Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats fed a vitamin E-deficient diet for 7--8 weeks postweaning showed no change in brain weight or the activity in brain of various enzymes involved in neurotransmitter synthesis and metabolism. Body and muscle weights were markedly reduced. Muscle choline acetyltransferase and acetylcholinesterase activities were significantly elevated on a protein basis, but the total amount of choline acetyltransferase/muscle was essentially normal and total acetylcholinesterase activity was slightly reduced. Total carnitine acetyltransferase and butyrylcholinesterase activities were markedly decreased. The results are quite different from those found in hereditary murine muscular dystrophy and suggest a myogenic etiology for the vitamin E-deficiency-induced condition.
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PMID:Cholinergic systems in muscle and brain in vitamin E-deficient rats. 74 Jan 30

Tests were set up on 73 Citellus fulvus to study the influence exerted by different doses of vitamin E (4 and 8 mg) introduced per os on the activity of the total cholinesterase in various divisions of the central nervous system and also the part played by the hormonal and seasonal factors in this effect. Each test series lasted 30 days (in spring, summer and autumn). The cholinesterase activity was determined after Vensen and Segonzak (1968). The results of the experiments revealed some characteristic trends in the change of the cholinesterase activity occurring under the effect of vitamin E that depended upon a number of factors, such as: the dose of tocopherol, the sex of the animal, time of the year, the brain division under study and the seasonal dynamics of the initial activity. It is shown that in the brain sectors where a material difference existed in the cholinesterase activity between the control males and females it vanished under the effect of tocopherol. On the other hand, in the brain sectors where no such difference existed, it appeared under the effect of tocopherol. The regular character of changes in the cholinesterase activity of the brain and spinal cord produced by different doses of vitamin E suggest the possibility of the brain cholinesterase activity disorders to a play a part in the development of neuro-muscular pathology in cases of the E vitamin deficiency.
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PMID:[Role of hormonal and seasonal factors in the effect of vitamin E on cholinesterase activity in the nervous system]. 121 Jan 81

Serum pancreatic secretory trypsin inhibitor (PSTI) was measured by radioimmunoassay in 5 patients with malabsorption syndrome. The serum level of PSTI was elevated to 123.8 +/- 25.8 ng/ml (Mean +/- SE) in patients with malabsorption syndrome, which was significantly higher than the 16.6 +/- 0.7 ng/ml level seen in 116 healthy control subjects. Serum PSTI levels in 5 patients with malabsorption syndrome showed inverse correlations with serum levels of cholesterol, cholinesterase and amylase, and not with serum levels of vitamin E, carotene, apoprotein A-IV, albumin, nor with immunoreactive elastase 1, respectively. These results suggest that elevated levels of serum PSTI represent a state of malnutrition due to impaired intestinal absorption.
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PMID:Elevated levels of serum pancreatic secretory trypsin inhibitor (PSTI) in patients with malabsorption syndrome. 243 66

The aim of the study was explaining of the combined action of low doses of sodium nitrite and fenitrothion on certain biochemical parameters in rat blood. The experiment was carried out on male adult Wistar rats. The animals were divided into 4 experimental groups: group I receiving 10 mg/kg of sodium nitrite, group II--2.5 mg/kg of fenitrothion (Owadofos), group III received a mixture of both these doses, group IV served as control. The preparations were given intragastrically through a tube for 90 days. After that time 2,3-diphosphoglyceric acid, vitamin E, SH groups in protein and non-protein compounds in erythrocytes, methaemoglobin and basic haematological parameters, as well as the activity of glucose-6-phosphate dehydrogenase, superoxide dismutase and choline esterase were determined. Sodium nitrite decreased the activity of glucose-6-phosphate dehydrogenase and vitamin E, with an increase of the activity of superoxide dismutase and protein SH groups and methaemoglobin level. fenitrothion caused similar changes as sodium nitrite and decreased the activity of choline esterase and the level of 2,3-diphosphoglyceric acid. No synergistic action of these compounds was noted. The level of non-protein SH groups was decreased. It seems that determination of the level of non-protein sulphohydryl groups may be one of the indicators of poisoning with sodium nitrite combined with phenitrotione.
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PMID:[Effect of the combined action of sodium nitrite and fenitrothion on certain biochemical parameters in rat blood]. 260 57

