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)

Dibucaine, fluoride and RO2-0683 inhibition studies were used to determine the serum cholinesterase (pseudocholinesterase) phenotypes at the E1 locus in a sample of 130 subject with Down's syndrome and fifty-three mentally retarded control subjects. No example of the Ef1 and Es1 allele was detected in either group, nor were any of the genotype E1a E1a detected. The gene frequency of E1a for the control group (0.0189) resembles closely that reported in the literature for normal European populations but in the Down's group was significantly lower (0.0038). The means and distribution of the dibucaine, fluoride and RO numbers in both groups were similar to those reported in normal subjects. The presence of the additional C5 cholinesterase type heterozygous for a variant cholinesterase on the E2 locus) was detected after starch gel electrophoresis, and the frequency was found to be raised in both groups. Several possible environmental factors (age, sex, maternal age, etc.) were investigated to account for this finding but with no success.
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PMID:Serum cholinesterase (pseudocholinesterase) in Down's syndrome: 1. Phenotype frequencies at the E1 and E2 loci. 14 99

Four-hundred and ninety individuals belonging to the Vysya caste from Andhra Pradesh were screened for pseudocholinesterase variants at the E1 and E2 locus. A high incidence of the silent allele (gene frequency=0.1112) was recorded with homozygotes exceeding 2% of the population. Dibucaine- and fluoride-resistant alleles were found in a heterozygous form with the usual alleles in four individuals each. No C5+ variant at the E2 locus was found.
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PMID:High incidence of the silent allele at cholinesterase locus I in Vysyas of Andhra Pradesh (S. India). 52 75

The kinetic properties of cholinesterase (ChE) present in plasma were compared with those of purified human ChE using the substrates succinyldithiocholine (SDTCh), acetylthiocholine (AcTCh) and butyrylthiocholine (BuTCh). SDTCh was hydrolysed at two sites; a site with a low Km (Km1 11.4 +/- 3.3 microM) with a Vmax of 0.06 mumol/min/ml and a site with a high Km (Km2 132.4 +/- 14.8 microM) and a Vmax of 0.107 mumol/min/ml. The Km2 site was absent in the sample of purified ChE. The related thiocholine esters, AcTCh and BuTCh were hydrolysed at two sites by both plasma and purified ChE. This indicated that the Km2 site which hydrolysed SDTCh was not ChE. The identity of this component in plasma remains unknown but it was shown not to be albumin. The anticholinesterase agents soman and pyridostigmine were used to demonstrate the direct relationship between inhibition of plasma ChE and hydrolysis of SDTCh at the low concentrations present clinically (20 microM). Whereas high concentrations of SDTCh (200 micron) could be partly hydrolysed by an enzyme present in plasma which is insensitive to ChE inhibitors. In a limited study on the plasma from two "atypical" individuals (Dibucaine number less than 20) all three substrates were hydrolysed at a single site with a higher Km than the Km2 site present in normal plasma. The clinical implications of these results are discussed.
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PMID:The hydrolysis of succinyldithiocholine and related thiocholine esters by human plasma and purified cholinesterase. 395 97

In 1973, a Cholinesterase Research Unit was established in Denmark (DCRU). The primary aim was to provide a central service for determining genotypes and activity of plasma cholinesterase (BChE) in patients showing abnormal response after succinylcholine. The purpose of the present study was, on the basis of 20 years experience with this Unit, to establish accurate reference intervals for BChE activity and inhibition values for the different genotypes of BChE. Also we wanted to evaluate the influence of age and sex on the BChE activity in genotypically normal patients. Plasma cholinesterase activity was measured using benzoylcholine as substrate. The genetic variations of the enzyme were identified using differential inhibitors, i.e.: Dibucaine, Sodium Fluoride, Succinylcholine, Urea and Ro-2-0683. We investigated 6,688 patients. The reference values for the 13 genotypes represented agree with previous findings. In genotypically normal patients, no age or sex differences were found in BChE activity in children below the age of 10 years. From the age of 10 years the activity decreased significantly in both males and females, the activity in females being significantly lower than in males. In females the activity was lowest in the age group 30-40 years, returning to prepuberty level at about 60 years of age. In males the activity decreased slightly up to 50-60 years of age. Hereafter the activity was stable or tended to increase slightly. Most genotypes could be recognized using the results of the different inhibition studies. We found the inhibitors Dibucaine, Sodium fluoride, Urea and Ro-2-0683 most helpful, whereas succinylcholine was of less value.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Identification of human plasma cholinesterase variants in 6,688 individuals using biochemical analysis. 779 80

