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PubMedDate not supplied

Detection of organophosphorous pesticides with an immobilized cholinesterase electrode.

A simple and reliable method based on cholinesterase inhibition is proposed to detect organophosphate pesticides in water. The potentiometric method to measure enzymatic activity was applied to an immobilized cholinesterase film coupled directly to a flat glass pH electrode. Under controlled laboratory conditions, it was possible to correlate inhibition of cholinesterase activity with intramembranal pH shifts induced by substrate hydrolysis. Measurements can be performed with such an enzyme electrode system in real time by monitoring the inhibition process, or after incubation of the enzymatic film. Technical grade compounds of methylparathion, azinphosethyl , and mevinphos were used as examples, and detected from ppm to several ppb after oxidative treatment. The sensitivity of the enzyme sensor depends on the inhibitory power of the pesticide molecules, and therefore determines additional toxicity information unavailable from other physico-chemical methods. This type of sensor could be used for screening purposes in the detection of pesticides in water pollution control and is intended to be complementary to existing analytical methods.

Cholinesterases↗
PubMed1989

Protecting agricultural applicators from over-exposure to cholinesterase-inhibiting pesticides: perspectives from the California programme.

California's requirement for medical supervision of applicators regularly handling Toxicity Category I and II organophosphate and carbamate cholinesterase-inhibiting pesticides is examined from a policy perspective by the California Department of Health Services (CDHS). Changes to increase the effectiveness of medical supervision and solutions to a number of practical implementation problems are discussed, including the pesticides which should be monitored, the use of individual cholinesterase baselines, the enzymes to be measured, and the frequency of cholinesterase testing.

Agricultural Workers' Diseases↗
PubMed2000

The recovery of plasma cholinesterase and erythrocyte acetylcholinesterase activity in workers after over-exposure to dichlorvos.

Plasma cholinesterase and erythrocyte acetylcholinesterase activities have a long history of use in monitoring both workers at risk of organophosphorus pesticide (OP) exposure and in investigating accidental exposures to OPs. On account of wide inter-individual variation, the establishment of unexposed, baseline enzyme activities is necessary for accurate interpretation. This paper describes the rate of recovery of the two enzymes' activity after substantial over-exposure of eight subjects to the OP dichlorvos. Plasma cholinesterase activity, immediately after exposure, was substantially more inhibited than erythrocyte acetylcholinesterase activity. The plasma enzyme activity showed an exponential pattern of recovery with a half-life of around 12 days, so recovery was essentially complete after about 50 days. This reported half-life of recovery is consistent with the reported de novo synthesis rate of plasma cholinesterase. The mean recovery of erythrocyte acetylcholinesterase activity appeared linear over time, attaining unexposed activity after about 82 days, which is somewhat shorter than the life-span of erythrocytes. These indicate the sort of time period, after an OP incident, before a valid unexposed level can be established in an individual; and substantiate the guidance given in the Health & Safety Executive's document MS17 on a minimum period of 60 days without exposure in order to establish pre-exposure baseline levels.

Acetylcholinesterase↗
PubMed1981

Succinylcholine neuromuscular blockade in subjects heterozygous for abnormal plasma cholinesterase.

The relationship between plasma cholinesterase genotype and duration and type of succinylcholine neuromuscular blockade was studied in 43 anesthetized patients heterozygous for abnormal plasma cholinesterase using train-of-four nerve stimulation. Twenty-eight patients were heterozygous for the usual and the atypical gene (E1uE1a), eight were heterozygous for the usual and the silent gene (E1uE1s), three were heterozygous for the usual and the fluoride-resistant gene (E1uE1f), three were heterozygous for the fluoride-resistant and the atypical gene (E1fE1a), and one was heterozygous for the fluoride-resistant and the silent gene (E1fE1s). Mean time to 90 per cent recovery of twitch height in patients with genotypes E1uE1a, E1uE1s, and E1uE1f (14.6, 12.4, and 12.0 min, respectively) was significantly prolonged compared to patients with normal cholinesterase genotype (9.3 min). No significant difference was found between the three groups of patients with one abnormal gene (E1uE1a, E1uE1s, and E1uE1f). In 13 (46 per cent) of the 28 patients with genotype E1uE1a the twitch height did not return to control for more than 15 min after the administration of succinylcholine and in three patients (10.7 per cent) for more than 20 min after succinylcholine. The four patients with abnormal genes on both chromosomes (E1fE1a and E1fE1s) all showed significantly prolonged paralysis following the administration of succinylcholine (mean time to 90 per cent twitch recovery was 30 min). Patients heterozygous for the usual and one of the abnormal genes (E1uE1a, E1uE1s, and E1uE1f) had typically depolarizing blocks following the administration of succinylcholine, 1 mg/kg. Patients with abnormal genes on both chromosomes (E1fE1a and E1fE1s), however, all showed desensitization type of neuromuscular blockade (phase II block).

