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PubMed1962

Mutation to neostigmine resistance in a cholinesterase-containing Pseudomonas.

Searle, Barbara W. (Stanford University School of Medicine, Palo Alto, Calif.) and Avram Goldstein. Mutation to neostigmine resistance in a cholinesterase-containing Pseudomonas. J. Bacteriol. 83:789-796. 1962.-In a strain of Pseudomonas fluorescens containing an inducible cholinesterase, the activity of that enzyme is rate-limiting for growth when acetyl-choline is the sole source of carbon or nitrogen. Under these circumstances, neostigmine, a cholinesterase inhibitor, becomes a growth inhibitor.A neostigmine-resistant mutant was isolated, and the properties of its cholinesterase were compared with those of the wild-type enzyme. There were no differences in penetration of cells by inhibitor, rate of enzyme-inhibitor combination, affinity of inhibitor or substrate for the cholinesterase, or protective effect of substrate upon the enzyme. However, the mutant consistently formed cholinesterase at about twice the wild-type rate. Mutation, in this case, appears to result in a specific change in the differential rate of enzyme biosynthesis. The relationship of this change to neostigmine resistance is discussed, and it is suggested that the effect observed here may be prototypic of a general type of mechanism responsible for acquired drug resistance.

Acetylcholine↗
PubMed1991

Expression of cholinesterase in the Schwann cells of peripheral nerves during development.

In peripheral nerves of mouse embryos Schwann cells exhibit a high activity of unspecific cholinesterase. At first (day 12 of embryonic development) this enzyme occurs in the nuclear envelope and in the granular endoplasmic reticulum. Thus, it is possible to differentiate between Schwann cells and fibroblasts which lack cholinesterase. Later on (day 16) the cholinesterase has shifted to the cell membrane of the Schwann cells. However, only that part of the plasmalemma which encircles single axons and the mesaxons exhibits an irregular deposition of the reaction end product. In newborns the first loops of the just formed myelin sheath are still stained. With maturation of the myelin sheath the enzyme activity disappears. The functional role of cholinesterase is unclear. Possible roles are discussed. The expression of cholinesterase in Schwann cells depends on the integrity of the axons. After a few hours, the cultivation of amputated limbs results in a reduction of the enzyme activity. After 1 day in culture cholinesterase disappears totally.

Animals↗
PubMed1990

[Variations in blood cholinesterase activity and exposure to chlorpyrifos in termite-control workers].

Chlorpyrifos, an organophosphate insecticide, has often been used as a termite-control agent since the advent of regulatory measures against the use of chlordanes in September 1986. A current concern is hazards such as organophosphorus poisoning among termite-control workers. In this study, the blood cholinesterase activity, the number of hours engaged in termite-control work, general conditions, and various test values were examined regularly in eight workers at a termite-control office. The results are summarized as follows. 1. The plasma cholinesterase level was within the normal range from October 1986 until April 1987 in all workers, but started decreasing after May following the initiation of the full-scale termite-control season. It remained lower than the normal range (0.6 pH) from June until August in five of the six termite-control workers. The lowest level observed during this period was less than 50% of the mean value for each worker prior to the busy season in the six termite-control workers and was less than 10% of the pre-season values in three of them. In two workers, engaged mainly in sales, the plasma cholinesterase activity remained higher than in termite-control workers throughout the season. The lowest level in this minimally-exposed group during this period was not less than 50% of the mean value for each worker before the busy season. With the arrival of the off season, the level began to recover and returned to normal in all workers in January 1988. 2. The red cell cholinesterase activity remained within the normal range throughout the observation period, but it was generally low during the busy season from June to September and relatively high during the off season from December 1987 to January 1988. On the average, the red cell cholinesterase activity during the season was about 30% lower than that in the off season. 3. No marked subjective or objective abnormalities were seen in the workers. The results of other tests were generally normal, although a slight decrease in the red cell and white cell counts as well as abnormalities in serum lipid and lipase were noted in some workers. Further observations are necessary. 4. A significant negative correlation was noted between the number of hours engaged in termite-control work and variations in the plasma cholinesterase activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1995

Profile of serum cholinesterase in systemic sepsis syndrome (septic shock) in intensive care unit patients.

Serum cholinesterase catalytic concentrations were estimated in 26 patients diagnosed as having systemic sepsis syndrome (septic shock) in the Intensive Care Unit (12 were admitted with the diagnosis of systemic sepsis syndrome while 14 patients developed the syndrome while in the unit) and in 66 normal, healthy subjects. The assay was performed for 7 consecutive days in the patient group. There was a very significant decrease in the level of cholinesterase in the patient group from the onset of the study as compared to the control group (P < 0.00001). This decrease remained during the course of the seven day study period, indicating hepatic dysfunction early in the diagnosis. When compared to other conventional liver function tests, serum cholinesterase seems to change earlier on in the diagnosis. Prothrombin time showed a pattern of change similar to that of serum cholinesterase. There was a significant relationship between the catalytic concentration of serum cholinesterase and the outcome of the systemic sepsis syndrome, the level being significantly lower in patients who died in comparison to those who lived. It seems that serum cholinesterase is a sensitive indicator of hepatic dysfunction in the systemic sepsis syndrome.

