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)

Following ingestion of [N-14CH3]cocaine (10 mg, 2.3 muCi) by 2 healthy subjects, breath, saliva, serum, and urine samples were collected serially. Labeled CO2 production was monitored as a measure of N-demethylation of cocaine. The cumulative excretion of 14CO2 in 5 hr was 2.4% and 6.2% of the administered dose with half-lives of 2.3 and 1.4 hr, respectively. The greater N-demethylation was found in a subject with lower plasma cholinesterase activity. Radioactivity excreted in 0 to 28 hr urine reached 65% to 75% of the dose. Ecgonine methyl ester, a product of cocaine hydrolysis by plasma cholinesterase, was identified as a major metabolite in the urine of both subjects and accounted for 32% to 49% of the urinary metabolites.
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PMID:Metabolism of cocaine in man. 63 29

Toxicological findings in 1,345 fatal general aviation accidents from fiscal year 1968 through 1974 are summarized. Methods used in examination of specimens for alcohol, drugs, carbon monoxide, cyanide, and cholinesterase activity are described. Blood ethanol levels in excess of 0.050% were found in 117 of the 1,345 pilots (8.7%). Drugs were found in 16 cases (1.2%). These and other toxicological findings indicate that in more than 40% of the cases, information worthy of consideration in developing the human-factors history of an accident or the cause of death from survivable crashes was obtained.
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PMID:Toxicological findings in fatal civil aviation accidents, fiscal years 1968-1974. 116 35

In the group of 107 patients poisoned by carbon monoxide (18 patients), ethanol (10), barbiturates (18), glutehimide (10), tranquilizers (19), organic solvents (10),salicylates (3), organochlorines (8), and sulfonamides (5)--the activities of 8 serum enzymes were determined for 6 consecutive days of treatment, the enzymes being as follows: aminotransferases, cholinesterase, alkaline phosphatase, lactate, alpha-hydroxybutyrate, glutamate, and sorbitol dehydrogenase. The antipyrine half-life was also assayed. It has been shown that the poisonings by particular groups of poisons do not bring about characteristic changes in the activity of enzymes that might be of any diagnostic value. The intensity of changes was connected withe depth and duration of toxic coma. Most frequently an increase ensued in the activity of AspAt and AlAt in the third 24-hrs period, and an increase in the activity of SDH in the first 24-hrs period. In the group under examination there were 26 drug abusers in whom a shortening of the antipyrine half-life was discovered. They were less responsive to toxic doses of drugs, and the enzymatic changes in them were less distinct. No changes in the activity of tested enzymes, which are characteristic of toxicomania, were found.
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PMID:The usefulness of the enzymatic tests in acute poisonings. 124 89

The action of the cholinesterase reactivator isonitrosine on gas homeostasis was studied in experiments on intact dogs. It has been found that oxygen consumption and CO2 release by tissues were enhanced within the period from 15 min to 6 days following isonitrosine administration. Simultaneously, oxygen return by the blood was improved. Such action of isonitrosine was unrelated to its effect on the cholinesterase activity of red blood cells.
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PMID:[The effect of isonitrozine on gas homeostasis]. 145 58

14C-carbofuran penetrated readily into seeds of Vicia faba and the rate of penetration was found to be dose dependent. The percentage of bound residues was generally low and did not exceed 3% of the applied dose. When the bound residues were fed to rats 46% of the radioactivity was eliminated via CO2 and urine, while tissues contained 25%. Carbofuran phenol and 3-hydroxy carbofuran represented the main metabolites in the urine. These data indicate that bean-bound carbofuran residues are highly bioavailable to rats. Feeding mice with bound carbofuran residues for 90 days led to inhibition of erythrocyte cholinesterase activity after 30 days (35-40%) while the plasma enzyme remained unaffected. Serum transaminases and blood urea nitrogen were significantly elevated, indicating injury to hepatic and renal structures. The results strongly suggest that the bound residues can induce adverse biological effects in mice.
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PMID:Bioavailability to rats and toxicity in mice of carbofuran residues bound to faba beans. 152 62

The novel combination of supercritical fluid extraction (SFE) with an enzyme assay system has been used to screen meat products to detect the presence of pesticides. Analytes are collected in water by expanding supercritical carbon dioxide to atmospheric pressure through a restrictor and into an aqueous phase. The solution is then tested for the presence of pesticide residues by enzyme assay. Two experimental approaches have been used. Alachlor-fortified lard and bovine liver were monitored by static SFE coupled with an enzyme immunoassay. SFE of carbofuran-fortified frankfurters was coupled with an enzyme assay based on cholinesterase inhibition. A major benefit of the SFE/enzyme assay technique over conventional screening techniques is that the analyst is not exposed to organic solvents.
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PMID:Supercritical fluid extraction/enzyme assay: a novel technique to screen for pesticide residues in meat products. 175 8