Adolescent↗
PubMed1995

Nonclassical roles of cholinesterases in the embryonic brain and possible links to Alzheimer disease.

Evidence about nonclassic functions of acetyl- (AChE) and butyryl-cholinesterase (BChE) during embryonic development of vertebrate brains is compared with evidence of their expression in Alzheimer disease (AD). Before axons extend in the early neural tube, BChE expression shortly precedes the expression of AChE. BChE is associated with neuronal and glial cell proliferation, and it may also regulate AChE. AChE is suggested to guide and stabilize growing axons. Pathologically, cholinesterase expression in AD shows some resemblance to that in the embryo. These findings are inconsistent with the "cholinergic hypothesis." Rather, it is suggested that cholinesterases in AD function nonclassically as in the embryo, possibly as part of a "neoembryonic" restorative program. These views may open new strategies for pharmacology and therapy for AD.

Aged↗
PubMedDate not supplied

Inhibition of human cholinesterases by drugs used to treat Alzheimer disease.

Current approaches to the treatment of cognitive and behavioral symptoms of Alzheimer disease emphasize the use of cholinesterase inhibitors. The kinetic effects of the cholinesterase inhibitors donepezil, galantamine, metrifonate, physostigmine, rivastigmine, and tetrahydroaminoacridine were examined with respect to their action on the esterase and aryl acylamidase activities of human acetylcholinesterase (AChE) and human butyrylcholinesterase (BuChE). Each of these drugs inhibited both AChE and BuChE, but to different degrees. Inhibition of BuChE by these compounds was approximately the same, or better, when acetylthiocholine, the analog of the neurotransmitter acetylcholine, was used as the substrate, instead of butyrylthiocholine. In addition, for these drugs, the inhibition of aryl acylamidase activity paralleled that observed for inhibition of esterase activity of AChE and BuChE. Given that drugs that are currently in use for the treatment of Alzheimer disease inhibit both AChE and BuChE, the development of drugs targeted toward the exclusive inhibition of one or the other cholinesterase may be important for understanding the relative importance of inhibition of BuChE and AChE in the treatment of this disease.

Acetylcholinesterase↗
PubMed1986

Plasma cholinesterase changes during the puerperium.

Changes in plasma cholinesterase activity during the puerperium were studied in 16 women who received epidural analgesia for labour followed by vaginal delivery, and in five women who underwent elective Caesarean section under epidural analgesia. A consistent fall in cholinesterase activity was demonstrated during the first 2 to 3 days post partum, followed by a rise to approximately normal nonpregnant values by the end of the puerperium. An additional patient who manifested prolonged paralysis following an emergency Caesarean section under general anaesthesia, including a suxamethonium infusion, was also studied. Possible mechanisms by which the transient decrease in cholinesterase activity is produced, and its clinical significance, are discussed.

Anesthesia, Epidural↗
PubMed1992

Suxamethonium block in the myasthenic patient. Correlation with plasma cholinesterase.

The neuromuscular block of suxamethonium 1.5 mg.kg-1 was investigated in three myasthenic patients (Class IIA), undergoing thymectomy. Two of the patients were receiving pre-operative pyridostigmine therapy. In the three patients, plasma cholinesterase activity was determined on the morning of surgery and was correlated with the neuromuscular response to suxamethonium as monitored by electromyography. The results suggest that the response to suxamethonium in the myasthenic patients can show wide variations according to the level of their plasma cholinesterase activity. The degree and duration of suxamethonium block is inversely related to the plasma cholinesterase activity.