Sumithion is the most active cholinesterase inhibitor. The cholinesterase inhibiting action of the organophosphates (OPs) is better compensated by vitamin E in normal animals, but by vitamin A in vitamin A-deficient animals. The lipid peroxidation (LP) is enhanced by the antioxidant vitamins in the liver of normal rats; although they decrease it in the liver of vitamin A-deficient animals, in no case do they prevent the LP-enhancing effect of the OPs examined. The OPs examined inhibit protein synthesis in the liver of vitamin A-deficient animals.
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PMID:Some further data on the effects of two organophosphate pesticides on the oxidative metabolism in the liver. 666 50

Rats were maintained on a vitamin E free diet containing 20% safflower oil for a period of 12 weeks at two dietary protein levels, 20% and 10% casein. Enhanced in vitro tissue lipid peroxidation and lysis of erythrocytes were noticed at both the protein levels. A reduction in body mass and tissue weights were observed in both the protein groups but more so at 20% protein level. Feeding of retinyl palmitate (100 000 IU/100 g body weight) for 4 consecutive days to -E rats inhibited liver and kidney in vitro lipid peroxidation. Ascorbic acid (150 mg/100 g body weight) given orally for 5 days to -E rats inhibited liver brain and kidney in vitro peroxidation. Lysis of erythrocytes from -E rats was further increased by dosing with both the vitamins "A" and "C", the latter being more effective. The stromal enzymes acetyl choline esterase and ATPase were lowered, following the hemolysis profile of the erythrocytes from the different groups. Glutathione content of erythrocytes were unaffected except in -E +C group. In all groups the higher protein level (20%) produced greater lysis as compared to 10% level. It is concluded that 20% protein is more injurious in vitamin E deficiency simultaneously made hypervitaminosis A or C.
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PMID:Effect of dietary protein and hypervitaminosis A or C on tissue peroxidation and erythrocyte lysis of vitamin E deficiency. 716 Sep 64

In order to study nutritional assessment and nutritional support therapy for elderly patients, we conducted energy supply therapy on 15 elderly (aged over 75) patients disabled with diseases such as cerebrovascular disease, pneumonia and heart failure. After recovery from acute phase, they were divided into 3 groups, and assigned to 3 different energy supply methods for 2 weeks: Six (3 males, 3 females) could take hospital diet, but only could absorb about 50% of the energy, amounting only 1,000 to 1,400 kcal/day. Additional 246 kcal was given by peripheral parental nutrition (PPN). Five (2 males, 3 females) were unable to take nutrition orally. Therefore, they were given high caloric nutrients by total parental nutrition (TPN), giving (1,222 kcal daily for a week), then 1,666 kcal for another week. Four (1 male, 3 females) also could not take meals orally, and had to be nourished by enteral nutrition (EN) with a nutrient preparation of 1,120 kcal for one week, then with 1,600 kcal for another week. In all 3 groups, the indices of rapid turnover proteins (pre-albumin, retinol binding protein and transferrin), choline esterase and vitamin A significantly elevated after 2 weeks of therapy, though the increase of pre-albumin and RBP in TPN group was slightly below the significant level. The increase in rapid turnover proteins and choline esterase was greater in the order of EN, TPN and PPN. Vitamin C, on the other hand, decreased significantly with treatment in all the groups, while vitamin E remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Nutritional assessment and nutritional support therapy in elderly patients]. 836 Oct 76