Impaired memory function is one of the most frequent and disabling symptoms observed after brain injury. A number of studies have examined the efficacy of using cholinergic agonists, such as physostigmine, in treating memory impairment resulting from various neurologic conditions. Few studies, however, have either combined the drug treatment with a memory training programme or monitored serum cholinesterase levels to increase the likelihood of achieving a therapeutic dose of the medication. The current study addresses both of these issues. Two single-case studies are reported in this investigation. In each case, a double-blind, placebo-controlled, single-subject, A-B-A design was used with A representing the base-line phases, B constituting the memory training combined with medication phase and A representing the return to base-line condition. Both patients sustained anoxia as a result of carbon monoxide poisoning. In the first case, a clinically significant improvement was seen in the patient's performance of both standardized and non-standardized measures of memory function as a result of the combined treatment regimen. No significant changes, however, were seen in the patient's performance on measures of attention and concentration, cognitive flexibility or motor speed. These findings were then replicated with the second anoxic patient. The results from this study point out the potential benefit of combining cholinergic agonists with specific memory training strategies in improving memory function after brain injury.
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PMID:Memory training combined with the use of oral physostigmine. 345 79

Clinical and pulmonary function changes induced by intravenous dichlorvos (2,2-dichlorvinyldimethyl phosphate) (DDVP) toxicosis, and reversibility of these changes after atropine treatment were investigated in six Friesian calves one to three months old. From one minute after dosage, all animals showed severe respiratory distress, excitation, weakness, muscle fasciculation and cholinesterase inhibition. Decrease in dynamic lung compliance and arterial oxygen tension and increase in total pulmonary resistance, viscous work of breathing and alveolar arterial oxygen gradient were highly significant (P less than 0.01). On the other hand, body secretions, heart rate, respiratory rate, tidal volume and arterial carbon dioxide tension were not significantly affected by DDVP injection. Atropine promptly and completely reversed these changes, except for muscle fasciculations, central depression and cholinesterase inhibition which disappeared progressively within 24 hours.
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PMID:Pulmonary function changes induced by experimental dichlorvos toxicosis in calves. 373 27

In rabbits anesthetized with 70% N2O-30% O2, the rate of efflux of acetylcholine (ACh) from the cerebral cortex doubled during hypercapnia (increase of end-tidal CO2 from 4 to 8%), and during mild nociceptive stimulation of the tail. Under 0.7% halothane anesthesia, the control rate of ACh efflux was lower than that under N2O; the rate rose 2-fold during hypercapnia and 4-fold during tail stimulation. In the absence of systemic atropinization, increase in ACh efflux was correlated with a shift in EEG from high- to low-voltage ('activated'); after systemic atropinization EEG remained in the high-voltage state, but the changes in ACh efflux with hypercapnia and stimulation were not affected. Following transection of the midbrain, ACh efflux was markedly depressed and did not change during hypercapnia. Taken in context with the previously known facts that the cerebral hyperemia of hypercapnia is potentiated by cholinesterase inhibition and attenuated by atropine or decerebration, the present results support the concept of a cholinergic regulation of the cerebral vasculature.
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PMID:Cortical acetylcholine efflux with hypercapnia and nociceptive stimulation. 402 96

The effects of infusions of ouabain on chemoreceptor activity recorded from the peripheral end of a sectioned carotid sinus nerve were studied in cats anaesthetized with pentobarbitone. Ouabain caused a marked increase in chemoreceptor discharge followed by a decline in discharge to frequencies near or below the pre-ouabain level; during the latter period further administration of ouabain had no effect. Infusion of ouabain during hypoxia further increased the chemoreceptor discharge, but this effect was short-lasting. On intracarotid administration ouabain was less effective in cats with the ganglioglomerular (sympathetic) nerves cut, whereas on intravenous administration no significant difference was observed. Following intravenous administration of ouabain the chemoreceptor peak discharge occurred with dose levels similar to those needed to cause cardiac arrhythmias, but following intracarotid administration the chemoreceptor discharge peaked at doses about 40% of those causing arrhythmias. During ouabain-induced excitation the stimulatory action of NaCN, CO2-equilibrated Locke solution and acetylcholine was potentiated, as was the chemo-inhibition induced by dopamine. During the post-excitatory period the responses evoked by these substances were reduced or abolished. Neither mecamylamine, a nicotinic antagonist, nor physostigmine, an anti-cholinesterase, affected the response of the carotid chemoreceptors to ouabain. The major finding of this study was that ouabain initially 'sensitizes' the carotid body chemoreceptors and then 'desensitizes' them. The most likely mechanism responsible for these effects is the well established Na+--K+-ATPase-inhibiting property of ouabain.
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PMID:Effects of ouabain on carotid body chemoreceptor activity in the cat. 687 75


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