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)

The method is suggested to isolate simultaneously microsomes and plasma membranes of neuroblastoma S 1300 N 18 cells by means of differential centrifugation in the step density gradient of Percoll/Ficoll with a high degree of purification determined from the activity of marker enzymes (acetyl cholinesterase Na+,K+-ATPase, alkali phosphatase, glucose-6-phosphatase, succinate-dehydrogenase, acid phosphatase) as well as from the content of DNA and RNA and with a sufficiently high protein yield. The purified fractions of microsomes and plasma membranes are established to contain no phosphatidyl glycerol and cardiolipin--safety markers of mitochondrial membrane purification. A degree of separation of microsomes, plasma membranes and proteins dissolved in cytosol may be estimated by the activity of the cholesterol-synthesizing system of enzymes with the use of sterol-transferring protein.
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PMID:[Rapid simultaneous isolation of microsomes and plasma membranes from neuroblastoma C 1300 N 18 cells]. 258 50

The aim of the study was explaining of the combined action of low doses of sodium nitrite and fenitrothion on certain biochemical parameters in rat blood. The experiment was carried out on male adult Wistar rats. The animals were divided into 4 experimental groups: group I receiving 10 mg/kg of sodium nitrite, group II--2.5 mg/kg of fenitrothion (Owadofos), group III received a mixture of both these doses, group IV served as control. The preparations were given intragastrically through a tube for 90 days. After that time 2,3-diphosphoglyceric acid, vitamin E, SH groups in protein and non-protein compounds in erythrocytes, methaemoglobin and basic haematological parameters, as well as the activity of glucose-6-phosphate dehydrogenase, superoxide dismutase and choline esterase were determined. Sodium nitrite decreased the activity of glucose-6-phosphate dehydrogenase and vitamin E, with an increase of the activity of superoxide dismutase and protein SH groups and methaemoglobin level. fenitrothion caused similar changes as sodium nitrite and decreased the activity of choline esterase and the level of 2,3-diphosphoglyceric acid. No synergistic action of these compounds was noted. The level of non-protein SH groups was decreased. It seems that determination of the level of non-protein sulphohydryl groups may be one of the indicators of poisoning with sodium nitrite combined with phenitrotione.
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PMID:[Effect of the combined action of sodium nitrite and fenitrothion on certain biochemical parameters in rat blood]. 260 57

Three dose levels of pyridostigmine (0.5, 2, and 5 mg/kg) were given iv to dogs anesthetized with sodium pentobarbital. Hemodynamic measurements made were cardiac output, blood pressure, left ventricular dP/dT, and heart rate. Pulmonary function data obtained were airway resistance, respiratory rate, and tidal volume. Activity of blood cholinesterase was also measured. Increasing doses of pyridostigmine promptly and progressively lowered the acetylcholinesterase activity of blood to a minimum of 40% of control at the 5 mg/kg dose. Airway resistance was most sensitive to the drug. Resistance increased significantly with 2 mg/kg, and the 5 mg/kg dose resulted in more than a 10-fold increase, which persisted for more than 2 hr. Tidal volume was decreased and minute volume was increased due to an increase in respiratory rate. With the higher doses, heart rate decreased and stroke volume rose sufficiently to compensate so that cardiac output was unchanged. The lowest dose produced minimal effects on both cardiovascular and respiratory systems, and since this dose is greater than that proposed for organophosphate poisoning in humans, it seems likely that this drug would not cause important effects in normal humans when used as a protective agent.
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PMID:Interactions of pyridostigmine with cardiopulmonary systems and their relationships to plasma cholinesterase activity. 273 58

