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:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric acid secretion, pepsin concentration in gastric juice and acetylcholinesterase and histidine decarboxylase activities in gastric mucosa of rats treated with dichlorvos (DDVP) were investigated. The increase of HCl secretion, the decrease of acetylcholinesterase activity and enhanced activity of histidine decarboxylase were observed. It is suggested that a higher gastric acid secretion is secondary to histamine production in gastric mucosa, induced by acetylcholine yields gastrin yields histidine decarboxylase mechanism.
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PMID:Dichlorvos intoxication and gastric secretion. 11 26

The effects of various agents that could be expected to perturb enzyme structure in a non-specific and reversible manner (alcohols, dimethylsulfoxide, dimethylformamide, dinitrobenzene, urea and guanidine - HCl) have been determined on reaction of acetylcholinesterase (acetylcholine hydrolase, EC 3.1.1.7) with a substrate, p-nitrophenyl acetate, and two irreversible inhibitors, diisopropylphosphorofluoridate and methanesulfonyl fluoride. In all three of these reactions an acyl group (acetyl, phosphoryl or sulfonyl respectively) bonds covalently with the active center of the enzyme. As expected, the reactions of p-nitrophenyl acetate and diisopropylphosphorofluoridate were severely retarded by most of these agents. By contrast, reaction of methanesulfonyl fluoride was usually depressed to a far smaller degree, and in two cases was faster. These findings are of interest in connection with: (1) differing requirements for the integrity of tha active center in catalysis with various substrate analogs, and (2) the mechanism by which cationic substrate analogs accelerate reaction of the enzyme with methanesulfonyl fluoride.
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PMID:Differential effects of denaturing agents on acetylcholinesterase: insensitivity of the reaction of methanesulfonyl fluoride compared to diisopropylphosphorofluoridate and p-nitrophenyl acetate. 17 35

Investigations were carried out on 32 male guinea pigs 2 to 3 months of age. The STH (produced by BIOMED, Warszawa, Poland) was administered intramuscularly every other day, in 7 injections of 20 Evans's units (E. U.) or 100 E. U./kg body weight each. Thyroid gland sections were stained with heamatoxylin and eosin and with the Azan method. The C cells were detected with the modified silver method of Grimelius and with the HCl-toluidine blue and HCl-lead haemotoxylin techniques. Moreover, reactions were performed for succinate and alpha-glycerophosphate dehydrogenases and also for non-specific esterases and non-specific acetylcholinesterase. STH evoked proliferation of the C cells, changed their morphology and activity pattern of the enzymes present therein, probably testifying to an enhanced secretory activity of these cells.
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PMID:Morphology and histochemistry of the "C" cells of guinea pig thyroid gland after treatment with STH preparation: Part II--young animals. 86 41

Coumaphos (8 or 15 mg/kg of body weight), triflupromazine HCl (1.1 mg/kg of body weight), or isotonic saline solution were given to 8 groups of sheep (5 per group) fed a low-or normal-dietary protein ration. One set of clinical signs, mortality rate, mean survival time, necropsy lesions, and plasma and erythrocyte cholinesterase (ChE) activity were monitored for each group. Observations suggested potentiation effect between the administered compounds. Inhibition of ChE activity was enhanced in groups given both drugs. Feeding of low-dietary protein ration adversely affected the development of clinical signs, mortality rate, mean survival time, and ChE activity. Recovery of ChE activity of triflupromazine HCl-treated animals was faster than in their respective controls, and sheep fed normal-dietary protein ration had faster ChE recovery than those fed the low-dietary protein ration. Inhibition of erythrocyte ChE found was a better index of organophosphorus toxicosis than that of plasma ChE.
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PMID:Influence of dietary protein on the effect of coumaphos and triflupromazine interaction in sheep. 98 39

