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)

When compared to values obtained in 17 normal weight normolipidemic control subjects (41.63 +/- 2.73 ml X min-1) antipyrine clearance determined in the saliva was found to be obviously decreased in the 10 patients with liver cirrhosis (21.88 +/- 0.79) and significantly increased in the 17 subjects with type IV hyperlipoproteinemia (59.91 +/- 4.59). Antipyrine clearance was positively correlated with both serum triglyceride concentration (r = 0.574; p less than 0.001) and serum cholinesterase activity (r = 0.705; p less than 0.001) and these correlations persisted even after the exclusion of cirrhotic patients. It is suggested that the accelerated hepatic secretion of very low density lipoproteins and of many export proteins and enzymes noted in most hypertriglyceridemic subjects is accompanied by an enhanced activity of liver microsomal enzymes involved in drug metabolism.
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PMID:Increased values of antipyrine clearance in type IV hyperlipoproteinemia. 377 12

The pretreatment of calves with a single dose of 10 mg kg-1 dieldrin or 21 daily doses of 10 mg kg-1 phenobarbitone increased the toxicity of diazinon as reflected by the development of more severe clinical signs and greater depression in whole blood cholinesterase activity in the pretreated calves. Induction by dieldrin or phenobarbitone of the hepatic microsomal enzyme amidopyrine-N-demethylase was also accompanied by a concurrent rise in the liver carboxylesterase activity.
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PMID:Effect of pretreatment with hepatic microsomal enzyme inducers on the toxicity of diazinon in calves. 380 24

The sensitivity of the mouse to organophosphorus-induced delayed neurotoxicity (OPIDN) has been investigated. One group of five mice received two single 1000-mg/kg po doses of tri-o-cresyl phosphate (TOCP) at a 21-day interval (on Days 1 and 21 of the study); a second group of five mice was given 225 mg/kg of TOCP daily for 270 days. A third group of five animals served as an untreated control. All animals were killed 270 days after the start of the experiment. Daily po dosing of 225 mg/kg TOCP caused a decrease in body weight gain, muscle wasting, weakness, and ataxia which progressed to severe hindlimb paralysis at termination. On the other hand, po administration of two single 1000-mg/kg doses of TOCP at a 21-day interval produced no observable adverse effects. Brain acetylcholinesterase (AChE) and neurotoxic esterase (NTE) activity were 35 and 10% of the control, respectively, in daily dosed animals while AChE and NTE in mice receiving two single 1000-mg/kg doses of TOCP were not significantly altered from the control group. Plasma butyrylcholinesterase activity was 12% of the control group in daily dosed animals. Hepatic microsomal enzyme activities of aniline hydroxylase and p-chloro-N-methylaniline demethylase and NADPH-cytochrome P-450 content in daily dosed animals were increased (141 to 161% of the control group) when compared to controls and mice receiving two single 1000-mg/kg doses of TOCP; the latter being not significantly different from each other. Degeneration of the axon and myelin of the spinal cord and sciatic fascicle were observed and were consistent with OPIDN. This study demonstrates that chronic dosing of TOCP produces OPIDN and induces hepatic microsomal enzyme activity in mice. It is concluded that while the mouse is susceptible to OPIDN, it is a less sensitive and a less appropriate test animal for studying this effect when compared to the adult hen.
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PMID:Characterization of delayed neurotoxicity in the mouse following chronic oral administration of tri-o-cresyl phosphate. 404 9

The target size of neurotoxic esterase (NTE), the putative target site for the initiation of organophosphorus-compound-induced delayed neurotoxicity, and acetylcholinesterase (AChE) from hen brain were examined by determining the rate at which the activities of the esterases were destroyed by ionizing irradiation. Samples of hen brain were prepared by slowly drying a microsomal preparation under vacuum. The dried samples were then irradiated with electrons from a 1 MeV Van de Graaff generator. The doses ranged from 0 to 28 Mrad. The radiation doses were calibrated by the rate of inactivation of T1-bacteriophage plaque induction. Following the irradiation procedure, the samples were resuspended in buffer and enzymic activity was measured. The target size of NTE from hen brain was determined to be about 105 kDa, whereas hen brain AChE was found to have a target size of about 53 kDa. The target size of NTE was found to be similar in experiments with rat brain and cat brain. In addition, commercial preparations of electric-eel electric-organ AChE and horse serum butyrylcholinesterase were found to have target sizes that were identical with each other, and also were very similar to that of AChE from hen brain.
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PMID:Target size of neurotoxic esterase and acetylcholinesterase as determined by radiation inactivation. 407 37