Children with cerebral palsy may be resistant to paralysis induced by nondepolarizing neuromuscular blocking drugs. Potency of a bolus of succinylcholine in children with cerebral palsy has not been studied previously. Therefore, we measured the response of the adductor pollicis to succinylcholine in children with cerebral palsy anesthetized with propofol and nitrous oxide. Forty children between the ages of 2 and 10.2 yr with spastic quadriplegic cerebral palsy were randomly assigned to receive 100, 175, 250, or 375 micrograms/kg of succinylcholine during anesthesia with propofol and nitrous oxide. The ulnar nerve was stimulated with a train-of-four supramaximal stimulus every 10 s and the compound electromyogram of the adductor pollicis recorded by a Datex NMT monitor. Plasma cholinesterase activity was measured in all patients with three different substrates (propionylthiocholine, benzoylcholine, and succinylcholine). Dibucaine number was also determined using inhibition of benzoylcholine degradation. ED50 of succinylcholine was 146.8 micrograms/kg with 95% confidence intervals of 111.4-193.7 micrograms/kg. ED95 of succinylcholine was 360.5 micrograms with 95% confidence intervals of 273.3-475.5 micrograms/kg. We conclude that children with cerebral palsy are slightly sensitive to succinylcholine, but probably not sufficiently to be clinically important.
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PMID:Dose response of succinylcholine at the adductor pollicis of children with cerebral palsy during propofol and nitrous oxide anesthesia. 776 64

Cocaine was the first drug to be used as a local anaesthetic. It was introduced into medicine in 1884 by Koller. Other drugs soon followed, for example, ethyl chloride spray, tropocaine, eugenol (oil of cloves) and Nupercaine. A wide range of uses for local anaesthetics soon developed and the term 'regional anaesthesia' was first used by Cushing in 1901 to describe pain relief by nerve blockade. Local anaesthetic drugs are water soluble salts of lipid soluble alkaloids. Each molecule is composed of an aromatic portion, intermediate chain and an amide portion. The portions are joined by either amide or ester linkages. Ester-linked drugs are hydrolysed in the plasma by plasma cholinesterase and their half-life varies from one to eight minutes. Amide-linked drugs are degraded by oxidative dealkylation in the liver. The half-life of these drugs varies from 1.5 to more than three hours. The addition of a vasoconstrictor, such as adrenaline, will prolong the duration of action of both the amide- and ester-linked drugs. Degradation of the amide-linked drugs depends on factors such as hepatic blood flow and liver conditions, such as cirrhosis, and congestive cardiac failure. Anaphylactic reactions are more common with ester-linked drugs than amide-linked drugs. The drugs are usually available for injection as hydrochlorides in a salt solution with small amounts of fungicides or preservatives added to give stability.
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PMID:Local anaesthesia in the operating theatre. 799 96

The interaction between suxamethonium and atracurium was investigated during anaesthesia with thiopentone, fentanyl, enflurane and nitrous oxide in oxygen with controlled ventilation. Electromyographic data (Relaxograph, Datex) from 30 patients in three, equal groups were analyzed. Group 1 received atracurium 0.23 mg kg-1. Group 2 received suxamethonium 1 mg kg-1 followed by atracurium 0.23 mg kg-1 when the EMG had recovered to 20% of its control value: a sequence intended to be representative of clinical practice. Group 3 received suxamethonium 1 mg kg-1 and atracurium 0.23 mg kg-1 in rapid succession. Plasma cholinesterase concentrations and Dibucaine and fluoride numbers were within normal limits in all patients. Suxamethonium given for endotracheal intubation (group 2) neither potentiated the subsequent atracurium blockade nor delayed spontaneous recovery. When suxamethonium and atracurium were given in rapid succession (group 3), the duration of suxamethonium blockade was reduced considerably but the recovery from the atracurium component of the blockade was not significantly different from groups 1 and 2. Although the intubation score at 60s was no worse in group 3, the duration of profound blockade suitable for intubation was reduced to such an extent that the simultaneous administration of suxamethonium and atracurium cannot be recommended in clinical practice when there is a requirement for rapid endotracheal intubation.
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PMID:Suxamethonium and atracurium: sequential and simultaneous administration. 843 69