The present experiments were performed to investigate the potential role of central adrenergic neurons in regulating occurrence of yawning in rats. Intraperitoneal injection of tacrine (THA) or 9-amino-2,3,5,6,7,8-hexahydro-1H-cyclopenta(b)-quinoline monohydrate HCl (NIK-247), cholinesterase inhibitors, induced yawning, which was markedly increased by pretreatment with the beta-adrenoceptor antagonist, pindolol. The yawning evoked by tacrine or NIK-247 given alone or in combination with pindolol was inhibited by pretreatment with scopolamine but not by mecamylamine or spiperone. Treatment with tacrine or NIK-247 increased acetylcholine content of the striatum, but this effect was not enhanced by pindolol, which per se did not affect basal acetylcholine content. Moreover, pretreatment with the central adrenaline synthesis inhibitors, (+-)-2,3-dichloro-alpha-methylbenzylamine HCl (LY-78335) and 2-cyclooctyl-2-hydroxyethylamine HCl (UK-1187A), increased tacrine-induced yawning. Subcutaneous injection of talipexole (B-HT 920), a dopamine D2 receptor agonist, evoked yawning, which was also increased by pindolol, LY-78335, and UK-1187A. These receptors antagonists and synthesis inhibitors per se did not cause yawning responses. The results suggest that the beta-adrenoceptor blockade and the inhibition of adrenaline synthesis facilitate the occurrence of yawning induced by cholinergic and dopaminergic agonists, and thus the central adrenergic neuronal systems may be implicated in the regulation of yawning responses.
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PMID:Role of adrenergic neuronal activity in the yawning induced by tacrine and NIK-247 in rats. 136 95

Male Sprague-Dawley rats when administered sc a sublethal dose of organophosphorus cholinesterase inhibitors such as the nerve agents, soman (100 micrograms/kg, sc), sarin (110 micrograms/kg, sc), tabun (200 micrograms/kg, sc), or VX (12 micrograms/kg, sc), developed seizures and severe muscle fasciculations within 15-20 min, lasting for 4-6 hr. Marked inhibition of acetylcholinesterase (AChE) and necrotic lesions in skeletal muscles such as soleus, extensor digitorum longus, and diaphragm were evident between 1-24 hr following injection. Pretreatment with memantine HCl (MEM, 18 mg/kg, sc) together with atropine sulfate (ATS, 16 mg/kg, sc), 60 min and 15 min, respectively, prior to nerve agents attenuated AChE inhibition, prevented myonecrosis, and muscle fasciculations as well as other signs of cholinergic toxicity. Pretreatment combining d-tubocurarine (d-TC, 0.075 mg/kg, sc) and ATS (16 mg/kg, sc) prevented the myonecrosis and fasciculation without protecting AChE against inhibition by these nerve agents. Neither MEM, d-TC, nor ATS in the concentration given interfered with the normal behavior of the rats. The role of d-TC and ATS interaction with presynaptic receptors regulating ACh release and MEM's role in modulating neural hyperactivity as protective mechanisms are discussed.
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PMID:Potential of memantine, D-tubocurarine, and atropine in preventing acute toxic myopathy induced by organophosphate nerve agents: soman, sarin, tabun and VX. 147 66

Basal and high K(+)-stimulated efflux of endogenous ACh from slices of brain was measured to evaluate the cholinomimetic effect of 9-amino-2,3,5,6,7,8-hexahydro-1H-cyclopenta[b] quinoline monohydrate HCl (NIK-247) on the central nervous system. The drug NIK-247 dose-dependently accelerated the efflux of ACh from slices of striatum. The maximum increase produced by 1.0 x 10(-4) M of NIK-247 was 329% in basal and 1332% in 30 mM K(+)-stimulated efflux. This drug was nearly twice as potent as THA (9-amino-1,2,3,4-tetrahydroacridine HCl) but had the same potency as physostigmine, in enhancing basal efflux, although there was no significant difference between the efficacy of these drugs in enhancing the K(+)-stimulated efflux. Both basal and 50 mM K(+)-stimulated efflux of ACh were increased by NIK-247, not only from the striatum but also from slices of frontal cortex and hippocampus. The activity was more effective in the striatum than in other tissues, and more effective on K(+)-stimulated than on basal efflux, regardless of the region of the brain. These effects of NIK-247 may be a result mainly of its inhibition of cholinesterase and its other biological characteristics, such as K+ channel blockade, capable of modulating release of ACh, may not be of major importance.
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PMID:Evaluation of a cholinomimetic drug, 9-amino-2,3,5,6,7,8-hexahydro-1H-cyclopenta [b] quinoline (NIK-247), as an enhancer of endogenous efflux of acetylcholine from brain slices. 154 4