Some enzymatic parameters of neuronal transmission as well as the occurrence and the properties or carboxylic ester hydrolases in the hippocampal region of the wistar rat are investigated by histochemical and comparable biochemical methods. The acetylcholinesterase-, the monoamine oxidase- and the GABA-transaminase reaction are found at fibre structures, the course of which is seen more or less clearly. The histochemical picture of these enzymes is very different in each hippocampal layer and mainly limited by the corresponding number of reacting fibres. The origin and attribution of the fibres to the afferent and efferent systems are discussed. The occurrence of the acetylcholinesterase, the monoamine oxidase and the GABA-transferase as well as of the biogenic amines and the GABA are hints for the existence of cholinergic as well as aminergic and GABA-ergic processes of transmission in the hippocampal region. In the hippocampal region, the cingular and the optic cortex carboxylic ester hydrolases acetylcholinesterase, unspecific cholinesterase and the A-, B- and C-esterase could be demonstrated. The acetylcholinesterase of the hippocampal region is for the most part firmly membrane-bound and exists at least in two multiple, formalin-sensitive forms which are histochemically located in fibre structures. The unspecific cholinesterase, localized in the hippocampal region within vessel and capillary walls, exists in an electrophoretic mobile, formalin-sensitive form. Nearly half of the enzymes is soluble. A preferred binding to definite cell organelles was not demonstrable. In the hippocampal region the 3 multiple forms of the A-esterase are formalin-instable lyoenzymes. Good solubility and high formalin-sensitivity are the reason, why A-esterases are not demonstrable with usually histochemical methods. In the hippo ampal region the B-esterase is tightly bound to n electrophoretic mobile formalin-sensitive form in the microsomal fraction. In the cytoplasm of the neurones the desmoenzyme appears more or less granular. The 3 multiple forms of the C-esterase are formalin-sensitive to a different degree. Good solubility and low formalin-sensitivity, compared to the A-esterases are responsible for the fact, that the C-esterases can be shown histochemically only after en-bloc-fixation. The reaction products are granular. The similar behaviour of C-esterase and acid phosphatase, stated by many tests, suggests the C-esterases of the B- and C-type results in the same reactivity of pyramidal and granular cells of the hippocampal region. Some small, very strongly reacting cells belong to other cell types (probably basket cells or polymorphic cells).
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PMID:[Histochemical and biochemical investigations of the hippocampus and neocortex of the Wistar rat. I. Carboxylic ester hydrolases, transmitter enzymes and transmitters of the normal animal (author's transl)]. 610 39

We estimated the concentrations, multiple forms, and lectin binding of five microsomal enzymes in particle free extracts from human kidney, pancreas, jejunal mucosa, and normal and cancerous liver. While arylesterase markedly reacted only with concanavalin A, arylamidase, alkaline phosphatase, gamma-glutamyltransferase, and cholinesterase were intensely precipitated by lectins from Ricinus communis 120, Canavalia ensiformis, Triticum vulgare and Phaseolus vulgaris S. Agglutinins from Glycine max, Arachis hypogaea and Ulex europaeus proved less effective. The reaction mainly depended on the origin of enzymes not on their species. Desialylation always decreased precipitation, and in extracts of normal liver parenchyma it even totally abolished precipitation, by Triticum vulgare lectin. Sialoenzymes therefore appear to be normal intracellular constituents. Differences between enzymes from normal and cancerous liver were not reflected by variant properties of the corresponding activities in sera. The same held true for multiple forms. The reasons for these differences are discussed.
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PMID:[Catalytic concentration, multiple forms, and lectin affinity of microsomal enzymes from human tissues: lectins as reagents, II (author's transl)]. 612 Feb 6

The apparent (app) Km and app Vmax for mouse hepatic microsomal oxidative detoxification of chlorpyrifos to 3,5,6-tricholoro-2-pyridinol were 16.10 +/- 6.8 microM and 263.2 +/- 22.5 nmol/liver/min, respectively. The app Km and app Vmax for the oxidative activation of chlorpyrifos to chlorpyrifos oxon were 20.0 +/- 6.5 microM and 126.1 +/- 14.6 nmol/liver/min, respectively, whereas the app Km and app Vmax for hepatic microsomal hydrolysis of chlorpyrifos oxon to 3,5,6-trichloro-2-pyridinol were 1.87 +/- 0.36 mM and 89,450.7 +/- 12,087.3 nmol/liver/min, respectively. Under first-order conditions the capacity of mouse hepatic microsomes to detoxify chlorpyrifos oxon exceeded their capacity to generate this potent cholinesterase inhibitor from chlorpyrifos by a factor of 7.6. Pretreatment of mice with phenobarbital (70 mg/kg daily for 4 days) resulted in a 2.5-fold increase in the app Vmax's for oxidative activation and detoxification of chlorpyrifos, and a 1.6-fold increase in the app Vmax for hydrolysis of chlorpyrifos oxon. The app Km's were not altered by phenobarbital pretreatment. Administration of beta-naphthoflavone (80 mg/kg/daily for 2 days) to mice resulted in a slight decrease in the app Vmax's for oxidative activation and detoxification of chlorpyrifos, without altering the app Km's of the same reactions, or the hydrolysis of chlorpyrifos oxon. Phenobarbital and beta-naphthoflavone increased and decreased, respectively, the predicted hepatic clearance of chlorpyrifos. The acute toxicity of chlorpyrifos was slightly antagonized by phenobarbital pretreatment, but was potentiated by beta-naphthoflavone administration. These pretreatments did not affect cholinesterase, nonspecific esterase, or plasma A-esterase activities. Collectively, these results suggest that chlorpyrifos oxon formed within the liver does not escape hydrolysis by the liver, and that extrahepatic sites of activation are important in directly mediating the acute toxicity of chlorpyrifos.
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PMID:The role of hepatic biotransformation in mediating the acute toxicity of the phosphorothionate insecticide chlorpyrifos. 620 Sep 55

