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)

This study was designed to assess the effects of a moderate increase in dietary sulphur (S) in cattle. Twelve animals were initially fed a basal concentrate (S = 0.2%) and then divided into two groups; one fed basal and the other high S (S = 0.75%) concentrates. Health, body weight gains, and activities of erythrocyte enzymes-glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), glucose-6-phosphate dehydrogenase (G6PD), acetylcholinesterase (AChE), plasma- asparate aminotransferase (AST), and whole blood concentrations of selenium (Se) were monitored at various stages of the study. Marked increases in the activities of GSH-Px, SOD and G6PD from the pretrial values were observed upon initial feeding of basal concentrate diet. Sex related differences were not evident in enzyme activities and Se concentrations of the blood. A high linear correlation (r = 0.92) between averages of GSH-Px activity and Se concentration of blood was observed in both sexes. Increasing the amount of S in the concentrate diet (from 0.2 to 0.75%) did not produce any statistically significant change in enzyme activities and Se concentrations, body weight gains, and health of the cattle during the 85 days feeding period. The results indicate that a moderate increase in the dietary S would not impair Se and copper status or cause related disorders in cattle.
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PMID:Effects of high dietary sulphur on enzyme activities, selenium concentrations and body weights of cattle. 360 49

1. Oxygen consumption in vitro and persistence in the general circulation of rabbit erythrocytes treated with the cholinesterase inhibitor paraoxon were determined.2. Paraoxon in vitro reduced oxygen consumption below a measureable level within 2 hours. By contrast, the metabolic inhibitor N-ethylmaleimide (NEM) produced complete inhibition within 15 minutes.3. Erythrocytes from rabbits orally dosed with parathion also exhibited marked depression of oxygen consumption.4. Glutathione (GSH) restored oxygen uptake to pretreatment levels within 15 min in erythrocytes previously inhibited with NEM or paraoxon.5. Erythrocytes treated with NEM were rapidly removed from the general circulation while paraoxon treated cells were removed at a rate comparable to untreated cells.
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PMID:Effect of paraoxon on erythrocyte metabolism as measured by oxygen uptake in vitro. 509 Nov 62

The activity of 18 red blood cell (RBC) enzymes and reduced glutathione (GSH) content were measured in 70 normal subjects, in 50 heterozygous beta-thalassaemia carriers and in 50 non-thalassaemic patients with haemolytic anaemia and high reticulocyte counts. In addition, pyrimidine 5'nucleotidase (P5N) activity was also determined in 34 patients with hypochromic, microcytic, iron deficiency anaemia. beta-Thalassaemia trait was associated with an increase in almost all of the enzyme activities, except for 2,3-bisphosphoglycerate synthetase (BPGS) and glutathione reductase (GR) which were normal and for acetylcholinesterase (AChE) and P5N which were slightly and markedly decreased respectively. The increases in enzyme activities were similar to those observed in patients with non-thalassaemic reticulocytosis except for glyceraldehydephosphate dehydrogenase (GAPD), phosphoglyceratekinase (PGK), pyruvate kinase (PK), glutathione peroxidase (GPX) and adenylate kinase (AK) which were higher than in non-thalassaemic group of patients with increased number of reticulocytes. No correlation was found between the severity of P5N deficiency and the intensity of basophilic stippling which was present in 46 of 50 thalassaemic carriers here studied. In addition, GSH content and UV absorption spectra of deproteinized thalassaemic RBC extracts were also found to be normal. The present findings provide further information on the metabolic status of RBC in beta-thalassaemia trait and suggest a possible molecular explanation for the frequently observed basophilic stippling in this disease.
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PMID:Pyrimidine 5'nucleotidase and several other red cell enzyme activities in beta-thalassaemia trait. 632 Aug 62

