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)

Brain from 47 avian and 17 mammalian species and the liver from 19 avian and 7 mammalian species has been examined for acetyl cholinesterase and nitrophenyl acetate esterase activities. Plasma from 27 avian and 7 mammalian species has been examined for acetyl cholinesterase, cholinesterase, nitrophenyl acetate esterase, glutamate, oxaloacetate transaminase, glutamate pyruvate transaminase, glutamate dehydrogenase, sorbitol dehydrogenase and lactate dehydrogenase activities. The studies have revealed that variations in enzyme activities occur between species but that there are discernible trends within families. The results indicate that comprehensive control enzyme data is necessary in order to assess the effects of exposure to agricultural chemicals in wildlife.
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PMID:Control enzyme levels in the plasma, brain and liver from wild birds and mammals in Britain. 613 42

The intralaminar distributions of transmitter and nontransmitter enzyme activities and amino acid levels were determined in the midtemporal cortices from normal individuals and established cases of Alzheimer's disease. In the normal, choline acetyltransferase (CAT) and acetylcholinesterase (AChE) activities were relatively high in the outer cortical layers, particularly, for CAT, in the two granular layers (II and IV). Both activities were reduced in Alzheimer's disease at all, although generally most extensively in the outer and middle layers of the grey matter whereas activities were near normal in the white matter. Further, the enzyme distribution patterns of these cholinergic activities were also disrupted in Alzheimer's disease and the activity of CAT throughout the cortex was generally reduced to that found in the white matter. No such differences in distribution were found for two other enzymes, pseudocholinesterase and lactate dehydrogenase. Assessment of the gamma-aminobutyric acid (GABA) system in the normal revealed a much more extensive intralaminar variation in the enzyme, glutamate decarboxylase, compared with the level of GABA itself. In contrast with the cholinergic enzymes, neither the levels nor intralaminar patterns of GABA were altered in Alzheimer's disease. From an analysis of free amino acids at the different cortical levels, the cortical pattern of glutamic acid in the normal was different from that for GABA, aspartic acid, or nontransmitter amino acids such as alanine. Neither of the putative amino acids, glutamate or aspartate, was altered in Alzheimer's disease. These findings demonstrate the relatively selective nature of microchemical changes occurring in the cortex in Alzheimer's disease and suggest that a functional abnormality in cholinergic input to the outer neocortical layers (I-IV) with predominantly receptive and associative functions may be an important feature of the disease.
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PMID:Intralaminar neurochemical distributions in human midtemporal cortex: comparison between Alzheimer's disease and the normal. 614 24

Activities of 12 enzymes (amylase, lipase, cholinesterase, nonspecific carboxyl esterase, lactate dehydrogenase (LDH), alkaline phosphatase, glutamate-oxalacetate transaminase (GOT), glutamate-pyruvate transaminase (GPT), gamma-glutamyl transferase (gamma-GT), leucine aminopeptidase (LAP), malate dehydrogenase (MDH) and peroxidase) were determined in the perienteric fluid and homogenate of Ascaris suum. With the exception of amylase, all activities were higher in the homogenate than in the perienteric fluid. The enzyme activities in the perienteric fluid were then compared with those in the human serum. Comparable activities were demonstrated for LDH, LAP, lipase and alkaline phosphatase, markedly higher activities in perienteric fluid were demonstrated for MDH, GOT, GPT and amylase, and much lower for cholinesterase. No gamma-GT activity was detected in the perienteric fluid.
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PMID:Activities of some enzymes in the perienteric fluid of Ascaris suum. 619 63

The activity was determined of sorbitol-dehydrogenase (SDH), cholinesterase (CE), leucine-aminopeptidase (LAP), acid phosphatase (AP), and glutamate-dehydrogenase (GDH) in blood plasma of lambs irradiated with 200, 320, and 450 Rad. Results showed that with the mild form of acute radiation sickness (treatment with 200 Rad) the activity of the blood enzymes did not change. With the severe (320 Rad) and the peracute (450 Rad) forms of the disease within the first 24 hours the activity of SDH and CE rose 3 to 5 times, and that of GDH and AP--twice within a period of 1 to 3 days following irradiation. In the case of a threefold increased activity of SDH and CE within 15 to 24 hours of treatment the diseased animals died. Parallel hematologic investigations revealed that well manifested leukopenia with these two forms of the sickness took place after the 24th hour. Activity determination of the investigated plasma enzymes within the first 15-24 hours following irradiation could be used as an adjunct test to the study of the hematologic indices for the early diagnosis of the severe and peracute forms of irradiation sickness as well as for the exit of the disease.
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PMID:[Enzyme activity in the blood plasma of lambs with acute radiation sickness]. 666 25