Health conditions were evaluated in 80 electrical workers exposed for many years to polychlorinated biphenyl (PCB) mixtures with a 42% mean chlorine content, who had blood PCB concentrations from 41 to 1319 micrograms/kg. The clinical study was based on personal history data, physical examination, and laboratory tests (red cell and leukocyte count; determination of haemoglobin, packed cell volume, bilirubin, serum protein electrophoretic fractions, pseudocholinesterase, AST, ALT, GGT, and OCT). Fifteen workers were found to have skin diseases--chloracne (4), folliculitis (4), oil dermatitis (1), juvenile acne (1), and dermatitis due to irritative or allergic agents (5). Sixteen workers showed more or less pronounced hepatic involvement, consisting most often of hepatomegaly with an increase in serum GGT, AST, ALT, and OCT values. In two workers bleeding cavernous haemangiomas were discovered, in one case associated with chronic myelocytic leukaemia. All the workers with chloracne were employed on electric capacitor impregnation with PCBs, and no definite association was found between chloracne and blood PCB concentrations. Conversely, a significant positive association was found between the abnormal liver findings and blood PCB concentrations, particularly trichlorobiphenyl blood concentrations. The abnormal hepatic findings observed are similar to those reported in experimental animals given PCBs, and in some workers such findings should probably be considered as clinical signs of hepatic microsomal enzyme induction.
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PMID:Occupational exposure to polychlorinated biphenyls in electrical workers. II. Health effects. 645 Dec 37

The levels of cocaine, benzoylecgonine and ecgonine methyl ester were measured periodically in the urine of dogs and rabbits by gas chromatography-chemical ionization selected ion monitoring mass spectrometry after subcutaneous injection of 2.9 mumol/kg (1.0 mg/kg) cocaine--HCl. Ecgonine methyl ester persisted much longer than benzoylecgonine. Urinary ecgonine methyl ester could be identified for 72 h in all the experimental dogs. The ester accounted for 6.6-27.1% of a dose of cocaine in dogs and 8.8-31.9% in rabbits 24 h after administration. Excretion of benzoylecgonine in urine was 6.3-19.2% in dogs and 7.5-32.9% in rabbits. This confirms that ecgonine methyl ester is one of the major metabolites of cocaine as well as benzoylecgonine. Excretion of the parent drug and its two hydrolyzed metabolites in faeces was very small, less than 1% of administered dose. Tri-o-tolylphosphate and eserine significantly inhibited cocaine hydrolysis to benzoylecgonine and ecgonine methyl ester, respectively. Parathion and EDTA, however, had no effects on cocaine hydrolysis in vivo. In vitro demethylation of cocaine to benzoylecgonine was demonstrated in the plasma from dogs and this production of benzoylecgonine was much more than that of non-enzymatic formation in buffer at physiological pH. It was concluded that a large part of the benzoylecgonine excreted in urine is an in vivo enzymatic product of cocaine. On the other hand, plasma cholinesterase and liver esterase mediated ecgonine methyl ester formation. This liver esterase was abundant in the soluble fraction and could be found in both of microsomal and mitochondrial fractions.
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PMID:In vivo and in vitro studies on cocaine metabolism: ecgonine methyl ester as a major metabolite of cocaine. 651 Aug 53

A single i.p. dose (120 mg/kg) of thiram given to male Sprague-Dawley rats caused a significant increase in the activity of SGOT and SGPT 24 hr post-treatment indicating liver damage. A considerable diminution in the serum cholinesterase activity was also noted in the treated rats as against the control animals. Additional evidence for thiram-induced liver toxicity is provided by the observation that there was approximately 50% inhibition of the activity of hepatic microsomal benzphetamine N-demethylase with a concomitant decrease in the concentration of cytochrome P-450, an important component of the mixed-function oxidase system. Although not significant, hepatic glutathione levels were also depleted by thiram, probably making the liver susceptible to toxic injury.
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PMID:Thiram-induced toxic liver injury in male Sprague-Dawley rats. 652 Mar 39


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