Groups of 21 male and 21 female Sprague-Dawley (SD) rats were fed diets containing pyriproxyfen at concentrations of 0, 80, 400, 2,000 and 10,000 ppm for 6 months. No death was found in any group. Alopecia in the neck and/or back, and soft feces were noticed in both sexes fed 10,000 ppm. A marked decrease in body weight gain was observed in both sexes fed 10,000 ppm throughout the treatment period, accompanying a decrease in food-consumption and an increase in water-intake during the initial stage of treatment. In terms of urinalysis, proteinuria, increases in K excretion, and, in number, yellowness or browish-yellowness in appearance, were observed in both sexes fed 10,000 ppm. In females fed 10,000 ppm, increases in bilirubin, Na excretion and specific gravity, and a decrease in ketone bodies, were observed. In hematology, decreases in erythrocyte count, hemoglobin concentration and hematocrit value, were observed in both sexes fed 10,000 ppm and in males fed 2,000 ppm. Also, an increase in MCH (in males), decreases in MCHC and platelet count (in females) were observed in 10,000 ppm group. Blood biochemistry revealed increases in total protein, albumin, alpha 2-globulin fraction, blood urea nitrogen, calcium (in both sexes fed 10,000 ppm), A/G ratio (in males fed 2,000 and 10,000 ppm), total cholesterol, phospholipid (in males fed 2,000 and 10,000 ppm, and in females fed 10,000 ppm), sodium (in females fed 2,000 and 10,000 ppm), gamma-glutamyl transpeptidase activity (in males fed 10,000 ppm) and alpha 1-globulin fraction (in females fed 10,000 ppm), and decreases in glucose, GOT (in both sexes fed 10,000 ppm), beta-globulin fraction (in males fed 2,000 and 10,000 ppm, and in females fed 10,000 ppm), GPT (in females fed 2,000 and 10,000 ppm), triglyceride, potassium (in males fed 10,000 ppm), and cholinesterase activity (in female fed 10,000 ppm). In organ weight, increases in liver (in males fed 2,000 ppm and 10,000 ppm, and in females fed 10,000 ppm), kidney (in both sexes fed 10,000 ppm) and thyroid (in females fed 10,000 ppm) and a decrease in pituitary (in females fed 2,000 and 10,000 ppm) were observed. Gross pathology revealed a higher incidence of blackish-brown coloration of the liver, and a lower incidence of accentuated lobular pattern of the liver (in males fed 10,000 ppm). An enlargement of the liver was seen in a few of both sexes fed 10,000 ppm. Histopathological examination showed that the sole effect attributable to treatment of this compound was on slight hypertrophy in the liver of both sexes fed 10,000 ppm, with a higher incidence.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A six-month chronic dietary toxicity study of pyriproxyfen in rats]. 273 65

This study shows our clinical and therapeutical experience in 48 cases of infant COFA intoxication admitted in the Intensive Care Unit of "Emilio Civit Children Hospital", Mendoza, Argentina in a periode of seven years. They were investigated to determine the presence of Parathion in blood and gastric washing with the sodium hydroxide qualitative method, and also cholinesterase was detected in blood with a colorimetric method (the monotest cholinesterase). Age range from one to ten years with predominance from 3 to 4 years; 27 were males and 21 females. In almost all the cases (90%) the toxic ingressed through several ways, and from 10 to 30 minutes appeared the characteristic signs: miosis and bronchorrhea. Clinically in 30 cases the intoxication was considered dangerous and mild in the others. The data obtained by laboratory techniques were diagnostic only in half of the cases. Atropine's sulphate was done to all cases until their recuperation, in doses from 2.5 mg to 20 mg. The evolution was highly satisfactory, only two died and two remained with seizures. Always had thanklessness and carelessness with the child from living together adults, who playing handle and waste the toxic. In two occasions the intoxication was familiar by contaminated food.
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PMID:[Parathion poisoning]. 275 76

