Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

If examinations of the liquor are to give an insight into the metabolic condition of the brain, then it is necessary for all sources of error to be removed. The use fo exact methods requires that the liquor be free of major pleocytosis. In vitro examinations showed that additions of blood caused the activity of LDH to be doubled within thirty minutes, while that of cholinesterase even increased sixfold. It is especially after craniocerebral injuries that extra care must be taken to insure that the liquor used is as clear as water.
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PMID:[Possible error in interpretation of liquor enzyme activities as demonstrated on the example of lactate dehydrogenase and cholinesterase]. 102 May 39

Water, saline and ethanol extracts of Eugenia caryophyllus inhibited brain acetylcholinesterase (AchE) activity. Inhibitory action of the saline extract was greater than that of other extracts. The most active fraction of the saline extract obtained by chromatography through Sephadex G25 and DEAE cellulose columns and elution with tris and phosphate buffers (pH. 7.1) exhibited reactions characteristic of phenols, amino compounds and uronic acid. It is, therefore, suggested that the active inhibitor is a complex glycoside containing phenol and uronic acid part structure.
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PMID:Biochemical studies of acetylcholine esterase inhibitor present in Eugenia caryophyllus. 102 8

The side effects of water soluble iodinated contrast media often mimic the clinical picture of acetylcholine intoxication. This prompted us to determine the amount of inhibition of human acetylcholinesterase by the following contrast media in vivo and in vitro: methyl glucamineiodipamide (Biligrafin forte), methylglucamine iothalamate (Conray 60), sodium-iothalamate (Conray 80). In vivo no correlation could be found between clinically manifest adverse reaction and enzyme inhibition after contrast media application. The in vitro values for 50% inhibition of erythrocyte acetylcholinesterase are: methylglucamine-iodipamide: 0.036 M, methylglucamine-iothalamate: 0.158 M, sodium-iothalamate: 0.3 M. Since in vitro, the maximal inhibitory effect of a given dose of contrast media can only be registered after a time interval when most of the contrast media in vivo has already been excreted by the kidneys or extracted by the liver, it seems very improbable that the enzyme inhibition seen in vitro should have any consequence whatsoever under clinical conditions. The in vitro inhibition of acetylcholinesterase is quickly reversible, with nearly all the activity regained 15 min after the removal of the contrast media.
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PMID:[The effect of tri-iodinated contrast media on acetylcholinesterase of human erythrocytes (author's transl)]. 103 75

Rats were continuously exposed to tritiated water (0, 1, 10 and 100 muCi HTO/ml body water) from conception to birth. Calculated, cumulative whole-body doses to the embryo and foetus were approximately 0, 6-6, 66 and 660 rad. The levels of several enzymes and established or presumptive central nervous system neurotransmitters were examined postnatally in whole brains. These were norepinephrine (NE), dopamine (DA), acetylcholinesterase (AChE) and monoamine oxidase (MAO). Intrauterine exposures to doses as low as 66 rad produced measurable and persistent decreases in brain weight and increases in NE concentrations at 21 and 45 days postnatally. No differences from control values were seen in the rate of turnover of NE or the concentrations of DA, AChE or MAO at 45 days. Exposure in utero to 6-6 rad produced no detectable postnatal effects on the brain neurochemical parameters measured.
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PMID:Some aspects of brain neurochemistry after intrauterine exposure to tritium. 108 Jan 41

It has been postulated that behavioral inhibition due to punishment or extinction may be mediated by brain acetylcholine, and drugs which have disinhibitory action are thought to interact with this system. This notion was tested by comparing the effects of scopolamine, physostigmine and chlordiazepoxide on punished and extinguished water consumption. Scopolamine hydrobromide (0.3, 0.5 mg/kg, i.p.), a centrally and peripherally acting antimuscarinic agent and physostigmine sulfate, (0.3 mg/kg, i.p.), a centrally and peripherally acting acetylcholinesterase inhibitor, lowered both non-punished and punishment suppressed water intake and lick rate, whereas their quaternary analogs which primarily act in the periphery, had no significant effect at comparable dose levels. Scopolamine and physostigmine suppressed punished water consumption at lower dose levels than nonpunished intake. In contrast, chlordiazepoxide (5.0, 10.0, 20.0 mg/kg, i.p.) enhanced punished as well as non-punished water intake. In a further experiment comparing punishment and extinction suppression, scopolamine and physostigmine did not affect punished or extinguished water intake; chlordiazepoxide (5.0, 10.0, 20.0 mg/kg) reliably increased punished, but not extinguished licking on the water nozzle. These results suggest (1) that scopolamine and chlordiazepoxide do not act via a common mechanism, and (2) that punishment and extinction suppression are not a pharmacological entity.
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PMID:Effects of scopolamine, physostigmine and chlordiazepoxide on punished and extinguished water consumption in rats. 116 84