Adolescent↗
PubMed1986

Grouping of human ejaculates according to the degree of coagulation and the relationship to the levels of choline and cholinesterase.

Human ejaculates were divided into 3 groups (I, II and III) according to the extent of their coagulation and the levels of free choline and cholinesterase were determined together with seminal vesicular N-acetylamino sugar and prostatic (zinc) marker components. Coagulation was determined as the percent coagulum (CG) at 5 min after ejaculation. The mean (+/- SEM) values for CG at 5 min in groups I, II and III were 6 +/- 2, 43 +/- 4 and 79 +/- 2, respectively. The time for 100% liquefaction in the 3 groups were 4.7 +/- 0.8, 12.9 +/- 1.4 and 19.1 +/- 2.1 min, respectively. Group III had significantly higher levels of choline and cholinesterase activity than groups I and II. The choline level was correlated significantly (r = 0.58) with the concentration of N-acetylamino sugar, but there was no correlation with the level of zinc. Evaluation of the level of choline in prostatic fluid, in semen from azoospermic men and in ejaculates with different CG values suggested that the level of choline may provide valuable information about activity of the seminal vesicles. Release of choline in group I was only 33 and 50% of that groups III and II, respectively. 60% of the total release of choline occurred during the liquefaction phase. The mean activity of cholinesterase in the prostate was only 27% lower than that found in seminal plasma. The liquefaction time and the concentration of choline, N-acetylamino sugar and zinc decreased significantly in ejaculates after 2 days of abstinence.

Acetylglucosamine↗
PubMed1977

Serum cholinesterase (pseudocholinesterase) in Down's syndrome: 1. Phenotype frequencies at the E1 and E2 loci.

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.

Adult↗
PubMed1977

Serum cholinesterase (pseudocholinesterase) in Down's syndrome: 2. Quantitative levels.

The observation elsewhere (Drew and Rundle, 1977) that increase frequencies of the C5 + variant of the serum cholinesterase in Down's syndrome may be due to a protective influence against adverse environmental factors has been investigated for such factors as age, sex, duration of institutionalisation, presence of the hepatitis -B antigen and maternal age. With the exception of the maternal age none of the factors tested appear to affect the circulating levels of cholinesterase. A maternal age effect in the Down's subjects was detected with lower levels of the enzyme being found in the subject positive for the C5 + variant born to mothers over thirty-five years when compared to the C5 + subjects born to mothers under thirty-five years. Further studies confirmed the presence of a relationship between maternal age, serum cholinesterase levels and haptoglobin phenotypes.

Adult↗
PubMed1975

Serum cholinesterase activity in burned patients. II: anaesthesia, suxamethonium and hyperkalaemia.

The importance of serum cholinesterase activity in burned patients was evaluated in relation to anaesthesia. Anaesthesia included a repeated administration of suxamethonium. Thirty-two patients with an estimated area of burn between 3 and 72% were studied during 39 anaesthetic procedures. A statistically significant inverse correlation was found between serum cholinesterase activity and the apnoea period following intravenous suxamethonium. In patients with very low enzyme activity, apnoea periods of 10 to 25 min were observed. No correlation was found between the changes in serum potassium following suxamethonium and either the serum cholinesterase activity or the changes in Pco2 and pH. The most reliable parameters in predicting a dangerous increase in serum potassium following intravenous suxamethonium were shown to be 1) the time elapsed from burn injury to anesthesia and 2) the degree of burn injury. However, abnormal reactions to suxamethonium were seen as early as 9 days following injury, and rises in serum potassium to over 6 mmol/l were observed even in patients with a total burn surface of around 8%, i.e., less than the surface of one arm.

Adolescent↗
PubMed1988

Half-life of plasma cholinesterase.

The half-life of plasma cholinesterase (acylcholine acylhydrolase EC 3.1.1.8) was determined in three patients homozygous for the atypical gene for plasma cholinesterase by measuring the rate of disappearance of enzyme activity following intravenous injection of concentrated human cholinesterase. Half-life values of 10.9, 11.1, and 11.3 days were estimated. The distribution volume was estimated to be 18.0, 18.2, and 13.8% of body weight, respectively.