Synaptosomes were incubated at various time intervals following injection of 120 micrograms/kg SC of soman or sarin or with various concentrations (10(-8) to 10(-2) M) of soman or sarin in vitro. Total cholinesterase (ChE) activities in each brain region were also measured. Following soman injection, sodium-dependent, high affinity choline uptake (SDHACU) was decreased from 1 to 4 hr in the cortex and from 1 to 2 hr in the hippocampus, but increased from 2 to 24 hr in the striatum. Similarly, following sarin injection SDHACU was decreased at 0.5 hr in the cortex and from 1 to 4 hr in the hippocampus, but increased at 1 hr in the striatum. Injection of soman severely inhibited (83-99%) total ChE activity in the cortex, hippocampus and striatum from 1 to 24 hr. In contrast, sarin did not severely inhibit ChE activity in these regions and maximal inhibition (40-60%) did not occur until 24 hr after injection. With both compounds, by 168 hr ChE activity in all regions had partially recovered. Incubation of synaptosomes with soman or sarin in vitro at concentrations below 10(-4) M did not affect SDHACU in any of the brain regions. These data demonstrated that acute soman and sarin injection produced similar effects upon SDHACU in different brain regions, although the time-course of these effects was different for the two compounds. These effects were probably neither due to a direct action of these compounds on the uptake process nor dependent on ChE inhibition.
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PMID:Effects of soman and sarin on high affinity choline uptake by rat brain synaptosomes. 276 46

Epicardial coronary artery strips of cattle hearts mounted in vitro respond to transmural stimulation with a neurogenic constriction, attributable to the endogenous release of acetylcholine. These responses were elicited with frequencies as low as 1.0 Hz and with pulse durations as low as 100 microseconds. The magnitude of the contractile response increased with increasing frequency of stimulation. Blockade of adrenergic neuronal mechanisms with guanethidine (5 x 10(-6) M) increased the size of the contractile responses at 10 Hz and they were antagonized markedly by the muscarinic antagonist atropine (4.3 or 8.6 x 10(-7) M), but not by the adrenergic antagonist phentolamine (3.6 x 10(-7) M). Contractions to field stimulation were increased greatly by the cholinesterase inhibitor physostigmine (1.1 x 10(-6) M). Blockade of neuronal sodium channels with tetrodotoxin (9.4 x 10(-7) M) reduced severely the contractions to field stimulation, as did cold storage of coronary vessels for 5 or 6 days. The contractile responses to stimulation were not inhibited significantly by antagonists of prostaglandin synthesis, or were they enhanced by denudation of the endothelium. It is concluded that cholinergic constrictor mechanisms, linked to medial muscarinic receptors, operate in the large coronary arteries, which are associated in humans with coronary spasm.
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PMID:Cholinergic contraction to field stimulation in coronary arteries of cattle. 278 63

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

The average biological intra-individual CV in 20 patients with chronic liver diseases (CLD), estimated for 14 analytes during a stationary phase, significantly exceeded that for a normal group in the cases of Na+, K+, Cl-, total protein, albumin, cholinesterase, hemoglobin, and alpha-amylase; it did not differ significantly from the normal group for cholesterol, alkaline phosphatase, aspartate aminotransferase, and alanine aminopeptidase; and it was significantly lower than in the normal group for alanine aminotransferase and gamma-glutamyltransferase. There were no significant sex-related differences in mean intra-individual variation in CLD patients. Individual values were gaussian-distributed for all analytes, including enzymes. The estimated biological component of intra-individual variation and the analytical variation as determined for each laboratory can be used to derive decision-making criteria in monitoring CLD.
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PMID:Intra-individual variation of analytes in serum from patients with chronic liver diseases. 288 11

Mothers who smoke cigarettes during pregnancy give birth to babies with lower birth weights than do nonsmoking mothers. One hypothesis to explain this finding is that nicotine depresses the activity of the placental cholinergic system, which has been linked to the placental transport of amino acids and other substances. The levels and activities of several components of the term placental cholinergic system were determined in smokers and nonsmokers to investigate whether this system is involved in the effect of smoking. There were no statistically significant differences in the levels, synthesis or release of acetylcholine in the tissues from smoking and nonsmoking mothers, nor in the activities of the choline uptake system or the enzymes choline acetyltransferase, cholinesterase or sodium/potassium adenosine triphosphatase. The results do not support the hypothesis that the lower birth weights of babies born to smoking mothers is mediated by an effect of nicotine or other tobacco components on the placental cholinergic system.
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PMID:The effect of cigarette smoking during pregnancy on the cholinergic system in isolated term human placental tissue. 293 60


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