The effect of adrenalectomy (Adx), SKF 525-A, phenobarbital (PB), and diethyl maleate (DEM) on the acute toxicity of fenitrothion was investigated in male rats by assessing the degree of plasma cholinesterase activity. PB, 60 mg/kg/day for 3 days, exerted no protective effect on the toxicity of fenitrothion (100 mg/kg, p.o.) given 24 h after the last injection. In adrenalectomized and SKF 525-A-pretreated rats, the toxicity of fenitrothion was lower than that of the controls. Fenitrothion toxicity was increased by administration of DEM (1 ml/kg), which depletes hepatic glutathione (GSH) levels. In vitro, the rates of fenitrothion decomposition and fenitrooxon formation by microsomes were markedly affected by PB, SKF 525-A and Adx. The decomposition of fenitrooxon by the microsomal fraction and GSH-dependent decomposition of fenitrooxon by the soluble fraction were not affected by PB, SKF 525-A and Adx pretreatment. The GSH-dependent decomposition of fenitrothion and fenitrooxon was increased by addition of GSH to the incubation mixture. The present results indicate that the GSH-dependent metabolic pathway plays an important role in the detoxication of fenitrothion.
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PMID:Effect of adrenalectomy, pretreatment with SKF 525-A, phenobarbital and diethyl maleate on the acute toxicity of fenitrothion in male rats. 686 Jan 45

A daily dose of 1 mg/kg and 10 mg/kg of methylmercury chloride (MMC) was injected to separate sets of rats for 2 days, 7 days, and 15 days. Low and high doses of four MMC antagonists, namely N-acetyl-DL-homocysteine thiolactone (NAHT), glutathione (GSH), D-penicillamine (DPA), and sodium selenite (SEL) were injected intramuscularly (i.m.) to MMC-treated animals after an interval of half an hour. The animals were sacrificed on the 3rd, 8th, and 16th day, respectively. An additional group of rats was treated with MMC for 7 days; thereafter, it was kept free of toxic exposure for 7 days and sacrificed on the 15th day. The brain was dissected and separated into olfactory bulbs, cerebral hemispheres, cerebellum, and medulla oblongata. Each part of the central nervous system (CNS) was studied separately. We found a dose- and duration-related acetylcholinesterase (AChE) inhibition in all CNS areas. The use of antagonists showed different effects in different CNS areas, but no appreciable recovery of AChE activity could be obtained with the doses used.
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PMID:Acetylcholinesterase fluctuations in central nervous system of rat during methylmercury intoxication and chelation therapy. 818 68

The glutathione (GSH) S-transferases are believed to have dual functions as hepatic detoxifying enzymes and intrahepatic binding proteins. Little is known about their alterations in human liver diseases. Therefore, we have studied the relationship between the enzyme activity and rose bengal (RB) binding in hepatic cytosol and plasma indocyanine green (ICG) kinetics in patients with various liver diseases. The enzyme activity was measured in samples of hepatic cytosol obtained from 52 patients. In addition, the content of cationic and neutral transferases was estimated in 17 biopsy samples by densitometry of Coomassie blue stained sodium dodecyl sulphate polyacrylamide gel electrophoretograms. RB binding studies also were performed on cytosol samples. ICG kinetic parameters were determined using the two-compartment open model in 17 patients who were given the dye (0.5 mg kg-1) intravenously. Correlations between the enzyme activity and liver function tests, content of the enzyme, RB binding and ICG kinetic parameters were evaluated. The following results were obtained. (1) The enzyme activities were high in alcoholic liver disease, fatty liver and Gilbert's syndrome, and low in cirrhosis. (2) The enzyme activities were positively correlated with serum cholinesterase activity, serum albumin level and hepaplastin test, and negatively correlated with ICG retention rate at 15 min. (3) The enzyme activity, its content and RB binding affinity of the cytosol were positively correlated with each other. (4) The enzyme activity was positively correlated with hepatic ICG distribution volume. These results are consistent with the role of the GSH S-transferases as ligandins in intracellular storage of dyes.
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PMID:Relationship between content of hepatic glutathione S-transferases and the kinetics of indocyanine green elimination in various liver diseases. 825 11

Blood and urine samples were taken from 34 persons occupationally exposed to lead and from 56 non-exposed control persons and blood lead and haemoglobin concentrations, red blood cell count, erythrocyte glutathione peroxidase (GSH-peroxidase) and acetylcholinesterase (AChE), and urinary delta-aminolevulinic acid were determined. Blood lead concentrations of the lead-exposed subjects were within the range of generally accepted as safe for occupationally-exposed adults in many countries (i.e. below 50 micrograms Pb/dl blood). Yet, significant dose-dependent elevations were found in erythrocyte GSH-peroxidase and urinary delta-aminolevulinic acid. The urinary delta-aminolevulinic acid concentration of lead-exposed smokers was significantly elevated over that of lead-exposed non-smokers. Smoking did not effect the urinary delta-aminolevulinic acid concentration of control persons. In addition, a statistically significantly lower red blood cell count was observed in the lead-exposed group. Our results indicate that the above described safety standard for blood lead concentrations in occupationally exposed adults, although generally accepted, needs revision.
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PMID:Effects of exposure to lead on selected biochemical and haematological variables. 868 81