The activity of serum enzymes, such as, creatine kinase (CK), pyruvate kinase (PK), aldolase (ALD), lactate dehydrogenase (LDH), sorbitol dehydrogenase (SbDH), malate dehydrogenase (MDH), glutamate-aspartate aminotransferase (AST), glutamate-alanine aminotransferase (ALT), myokinase (MK), glucosephosphate isomerase (GPI), alkaline phosphatase (AlkP), pseudocholinesterase (PsCHE) isocitrate dehydrogenase and gamma-glutamyltranspeptidase (gamma-GTP), was determined in 256 patients with progressing myodystrophy (PMD) (Duchenne's form in 125, Becker's form in 14, pelvicohumeral form in 36, humeroscapulofacial form in 19, ocular form in 10, other rare forms in 34, and nonidentified forms in 13 patients). In the control group (64 men, 56 women and 50 children), the activity of the enzymes was found to depend on the patients' sex and age. With regard to both parameters, i. e. the degree of the enzyme activity rise and the frequency of the pathological values the most informative were CK, then PK and ALD, and then all the other enzymes. Of all the PMD forms the enzymatic activity appeared to be the highest in patients with the pseudohypertrophic malignant form. By determining the activity of five enzymes (CK, ALD, LDH, AST and ALT) and taking into consideration the patient's age, the onset and the duration of the disease one can distinguish between sick and healthy subjects, as well as between various forms of PMD.
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PMID:[Serum enzyme dynamics in progressive muscular dystrophies]. 703 17

Studied was the dynamics of the changes taking place in the activity of a number of enzymes in the blood plasma (glutamate oxalacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), lactate dehydrogenase (LDH), alkaline phosphatase (AP), aldolase (ALD), creatine phosphokinase (CPK), guanase, and cholinesterase (CE). The calculation of the correlation coefficients and the regression lines revealed that GOT, GPT, LDH, ALD, and guanase raised their activity following treatment of the test animals up to a higher extent and at a higher rate. Lower rate changes were those in the activity of AP, leucinaminopeptidase, and CE. No changes whatever were found in the activity of CPK. On the basis of these results the diagnostic value is determined of both the individual enzymes and the enzyme constellation as a whole.
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PMID:[Changes in serum enzyme activity after the tetrachloromethane treatment of guinea pigs]. 716 46

Following sequential intraocular transplantations of areas containing NE cell bodies (locus coeruleus or superior cervical ganglion) and of NE fiber target areas (hippocampus), both pieces mature in a manner analogous to that observed for individual transplants. NE-containing nerve fibers, derived from either LC or SCG transplants, can be seen to invade the hippocampal formation. When LC is used, the invading fibers markedly hyperinnervate the hippocampus while SCG-derived fiber densities approximate those seen with innervation from the adrenergic ground plexus of the iris. Electrophysiological recordings from neurons in the LC reveal an atropine-sensitive excitatory response to illumination, suggesting innervation of the LC by cholinergic nerve fibers from the iris. This is supported by the fact that dense cholinesterase-positive staining can be found in the LC piece. Application of an epileptogenic agent, such as penicillin, results in a marked excitation of neurons in the LC without inducing epileptiform activity in the hippocampus. In contrast, single hippocampal grafts seize readily after penicillin. Local application of the inhibitory agent GABA into the LC allows penicillin-induced epileptiform activity to generate in the hippocampus, suggesting that functional inhibitory innervation develops between NE fibers derived from LC and pyramidal neurons in the hippocampus. Supporting this, subsequent excitation of LC neurons by iontophoresis of glutamate terminates the hippocampal seizure. Prior administration of reserpine (2.5 mg/kg) disrupts the inhibitory influence of LC innervation on the hippocampal EEG following penicillin. After reserpine, the hippocampal portions of double grafts behave like single hippocampal transplants. It is concluded that sequential transplantations of cell body and target regions of the CNS to the anterior chamber of the eye creates a functional, yet isolated, neuronal pathway which can be utilized to study the development of neuronal connections.
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PMID:Conditions for adrenergic hyperinnervation in hippocampus: II. Electrophysiological evidence from intraocular double grafts. 739 24