We report Raman spectra of various cholinesterases: lytic tetrameric forms (G4) obtained by tryptic digestion of asymmetric acetylcholinesterase (AChE) from Torpedo californica and Electrophorus electricus, a PI-PLC-treated dimeric form (G2) of AChE from T marmorata, and the soluble tetrameric form (G4) of butyrylcholinesterase (BuChE) from human plasma. The contribution of different types of secondary structure was estimated by analyzing the amide I band, using the method of Williams. The spectra of cholinesterases in 10 mM Tris-HCl (pH 7.0) indicate the presence of both alpha-helices (about 50%) and beta-sheets (about 25%), together with 15% turns and 10% undefined structures. In 20 mM phosphate buffer (pH 7.0), the spectra indicated a smaller contribution of alpha-helical structure (about 35%) and an increased beta-sheet content (from 25 to 35%). This shows that the ionic milieu profoundly affects either the conformation of the protein (AChE activity is known to be sensitive to ionic strength), or the evaluation of secondary structure, or both. In addition, we analyzed vibrations corresponding to the side chains of aromatic and aliphatic amino acids. In particular, the analyses of the tyrosine doublet (830-850 cm-1) and of the tryptophan vibration at 880 cm-1 indicated that these residues are predominantly 'exposed' on the surface of the molecules.
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PMID:A comparative Raman spectroscopic study of cholinesterases. 179 30

Octadecyl-bonded silica, commonly used for reverse-phase high-pressure liquid chromatography, was modified using surfactants bearing ionizable groups and the modified packing used in ion-exchange chromatography of proteins. The surfactants 2-(n-hexadecylheptaethoxy)acetic acid, 1-(n-hexadecyloctaethoxy)ethylene-diamine, and N-(n-hexadecyloctaethoxy)pyridinium were adsorbed onto test columns packed with octadecyl-bonded silica particles. The proteins lysozyme, bovine serum albumin, trypsin, horse serum cholinesterase, and bovine liver carboxylesterase were used to study the ion-exchange characteristics of the modified packings. The retention order of the proteins on the surfactant-modified stationary phases were as predicted by the isoelectric point of each protein. In addition, the interaction of enzymes with the packings did not result in significant loss of enzymatic activity. Surfactant removal was possible with the use of organic solvents and this allowed the octadecyl-bonded surface to be used again in the reverse-phase mode. During the course of the experiments, no degradation in the packing's performance was observed due to loss of adsorbed surfactant, even after over 85,000 column volumes of sodium chloride and Tris-HCl buffers were circulated through the column.
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PMID:Reversible conversion of octadecyl-bonded silica to ion-exchange surfaces for protein separations. 254 Jun 75

Male Sprague-Dawley rats administered with a sublethal acute dose of carbofuran (1.5 mg/kg, sc) developed the observable toxic signs of anticholinesterase nature within 5-7 min. The toxic signs with increasing propensity to maximal severity including tremors, generalized muscle fasciculations, and convulsions were evident during 15 min to 1 h and lasted for 2 h. Thereafter, signs were seen up to 3 h with reduced intensity. By the end of 3.5 h toxic signs were completely subsided. Maximal acetylcholinesterase (AChE) inactivation occurred at 1 h in discrete brain regions (cortex, stem, striatum, and hippocampus) and hemidiaphragm muscle when most severe signs of toxicity were also evident. A single sc dose of memantine HCl (MEM, 18 mg/kg) and atropine sulfate (ATS, 16 mg/kg) 60 and 15 min, respectively, prior to carbofuran administration completely prevented the expected gross toxic signs and significantly (p less than .01) attenuated the carbofuran-induced inhibition of AChE activity. When given therapeutically, this combined treatment completely reversed the clinical evidence of carbofuran toxicity within 15 min and also markedly reduced AChE inactivation. Memantine or atropine when given alone was less effective compared to their combined administration. The results of this study suggested that, in addition to cholinolytic effects of atropine, memantine may prevent and antagonize the acute toxicity of carbofuran by (a) protection of AChE activity and its rapid reactivation from inhibition and (b) rapid elimination of carbofuran.
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PMID:Prevention and antagonism of acute carbofuran intoxication by memantine and atropine. 277 46


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