APACHE↗
PubMed2003

[Reference values for erythrocyte cholinesterase activity in the working population of Antioquia, Colombia, according to the Michel and EQM techniques].

OBJECTIVE: To establish reference values for erythrocyte cholinesterase (EC 3.1.1.7) activity for the active working population of two regions of the department of Antioquia, Colombia, that are located at different altitudes above sea level. METHODS: We took representative samples from populations of active working persons 18 to 59 years old from two regions in the department of Antioquia: (1) the Aburrá Valley (1 540 m above sea level) and (2) the near east of the department (2 150 m above sea level). We excluded workers who were using cholinesterase-inhibiting substances in their work or at home, those who had a disease that altered their cholinesterase levels, and those who said they were not in good health. We measured the erythrocyte cholinesterase activity using two methods: (1) the Michel method and (2) the EQM method (EQM Research, Cincinnati, Ohio, United States of America). We carried out the measurements with 827 people, 415 from the Aburrá Valley and 412 from the near east region. We compared proportions using the chi-square test and Fisher's exact test. We utilized the Student's t test for independent samples to compare two averages. To simultaneously compare three or more averages, analysis of variance was used, followed by the Newman-Keuls multiple-range test. When the variables were not normally distributed or when the variances were not homogeneous, Kruskal-Wallis nonparametric analysis of variance was used to compare the medians. Three computer software programs were used in the statistical analysis: SPSS 9.0, SGPlus 7.1, and Epi Info 6.04. In all the statistical tests the level of significance was set at P < 0.05. RESULTS: The average erythrocyte cholinesterase activity value that we found for the studied population by using the Michel method was 0.857 delta pH/hour (95% confidence interval (CI): 0.849 to 0.866), and the average value found through the EQM method was 35.21 U/g hemoglobin (95% CI: 34.82 to 35.60). With the Michel method: (1) the enzymatic activity differed significantly between the two regions, according to the Newman-Keuls test; (2) within each region, the enzymatic activity was significantly higher among males than among females, according to the Newman-Keuls test; and (3) in none of the region-sex strata was there a statistically significant influence of age on the enzymatic activity. Using the EQM method, there were no statistically significant differences by region, sex, or age group. CONCLUSIONS: The erythrocyte cholinesterase activity values found by the two analytical techniques were significantly higher than the values from outside Colombia that are now being used as reference values in the country, which poses both clinical and epidemiological problems. We recommend that the data from this study be adopted as the reference values in Colombia.

Adolescent↗
PubMed2005

Decreased persistence to cholinesterase inhibitor therapy with concomitant use of drugs that can impair cognition.

STUDY OBJECTIVES: To assess persistence with cholinesterase inhibitor therapy 6 months after the start of treatment, and to determine whether the likelihood of persistence is associated with the coprescription of drugs that can impair cognition. DESIGN: Retrospective cohort study. SETTING: Community (home residence) or long-term care facility. PATIENTS: A total of 1183 patients enrolled in the Rhode Island Medicaid program, aged 45 years or older, who were dispensed a cholinesterase inhibitor from January 1, 2000-June 30, 2002. MEASUREMENTS AND MAIN RESULTS: Patients were considered persistent with treatment if they filled at least five prescriptions for a 1-month supply of the same cholinesterase inhibitor, without an extended gap in days between refills. We compared rates of persistence among patients receiving and those not receiving drugs that can impair cognition. Covariates assessed were patient age, sex, race, and care setting. Approximately one in four patients discontinued cholinesterase inhibitor therapy within 6 months. Patients aged 85 years or older were more persistent than younger patients (77% vs 71%, p<0.05). Caucasian patients were more likely to be persistent than non-Caucasian patients (74% vs 52%, p<0.001). Patients living in the community were less likely to persist than those residing in long-term care facilities (58% vs 76%, p<0.001). After adjusting for race and care setting, patients who were prescribed drugs that can impair cognition were more likely not to have persisted with cholinesterase inhibitor therapy at 6 months than those who did not receive such drugs (odds ratio 1.56, 95% confidence interval 1.13-2.16). CONCLUSION: A substantial percentage of patients who began receiving cholinesterase inhibitor therapy had discontinued the therapy within 6 months. Many patients also received prescriptions for agents that can impair cognition. Our findings indicated a modest but statistically significant increase in likelihood of treatment discontinuation among patients who also received prescriptions for drugs that can impair cognition. Iatrogenic causes of dementia are important to recognize and address so that therapies for enhancing cognition can be fully effective.

Age Factors↗
PubMed1994

Pesticide exposures, cholinesterase depression, and symptoms among North Carolina migrant farmworkers.