Alzheimer's disease is a progressive neurodegenerative disorder primarily manifesting as a loss of memory. Senile plaques and neurofibrillary tangles are the major histopathological alteration in the brain of Alzheimer's disease patients. A considerable deficiency of cholinergic neurons is a consistent finding in Alzheimer's disease. Therefore, many therapeutic strategies to augment cerebral concentration of acetylcholine such as cholinergic precursors, cholinergic receptor agonists, cholinesterase inhibitors and acetylcholine release modulators have been evaluated in Alzheimer's disease. Although cholinesterase inhibitors such as tacrine and galanthamine offer modest clinical benefits, other cholinergic agents have proved to be of limited therapeutic value. Efforts to enhance monoaminergic neurotransmission have also been largely disappointing. Therefore, emphasis is not being put on the use of combination of two class of drugs. Moreover, use of therapeutic agents based on the putative pathogenic etiology of the disease such as excitotoxicity, amyloidosis, aluminium accumulation, inflammatory mechanisms and free radical production is being evaluated. Desferrioxamine, non-steroidal anti-inflammatory drugs, prednisone, dapsone, vitamin E and idebenone are some such agents that are currently under investigation for the preventive or palliative effect in Alzheimer's disease. Neurotrophic factors such as nerve growth factor, brain derived neurotrophic factor and epidermal growth factor have shown promising results in animal studies. However, novel methods for delivering these molecules into the brain required to be developed before launching their clinical trials in man.
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PMID:Pharmacological basis of drug therapy of Alzheimer's disease. 956 41

Genetic vulnerability factors are becoming more important in AD, yet only a minority of cases are familial, and of these only a portion are genetically determined. Because, early in the course, neurodegeneration is occurring in vulnerable cholinergically innervated regions and not throughout the brain as a whole, AD may be conceptualized as a corticolimbic system neurodegenerative disorder involving the entorhinal cortex, hippocampus, and amygdala. This conceptualization has obvious implications for the development of therapies since future interventions may be designed to prevent or slow neurodegeneration or improve clinical signs by modulating risk factors, beta-amyloid deposition, and phosphorylation of tau proteins; inhibiting inflammatory or oxidative processes; or enhancing cholinergic function in various ways. The recently reported effects of antioxidants, including vitamin E and selegiline, in prolonging time to institutionalization, death, or significant worsening, is one example of the feasibility of this approach, as are the observations that anti-inflammatory use may reduce AD risk and that long-term cholinesterase inhibitor use may delay nursing home placement. At present, approaches that are focused on neurotransmitter systems may prove more immediately accessible targets for therapeutic intervention.
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PMID:Cholinergic deficiency in Alzheimer's disease. Pathogenic model. 958 Dec 21

Alzheimer's disease (AD) is characterized by a gradual decline in 3 domains: cognition, behavior, and function. Ideally, an effective treatment would target all 3 types of impairment. However, available treatments for AD diminish only certain symptoms and cannot halt the dementing process. Most pharmacologic agents currently available or in development target a specific symptom cluster (e.g., cognitive loss), and are based on the known neurobiology of the disease (e.g., neurotransmitter deficit) or hypothesized antidementia approaches (e.g., anti-inflammation, antioxidation). Two currently available cholinesterase inhibitors improve memory and other aspects of cognition during short-term treatment. Additional cholinergic agents will soon become available. Other promising agents under study for cognitive enhancement or protection include vitamin E, selegiline, estrogen, and nonsteroidal anti-inflammatory drugs. As scientists uncover the basic pathogenetic mechanisms of AD, additional treatments will likely emerge. Therapies for behaviors associated with dementia (e.g., depression, agitation, anxiety) are sometimes effective. Choices of specific medications, including antidepressants, antipsychotics, and anxiolytics, depend on specific side-effect profiles. Psychotherapies aimed at enhancing cognition are ineffective for dementia but nonpharmacologic interventions may minimize depression and agitation and may improve quality of life.
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PMID:Treatment of Alzheimer's disease: current approaches and promising developments. 961 51


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