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)

The effects of methylmercury chloride and other mercury compounds on cholinergic parameters were studied in vitro. Methylmercury chloride (MMC) and phenylmercury acetate inhibited choline acetyltransferase (ChA) with 20 microM of I50, and mercury nitrate (MN) with 100 microM of I50. All the three compounds had little effect on cholinesterase activity. MMC inhibited a high affinity choline uptake with 41 microM of Ki, as well as a low affinity choline uptake with 250 microM of Ki. MMC did not affect a spontaneous and potassium-stimulated ACh release from brain tissue slices incubated in eserinized Krebs-Ringer's solution up to the concentration of 100 microM. It was shown that the organic mercury compounds, such as methylmercury, were potent inhibitors of the choline uptake systems, as well as ChA activity.
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PMID:Effects of methylmercury chloride on various cholinergic parameters in vitro. 54 84

The plasma cholinesterase variants of 190 mentally ill individuals having lithium prophylaxis have been examined. A significantly increased frequency of the E1f gene is reported. The effect of lithium nitrate and sodium nitrate on the plasma cholinesterase variants have been shown to be identical in the concentration range 25.0-50.0 mmol/l. The usual enzyme is slightly less sensitive to inhibition by either salt than the dibucaine resistant variant. The evidence suggest that the increased frequency of the E1f gene could be a genetic marker associated with some mental illness and not the result of lithium prophylaxis.
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PMID:Plasma cholinesterase variants in patients having lithium therapy. 85 31

This systematic study describes the determination of approximately 150 pesticides (mainly insecticides and fungicides) on high-performance thin-layer chromatography (HPTLC) layers, using modern techniques for spotting and evaluation. Standardized mobile phases and reagents for visualization form the basis for the confirmation of gas-chromatographic results by HPTLC. The very high sensitivity of cholinesterase inhibition can be utilized only on plates coated with silica gel. Several other currently important pesticides can be separated on C-18 reversed phase layers and detected using silver nitrate-UV irradiation or chlorine-o-tolidine. Computer-assisted densitometric evaluation allows direct quantitative determination of the pesticides.
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PMID:[Identification and quantitative determination of currently important plant protectants by HPTLC]. 199 14

1. Frog sartorius muscles were treated with an irreversible cholinesterase inhibitor and then incubated in isotonic potassium propionate solution (isotonic KPr). Total and bound, presumably vesicular, acetylcholine (ACh) in the tissue and ACh in the medium were assayed by mass fragmentography, miniature end-plate potentials (MEPPs) were recorded and the end-plates were investigated by electron microscopy. 2. Incubation in isotonic KPr for 30 min stimulated ACh release and concomitantly decreased total and bound ACh. Nerve stimulation for 30 min by trains of impulses (0.1 s trains of 100 Hz, 1 train s-1) in normal-potassium propionate-containing solution had the same effects. 3. When the tissue was incubated in normal-K+ Ringer solution for 3 h, following chemical or electric stimulation, bound ACh recovered to about 75% of the initial value, provided that Cl- ions were present in the medium. In the presence of propionate instead of Cl- ions almost no recovery of bound ACh took place. There was also recovery of bound ACh in the presence of either NO3- or gluconate ions. In NO3- it was the same as in Cl-, but in gluconate it was less than found in Cl- -containing medium. 4. Recovery of total ACh, in contrast to bound ACh, took place even in the presence of propionate ions, showing that extracellular Cl- is not required for the synthesis of ACh. 5. In terminals recovered in normal Ringer solution, many synaptic vesicles were found, but terminals 'recovered' in propionate solution were depleted of vesicles. 6. From these and other results it is concluded that the recycling of synaptic vesicles normally requires the presence of extracellular chloride.
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PMID:The effect of anions on bound acetylcholine in frog sartorius muscle. 278 83

The multiplicity of soluble esterases in Raillietina tetragona, R. echinobothrida and R. cesticillus was studied by use of slab polyacrylamide gel electrophoresis. Five fractions of esterase activity were observed in R. tetragona, seven in R. echinobothrida and three in R. cesticillus. The various fractions of esterase activity of closely related species of Raillietina showed differential behaviour towards various chemicals. Based on the inhibitory effect of inhibitors p-CMB, EDTA, malathion, silver nitrate and eserine sulphate, the various esterases have been classified into arylesterase, carboxylesterase, acetylesterase and cholinesterase.
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PMID:A comparative study on esterases from three species of Raillietina. 654 Feb 80

The effects of hemicholinium-3 (HC-3) or 4-(l-naphthylvinyl)pyridine (4-NVP) alone and together with cholinolytics and/or cholinesterase inhibitors on brain acetylcholine (ACh) levels and survival were studied. Intracerebroventricular (ICVT) injection of 10 micrograms HC-3 280 min before euthanasia by microwave irradiation reduced rat cerebral ACh levels from 28.4 to 5.4 nmoles ACh/g wet tissue. In rats pretreated with HC-3 alone or with other pretreatment drugs prior to giving up to 2.7 LD50 of soman, iv, cerebral ACh levels increased very little, but in animals not receiving HC-3, brain ACh levels increased to 67.1 nmoles. Treatment of unpoisoned rats with 4-NVP resulted in a significant (26%) reduction in ACh. The inclusion of atropine with 4-NVP caused sign-free doses of physostigmine to produce toxic signs in rabbits and did not enhance the efficacy of carbamate pretreatment against soman. Pretreatment of rabbits with pyridostigmine and atropine methyl nitrate (AMN) failed to provide any protection against soman, but when HC-3, ICVT, was included with those drugs, the protective ratio (PR), against soman was increased excess ACh is a primary lesion in organophosphorus anticholinesterase intoxication and that the central nervous system is quite sensitive to excesses of ACh.
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PMID:Effects of inhibitors of acetylcholine synthesis on brain acetylcholine and survival in soman-intoxicated animals. 710 25