We examined a chloride (Cl-)-dependent K+ transport (K(+)-Cl- cotransport) and regulatory volume decrease in dog red blood cells with high K+, low Na+, and high glutathione (GSH) content (HK/HG) due to the presence of an Na(+)-K+ pump. The HK/HG cells were separated according to their density, and the age-marker enzyme activities, such as glucose-6-phosphate dehydrogenase and cholinesterase, were determined. Unexpectedly, we found that young cells were heavier (more dense) and smaller in size compared with the old cells, which were lighter (less dense) and larger. The K(+)-Cl- cotransport was nearly 10-fold higher in the most dense cells, representing a 12% fraction of the total population compared with the lightest cohort. Although K(+)-Cl- cotransport in both the dense and the light cells was activated by N-ethylmaleimide, swelling and depletion of cellular divalent cations and the activation of the transport in the dense cells was greater. Both the dense and light cells regulated their volume when they were isosmotically swollen. Therefore, the lower activity of K(+)-Cl- cotransport might not explain the relative large volume in old HK/HG cells. The concentration of GSH and glutamate was higher in the light cells. Thus the higher the GSH and glutamate concentration, the greater the cell volume and the lower the K(+)-Cl- cotransport.
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PMID:K(+)-Cl- cotransport and volume regulation in the light and the dense fraction of high-K+ dog red blood cells. 932 78

Pyrethroid pesticides are used preferably over organochlorines and organophosphates due to their high effectiveness, low toxicity to non-target organisms and easy biodegradibility. However, it is possible that during the pyrethroid metabolism, there is generation of reactive oxygen species (ROS) and pyrethroids may produce oxidative stress in intoxicated rats. The present study was therefore, undertaken to determine pyrethroid-induced lipid peroxidation (LPO) and to show whether pyrethroid intoxication alters the antioxidant system in erythrocytes. A single dose of cypermethrin and/or fenvalerate (0.001% LD50) was administered orally to rats and the animals were sacrificed at 0, 1, 3, 7 and 14 days of treatment. The results showed that lipid peroxidation (LPO) in erythrocytes increased within 3 days of pyrethroid treatment. The increased oxidative stress resulted in an increase in the activity of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT). The increase in reduced glutathione (GSH) content in erythrocytes may probably be an initial adaptive response to increased oxidative stress in pyrethroid intoxicated rats. Erythrocytes and serum acetylcholinesterase (AChE) activity was measured in pyrethroid-induced oxidative stress as it may mimic inhibition in target tissues such as muscle and brain. The inhibition in erythrocytes and serum AChE activity was partially relieved over a period of time indicating recovery from pyrethroid intoxication. The increase in erythrocyte LPO correlated with the inhibition in erythrocyte AChE activity and so erythrocyte AChE can be a marker enzyme in pyrethroid toxicity. The results show oxidative stress and alteration in antioxidant enzymes in erythrocytes of pyrethroid intoxicated rats.
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PMID:Lipid peroxidative damage on pyrethroid exposure and alterations in antioxidant status in rat erythrocytes: a possible involvement of reactive oxygen species. 1035 40

The effects of huperzine A (HupA), a novel acetylcholinesterase inhibitor, on Abeta(25-35)-induced cell lesion, level of lipid peroxidation, antioxidant enzyme activities were investigated in the rat pheochromocytoma line PC12. Following a 48 h exposure of the cells to Abeta(25-35), a significant reduction in cell survival and activities of glutathione peroxidase (GSH-Px) and catalase (CAT), as well as increased production of malondialdehyde (MDA) and superoxide dismutase (SOD) were observed. Preincubation of the cells with HupA prior to Abeta(25-35) exposure elevated the cell survival and GSH-Px and CAT activities, and decreased the level of MDA and SOD activity. The results indicate that HupA has protective effects against Abeta-induced cell toxicity, which might be beneficial for the treatment of Alzheimer's disease.
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PMID:Protective effects of huperzine A on beta-amyloid(25-35) induced oxidative injury in rat pheochromocytoma cells. 1083 8


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