People with genetic variants of cholinesterase (ChE) have been reported to have prolonged apnea with the use of myorelaxant succinylcholine. For the silent type variant ChE, two cases of mutation have been reported. In one case, the exon 2 of ChE gene was disrupted by a 342 bp insertion of Alu element. In the other case, a frame shift mutation was identified at Gly-117 (GGT-->GGAG) to create a stop codon at nucleotide 384. Dibucaine resistant ChE was examined and found to have a point mutation at nucleotide 209 (A-->G) that converted Asp-70 to Gly, and consequently reduced the affinity of ChE for choline esters. In addition, another two types of a point mutation reducing ChE activity were reported on K variant (Ala-539-->Thr) and a case of (Gly-365-->Arg) in a patient with liver cirrhosis.
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PMID:[Gene analysis of human cholinesterase variants]. 846 62

A toxic shock syndrome occurred after a femoral nail removal requiring revision surgery. After administration of suxamethonium (1 mg.kg-1), an apnoea prolonged over 45 minutes was observed. The trachea was extubated 105 minutes after suxamethonium administration. For the nail removal, two days before, the anaesthetic had been given by the same anaesthesiologist, with a similar protocol. Apnoea extended over 20 minutes. The day of the revision surgery, plasma cholinesterase activity was 410 UI.L-1 and reached 910 UI.L-1, 9 months later. Dibucaine number was 20 and fluorure number 17. The apnoea was in relation with a genetic plasma cholinesterase deficiency increased by the toxic shock syndrome. Shock and hepatic insufficiency were suspected to contribute to the decrease in plasma cholinesterase. Suxamethonium should be avoided in case of toxic shock syndrome.
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PMID:[Prolonged apnea after suxamethonium administration during staphylococcal toxic shock]. 873 39

The purpose of these experiments was to determine the reversibility of alpha-chaconine and alpha-solanine inhibition of human plasma butyrylcholinesterase (BuChE). For the substrate alpha-naphthylacetate, optimal assay conditions were 0.50 M sodium phosphate buffer and a substrate concentration of 3-5 x 10(-4) M. Dibucaine (1 x 10(-5) M) indicated the usual phenotype for all subjects; alpha-chaconine and alpha-solanine at 2.88 x 10(-6) M inhibited BuChE about 70 and 50%, respectively. One- and 24-hr incubations at 1 x 10(-5) M with alpha-chaconine, alpha-solanine, paraoxon, eserine, and ethanol yielded reversible inhibition with dilution except for paraoxon. Twenty-four-hour dialyses of incubations showed no inhibition except for paraoxon. PAGE enzyme activity gels of 1- and 24-hr incubations also showed no inhibition except for paraoxon. alpha-Chaconine and alpha-solanine are reversible inhibitors of human butyrylcholinesterase. At estimated tissue levels, alpha-chaconine, alpha-solanine, and solanidine inhibited BuChE 10-86%. In assays which combined alpha-chaconine, alpha-solanine, and solanidine, inhibition of BuChE was less than additive. No inhibition of albumin alpha-naphthylacetate esterase (an arylesterase) was noted with any inhibitor. The importance of these data to adverse toxicological effects of potato alkaloids is discussed.
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PMID:Inhibition of human plasma and serum butyrylcholinesterase (EC 3.1.1.8) by alpha-chaconine and alpha-solanine. 892 46


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