In studies of potential exposure of a volunteer working under controlled conditions during apple hand-thinning operations at 1, 24, 48, 72, 96, 168, and 240 hr after application of conventional 0.03% parathion spray, both dermal and respiratory exposure values were greater where water-wettable powder formulations were used than where emulsifiables were used. Residue levels of parathion on leaves from the two types of applications were about the same. Only trace amounts of paraoxon could be detected at one and seven days after application. Highest exposure values (14.2 mg/hr dermally and 0.15 mg/hr respiratorily) were obtained within 24 hr of application. Exposure was considerably less after residues were 72 hr old. Greatest exposure was on the forearms and hands. Urinary p-nitrophenol excretion indicated slightly more absorption following exposure in water-wettable powder experimental plots. Potential exposure values indicate that absorption could reach hazardous levels after one or two hr of work, even at the 96-hr residue period, if all the pesticide were absorbed. Considering that only a small fraction of the total amount would be absorbed, it is calculated that at 75-hr residue period poisoning should not occur. There was no significant change in blood cholinesterase activity of the volunteer worker. Variation in spray deposit within an orchard due to poor tank mixing did not appear to be great enough to be considered an important factor affecting exposure.
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PMID:Exposure of apple thinners to parathion residues. 119 Aug 38

The article deals with the hydrophobic character (distribution coefficient in the systems hexane - water and chloroform - water) and certain peculiarities of distributing three cation-containing phosphoroganic inhibitors of cholinesterase and their uncharged analogues in the organisms. The distribution coefficients in the charged and uncharged compounds in the system hexane - water differ inconsiderably, whereas in the system chloroform-water by the thousands and millions times. In rabbits with intravenous administration the content of all inhibitors in blood decreases rapidly, the uncharged compounds accumulate selectively in the lungs and the charged ones are distributed evenly in the tissues.
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PMID:[The distribution of cholinesterase charged phosphorganic inhibitors and their uncharged analogues in tissues]. 120 7

Abolition of cholinergic inhibition in the heart of fresh-water bivalves in absence of cholinesterase can be attained by inactivation of the acetylcholine receptor (R). The role of Ca in this process was studied. Determination of Ca in the perfusate at different stages of cholinergic inhibition showed that the concentration of Ca increased during the sistolic arrest, and the initiation of beats was accompanied by binding of Ca. This coincided with the onset of ATP release and went on till the complete desensitization. The increase of external Ca concentration up to 1.10-2M increased the half-time of desensitization while the binding of Ca with EDTA decreased it and eliminated the ATP anti-acetylcholine effect. Another bivalent ion, UO2, which binds phosphate groups, competes with Ca. The role of Ca and ATP in chemical inactivation of the acetylcholine receptor is discussed.
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PMID:[The role of Ca ions in desensitization induced by acetylcholine]. 120 72

C57B1/6J, a specific inbred strain of mice with high alcohol preference and DBA/2J, a specific inbred strain with poor preference for alcohol were studied. Brain content of acetylcholine, uptake of 14C-Choline by whole brain homogenate were significantly higher in the C57B1/6J mice whereas brain acetylcholinesterase was higher in the DBA/2J mice. No significant difference was found for the level of brain serotonin, uptake of 3H-norepinephrine or 3H-dopamine. Treatment with a specific inhibitor of choline transferase, 4-(1-napthylvinyl) pyridine salt (10 mg/kg, twice daily) shifted the selection of alcohol to water in the C57B1/6J mice. These findings suggest a direct involvement of central cholinergic mechanism in alcohol preference.
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PMID:Neurochemical correlates of alcohol preference in inbred strains of mice. 122 97

The content and hydrophobic properties (distribution coefficient in hexan : water) of organophosphorus inhibitors OPT of the following structure--R-O (CH3)/P/O/S C2H4SC2H5 have been studied in rat brain. On enlargement of the O-alkyl radical from ethyl to isopropyl and pinacolin hydrophobecity increases from 1 to 12 and 39, while the relative content of the chloroform extractable free OPT in brain, under conditions of uniform distribution, decreases from 11--18% to 3.2%. On incubation of the homogenate at 37 degrees C the further inhibition of the specific cholinesterase of the brain indicates the presence of an absolutely free form of OPT, the amount of which is not dependent on the degree of its hydrophobicity.
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PMID:[Forms of deposition of phosphoorganic cholinesterase inhibitors in the brain]. 123 72


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