We investigated the effect of Probucol in preventing fatty liver in monosodium-L-glutamate (MSG) treated obese mice and control mice fed a high fat diet. MSG mice became significantly obese 9 weeks after birth with higher levels of serum blood glucose, total cholesterol, HDL-cholesterol, GPT, and cholinesterase, and had greater triglyceride contents in their livers relative to control mice. Morphologically, MSG obese mice also had a marked fatty liver. Administration of Probucol mixed with the high fat diet for 2 weeks significantly decreased the serum levels of total cholesterol and HDL-cholesterol, and liver triglyceride contents in both MSG and control mice. Morphologically, the livers were less fatty after Probucol treatment. These results suggest that Probucol prevents the development of fatty liver, and in addition reduces hypercholesterolemia.
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PMID:Probucol prevents the progression of fatty liver in MSG obese mice. 755 75

The role of muscarinic transmission in the activation of cholinergic neurons ascending to the neocortex from the nucleus basalis magnocellularis (NBM) was investigated. The release of acetylcholine (ACh) from the neocortex of urethane-anesthetized rats was measured using microdialysis, and a second microdialysis probe was inserted into the NBM to apply drugs to the NBM and to measure ACh release from this area. Cholinergic neurons in the NBM were activated synaptically by stimulating the pedunculopontine tegmentum (PPT). Systemically administered scopolamine greatly increased the PPT stimulation evoked cortical release of ACh when the cortical probe was perfused with the cholinesterase inhibitor neostigmine. PPT stimulation evoked release was also high when the cortical probe was perfused with atropine plus neostigmine, but it was not increased any further by systemic scopolamine or by scopolamine perfused through the NBM probe. When neostigmine was perfused through the NBM probe, PPT stimulation evoked cortical ACh release was halved, but the release was restored when the NBM solution also contained scopolamine. The resting release of ACh within the NBM was increased by local neostigmine, but evoked release in the NBM was large only in the presence of local scopolamine. Both of these increases were blocked by perfusion of the NBM with tetrodotoxin. These results suggest that muscarinic transmission within the NBM does not control the activation of cholinergic neurons under physiological conditions, when the diffusion of ACh is limited by its hydrolysis. However, when ACh is allowed to diffuse to a wider area, it may inhibit the release of an excitatory transmitter, probably glutamate, via presynaptic muscarinic receptors.
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PMID:Pharmacological but not physiological modulation of cortical acetylcholine release by cholinergic mechanisms in the nucleus basalis magnocellularis. 783 77

The effects of a subacute intoxication with diisopropyl fluorophosphate (DPF) on total muscarinic acetylcholine receptor sites (mAChRs) and M-1 AChRs were evaluated in the cerebral cortex of young (2-4 months) and aged (22-24 months) Fischer 344 rats. Since M-1 AChRs are coupled to the metabolism of phosphoinositides, carbachol-induced accumulation of inositol phosphates (IP) and its inhibition by glutamate and NMDA was also measured in the cortical slices. DFP treatment caused about 75% inhibition of cholinesterase and 35% down-regulation of mAChRs (measured as [3H]quinuclidinyl benzylate binding) in both young and aged rats. The down-regulation of M-1-ACHRs (measured as [3H]pirenzepine binding) was more pronounced in aged (30%) than in young (17%) DFP-treated rats. There was a significant increase in carbachol-induced IP accumulation in aged, with respect to young, untreated rats. DFP treatment caused a considerable decrease in such IP accumulation in aged but not in young rats. Glutamate and NMDA antagonized carbachol-induced IP accumulation in untreated young and aged rats (and the effects of NMDA were reversed by carboxy-piperazinyl-propyl phosphonic acid). In DFP-treated rats such antagonism was somewhat less pronounced. The data appear of interest in relation to the use of anticholinesterase compounds in the therapy of senile dementia of Alzheimer's type. They suggest that beside their primary action (increasing brain ACh levels) such compounds also act on post-receptor mechanisms and on the interactions between cholinergic and glutamatergic neurotransmitter systems.
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PMID:Carbachol-induced accumulation of inositol phosphates and its modulation by excitatory amino acids in cortical slices of young and aged rats with down-regulation of muscarinic M-1 receptors. 789 49


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