Adult↗
PubMed1993

Mivacurium-induced neuromuscular blockade in patients with atypical plasma cholinesterase.

The duration of action of mivacurium was evaluated during a modified neurolept anaesthesia in 17 patients heterozygous for the usual and the atypical plasma cholinesterase (pChe) gene (E1uE1a) and in five patients homozygous for the atypical gene (E1aE1a). The response to train-of-four nerve stimulation was recorded using a Myograph 2000. Five heterozygous patients were given a small dose of mivacurium 0.03 mg kg bw-1 intravenously (Group 1). The mean (range) suppression of the first twitch in the train-of-four response (T1) was 91% (69-100%). The time to 90% T1 recovery was 23.9 min (14.0-31.3 min). Twelve other heterozygous patients (Group 2) received mivacurium 0.2 mg kg bw-1 (2.5 x ED95). In these patients the time to 100% T1 suppression was 1.4 min (1.1-2.0 min). The time to reappearance of the T1 response, to 90% T1 recovery, and the recovery index (25.3 min (14.5-34.5), 45.5 min (30.9-59.2), and 9.8 min (6.8-19.6), respectively) were significantly longer than reported in phenotypically normal patients. Five patients homozygous for the atypical gene (Group 3) were given 0.03 mg kg bw-1 mivacurium. The time to reappearance of T1 response following this low dose of mivacurium ranged from 26-128 min. In all five patients the neuromuscular block was successfully antagonized with neostigmine preceded by atropine. In conclusion, mivacurium-induced neuromuscular blockade was moderately prolonged in patients heterozygous for the usual and the atypical gene for plasma cholinesterase. Patients homozygous for the atypical plasma cholinesterase gene appear to be markedly sensitive to mivacurium.

Adolescent↗
PubMed1995

Identification of human plasma cholinesterase variants in 6,688 individuals using biochemical analysis.

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)

Adolescent↗
PubMed1980

Polyacrylamide gel electrophoresis of amniotic fluid cholinesterases: a good prenatal test for neural tube defects.

The qualitative assay of the cholinesterases (ChE) in amniotic fluid on polyacrylamide gel gave a single major band (cholinesterase) in all samples from normal pregnancies, and two major bands (cholinesterase and acetylcholinesterase) in all cases from fetuses with open neural tube defects. Five fluids which were true false positive on alpha-fetoprotein (AFP) assay (elevated AFP in a clear fluid but normal fetus) had a single band, and two fluids which were false negative on AFP testing (normal AFP but spina bifida fetus) had two bands. The second 'diagnostic' ChE band sometimes occurred, together with other extra bands, in some fluids which were very severely contaminated by maternal or fetal blood, but in four of six fluids from normal fetuses where fetal blood staining was sufficient to cause the AFP to be elevated, there was only one ChE band. It is suggested that the qualitative assay of ChE should be performed in addition to AFP in the prenatal diagnosis of neural tube defects.

Amniotic Fluid↗
PubMed1961

Localization of cholinesterases in the chicken nervous system and the problem of the selective neurotoxicity of organophosphorus compounds.

Using the thiocholine method, a restricted survey has been made of cholinesterases in the spinal cord and brain stem of the chicken. No simple relation between sites of selective damage in organophosphorus neurotoxicity and centres of cholinesterase activity could be adduced. Moreover, no significant differences between species susceptible and insusceptible to poisoning by these compounds were found by this method. It is concluded that, while cholinesterase may well play an intermediary role in the intoxication, other factors determine the selective damage to certain neurones and their processes.

Animals↗
PubMed1984

Perivascular cholinesterase and morphological blood-brain barrier function.

Little is known about the function of cholinesterase activity present in the walls of cerebral microvessels. It has been shown that systemically administered physostigmine, a cholinesterase inhibitor that penetrates the blood-brain barrier, causes barrier opening. This has led to suggestions that perivascular cholinesterase is involved in the maintenance of morphological blood-brain barrier function. The present study demonstrates that the physostigmine-induced barrier opening is fully attributable to the acute hypertension and hypercapnia the agent gives rise to. Thus, it is discussed whether the enzyme activity may function as an enzymatic barrier to cholinergic agents.

Animals↗