30 years, according to a standard programme for otoneurological examination and application of modern otoneurological methods. The biochemical investigations were performed to 32 healthy and 19 sick drivers with vestibular disorders, prior to and post vestibular provocation. The following biochemical indices were studied: serotonin, histamine, cholinesterase activity, glucose, GOT, GPT, alkaline phosphatase, calcium, potassium, sodium, chlorides, inorganic phosphorus. The biochemical changes, associated with vestibular loading of organism were established not to be strongly manifested and coming out of the frames of the normal values, nevertheless, they are significant for a given subject and should not be neglected. The data are of importance in the vocational selection of driver-applicants, prophylaxis and treatment of those working under stress situations and extreme impacts.
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PMID:[Otoneurological and biochemical research on the drivers of motor vehicles]. 349 83

Male and female F344/N rats and B6C3F1 mice were exposed to lethal and sublethal concentrations of methyl isocyanate by inhalation. Mortality, clinical signs, body and organ weights, and changes in clinical pathology and hematology were monitored immediately after 2-hr exposures and during the ensuing 3 months. Additional studies investigated the possible involvement of cyanide in the toxicity of methyl isocyanate. During exposures, signs of restlessness, lacrimation, and a reddish discharge from the nose and mouth were evident in rats and mice. Following exposures, rats and mice were dyspneic and weak. Deaths of rats and mice exposed to lethal concentrations (20 to 30 ppm) began within 15-18 hr, with males more prone to early death than females. A second wave of deaths occurred after 8 to 10 days, affecting primarily female rats and mice exposed to 20 to 30 ppm of methyl isocyanate, and male and female rats exposed to 10 ppm. Most deaths occurred during the first month following the exposures and were preceded by periods of severe respiratory distress. Body weights decreased in proportion to dose early, but then weight gain resumed in survivors at control rates. The only organ with a consistent, dose-related weight change was the lung, which was heavier throughout the studies in animals exposed to high concentrations of methyl isocyanate. No significant clinical pathology, or hematologic changes were observed in exposed rats. Blood and brain cholinesterase were not inhibited. Studies attempting to measure cyanide in the blood of methyl isocyanate-exposed rats, and attempting to affect lethality with a cyanide antidote (sodium nitrite and sodium thiosulfate) gave negative results.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Toxicity of inhaled methyl isocyanate in F344/N rats and B6C3F1 mice. I. Acute exposure and recovery studies. 362 44

The prevalence of the atypical phenotype of pseudocholinesterase was looked for in 345 individuals living in Zaria district of Northern Nigeria by the differential inhibitory actions of dibucaine and sodium fluoride. The frequency of the atypical gene, Ea1 was found to be 0.9% and the frequency of the fluoride insensitive phenotype Ef1, was 0.74%. The atypical enzyme or the intermediate phenotype was not observed in any of the 42 patients with sickle-cell disease.
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PMID:The prevalence of atypical serum cholinesterase in a Nigerian population. 362 11

The hypothesis that the toxic effects of imidocarb mediated by reduced cholinesterase activity might be intensified by hypomagnesaemia was tested in calves. Hypomagnesaemia was induced in 12 males (50 kg) using an artificial milk based on a commercial nondairy coffee creamer. Although plasma magnesium levels reached 0.33 mmol litre-1 in two weeks no clinical signs were detected. In 12 control calves a daily magnesium supplement of 0.6 g was inadequate although the published requirement is 0.45 g; it was raised to 1.2 g to keep plasma magnesium normal. Lighter calves developed hypomagnesaemia more readily and fast-growing calves had lower plasma urea concentrations. Plasma calcium, but not plasma magnesium, showed significant positive correlation with plasma albumin. The only statistically significant effects of hypomagnesaemia were slight elevations of white cell count and plasma sodium. The hypomagnesaemic and normomagnesaemic calves were divided into two equal groups and treated with 3.3 mg kg-1 of imidocarb dipropionate or a placebo. The drug produced the expected clinical signs of mild toxicity and depression of cholinesterase but no other adverse effects. Transient slight depressions of plasma calcium and potassium concentration, a transient rise of plasma sodium and elevation of creatine kinase occurred. None of the effects of imidocarb treatment was intensified by hypomagnesaemia except, perhaps, constriction of the pupils; generally, hypomagnesaemic animals were affected less.
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PMID:Effect of induced hypomagnesaemia on the toxicity of imidocarb in calves. 370 46

Using fully mechanized analytical equipment, interference by haemolysis in the determination of 26 clinical chemical parameters was determined quantitatively by adding haemolysate to serum. Haemoglobin concentrations up to 6.6 g/l caused essentially no interference in the following determinations: albumin (immuno-nephelometric), alpha-amylase, calcium, chloride, cholesterol, cholinesterase, creatinine, iron, glucose, glutamate dehydrogenase, uric acid, urea, sodium, inorganic phosphate, total protein, transferrin and triglycerides. In the presence of haemoglobin, erroneously high values were found for: lactate dehydrogenase (haemoglobin higher than 0.2 g/l), aspartate aminotransferase, potassium and acid phosphate (haemoglobin higher than 1.5 g/l), creatine kinase (haemoglobin higher than 2.5 g/l) and alanine aminotransferase (haemoglobin higher than 3.4 g/l). Erroneously low values were found for bilirubin (haemoglobin higher than 0.8 g/l), alkaline phosphatase and albumin (by electrophoresis) (haemoglobin higher than 1.5 g/l) and gamma-glutamyltransferase (haemoglobin higher than 3.0 g/l).
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PMID:Haemolysis as an interference factor in clinical chemistry. 371 97


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