These experiments studied the effect of scopolamine on memory formation and subsequent memory recall. Different groups of rats were trained on a Y-maze brightness discrimination task 20 min after IP injection of 2 mg/kg scopolamine HBr, an anticholinergic. Retention tests were then conducted 1 day or 2, 4, or 6 weeks after training. Deficits in retention performance were observed at 1 day and 2 weeks after training but not at the longer intervals. In addition, other rats were trained in the same manner and after the same dose of scopolamine but were then retention tested 20 min after 0.5 mg/kg physostigmine salicylate, a cholinesterase inhibitor. These subjects also showed deficits at 1 day and 2 weeks but were not different from controls at the longer intervals. Amnesia was not, however, produced after treatment with scopolamine methyl nitrate or by injections of scopolamine HBr administered immediately after training. These results suggest that scopolamine, present in the central nervous system during training or within the first few moments thereafter, modifies the formation of the memory trace in such a way that memory is not available for recall for a period of weeks.
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PMID:Time dependent changes in anterograde scopolamine-induced amnesia in rats. 723 57

A method of DNA immobilization on cellulose nitrate films has been developed. Modified films of uniform and stable surface have been used to devise two variants of solid-phase enzyme immunoassays of antibodies. The co-immobilization of enzyme label (cholinesterase) and the DNA molecules makes it possible to carry out the procedure of solid-phase enzyme immunoassay without any separation of components. Thus, it takes only 15 min to diagnose an autoimmune disease (Aleutian disease of minks) with the immunoenzyme amperometric sensor, with a lower detection limit for antibodies of 0.5 x 10(-10) M. For scaled diagnosing, solid-phase enzyme immunoassay on DNA-modified films with prior separation of components and spectrophotometric registration of peroxidase activity has been developed. The time for determination was 30 min, with a lower detection limit of 7.4 x 10(-12) M.
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PMID:New variants of enzyme immunoassay of antibodies to DNA. 891 84

The influence of non-ionogenic surfactants, i.e., Tween-20, Triton X-100 and PEG-10,000, on the response of cholinesterase-based potentiometric biosensors and their sensitivity towards reversible and irreversible inhibitors were investigated. Acetyl- and butyrylcholinesterases were immobilized on nylon, cellulose nitrate films and tracing paper and were introduced into an assembly of potentiometric biosensors. The effect of surface-active compounds depends on the hydrophilic properties and porosity of the enzyme support material and the inhibition mechanism. In the range 0.002-0.3% m/v the surfactants show a reversible inhibiting effect on biosensor response. At lower concentrations (down to 10(-4)% m/v) the surfactants alter the analytical characteristics of reversible and irreversible inhibitor determination. The use of surface-active additives improves the biosensor selectivity in multi-component media.
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PMID:Influence of surface-active compounds on the response and sensitivity of cholinesterase biosensors for inhibitor determination. 900 8

Pyridostigmine bromide (PB) is a reversible cholinesterase inhibitor used routinely in the treatment of myasthenia gravis and recently by the US Army as a prophylactic agent against potential nerve gas attack in the Persian Gulf War. Pyridostigmine has been implicated as one of several possible causative factors associated with Persian Gulf illnesses. To investigate toxic interactions between PB and other drugs, male ICR mice received contralateral ip injections of either a selected adrenergic drug or caffeine, followed 15 min later by PB. Representative isobolograms plotted for each drug interaction illustrate that a beta-adrenoceptor agonist (isoproterenol), selective beta 2-adrenoceptor agonists (salbutamol, terbutaline), alpha 1- and alpha 2-adrenoceptor antagonists (yohimbine, phentolamine, prazosin), as well as the stimulant caffeine, strongly potentiate the lethal effect of PB. Agents with agonist activity at both alpha- and beta-adrenoceptors (epinephrine, norepinephrine) additively increase PB-induced lethality. The potentiation of toxicity between PB and these agents was counteracted by pretreatment with atropine and atropine methyl nitrate. An alpha 2-adrenoceptor agonist (clonidine) and beta-adrenoceptor antagonists (propranolol, nadolol, acebutolol) did not increase PB-induced lethalities. These data demonstrate a toxic synergism between PB, several commonly used classes of adrenergic agents and caffeine when exposure occurs in different combinations. Future studies into the mechanism(s) of these interactions may bring into question the usage of PB as a protective agent in combat conditions as well as delineate any possible contributions of the drug to Persian Gulf illnesses.
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PMID:Potentiation of pyridostigmine bromide toxicity in mice by selected adrenergic agents and caffeine. 925 Nov 70


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