OBJECTIVES: We conducted a clinic-based study of erythrocyte cholinesterase levels, pesticide exposures, and health effects among farmworkers and nonfarmworkers to determine risks for exposure and associated morbidity. METHODS: Two hundred two farmworkers and 42 nonfarmworkers were recruited sequentially at two community health centers. Erythrocyte cholinesterase levels were measured colorimetrically. Questionnaires obtained data on demographics, occupational history, exposures, and symptoms. RESULTS: Cholinesterase levels were significantly lower among farmworkers (30.28 U/g hemoglobin) than among nonfarmworkers (32.3 U/g hemoglobin). Twelve percent of farmworkers, but no nonfarmworkers, had very low levels. Farmworkers applying pesticides also had lower cholinesterase levels. One half of farmworkers reported being sprayed by pesticides and working in fields with an obvious chemical smell. Of reported symptoms, only diarrhea was associated with cholinesterase levels. Reported exposures, however, were strongly associated with symptoms. CONCLUSIONS: Farmworkers reported many pesticide exposures that violate state and federal regulations. Farmworkers had cholinesterase levels significantly lower than those of nonfarmworkers, although only spraying pesticides was associated with very low levels.

Acetylcholinesterase↗
PubMed2004

Cost effectiveness of cholinesterase inhibitors in the treatment of Alzheimer's disease: a review with methodological considerations.

Cholinesterase inhibitors have been available for the treatment of Alzheimer's disease since 1993. They have significantly positive effects on cognitive functioning and other domains of functional capacity, such as activities of daily life in terms of efficacy, but the clinical value of these effects are under discussion. Cholinesterase inhibitors may also influence behavioural and psychological symptoms in Alzheimer's disease. Cholinesterase inhibitors are also regarded as rather expensive and, therefore, the question of cost effectiveness is essential. Pharmacoeconomic evaluations of cholinesterase inhibitors have so far been conducted in retrospect on efficacy data from prospective randomised clinical trials combined with economic data from other sources. There are no published specific cost-effectiveness studies of cholinesterase inhibitors which prospectively collected empirical data on costs and outcomes. There is only one published randomised clinical trial with such empirical data with a cost consequence analysis design, indicating cost neutrality. Several types of models to describe the long-term effects have been published, indicating cost effectiveness. However, due to methodological considerations, the validity of these models is difficult to judge. A research agenda for the cost effectiveness of cholinesterase inhibitors is proposed, including long-term studies with empirical data on resource use, costs and outcomes, studies on quality of life, informal care and behavioural and psychological symptoms, combination and comparative studies on mild cognitive impairment.

Alzheimer Disease↗
PubMed1991

Quantification and phenotyping of serum cholinesterase by enzyme antigen immunoassay: methodological aspects and clinical applicability.

An enzyme antigen immunoassay for a specific determination of serum cholinesterase is described. Polyclonal and monoclonal antibodies against cholinesterase have been used. Hydrophobic binding of the specific antibody to a microtitre plate was followed by incubation with the samples, and the activity of the bound cholinesterase was assayed by the Ellman method. The procedure has been optimized and characterized, with respect to antigen specificity, and the applicability of the assay for cholinesterase phenotyping is demonstrated. The cholinesterase activities, dibucaine-, scoline-, fluoride- and urea numbers were comparable with established reference values. The high sensitivity and specificity of the assay has been used for determination of cholinesterase in amniotic and cerebrospinal fluids, and its applicability in clinical medicine is indicated.

Acetylcholinesterase↗
PubMedDate not supplied

[Role of hormonal and seasonal factors in the effect of vitamin E on cholinesterase activity in the nervous system].

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.

Animals↗
PubMed1992

Monitoring organophosphate insecticide-exposed workers for cholinesterase depression. New technology for office or field use.

A serious limitation to the diagnosis of mild organophosphate poisoning and to the preventive screening of organophosphate-exposed workers has been the large interindividual variability in erythrocyte cholinesterase. This makes it necessary to obtain a pre-exposure baseline measurement of enzyme activity as a basis for evaluating subsequent declines. To evaluate a new battery-operated colorimetric erythrocyte cholinesterase kit, 23 workers at a Mexican pesticide formulation plant were examined. All workers had normal cholinesterase, and exposed and unexposed workers were found to have similar mean cholinesterase levels. Although erythrocyte cholinesterase was found to have a coefficient of variation of 12% (similar to that reported in previous studies), hemoglobin-adjusted erythrocyte cholinesterase had a markedly reduced coefficient of variation (7.4%). The 90% confidence interval (24.9-31.7 IU/g hemoglobin) resulted in a lower normal limit that is 78% of the upper limit. Even if a pre-exposure baseline were high normal but unknown at the time of examination, the supervising clinician can be confident that any person with a normal result will be no less than 78% of baseline. The kit is moderately priced, easy to use in the field setting, and the low variability to the assay should allow improvement in diagnosis, screening, and in the epidemiologic evaluation of exposure.

Adult↗
PubMed1987

Clinical confirmation of organophosphate poisoning by serial cholinesterase analyses.

Three groups of agricultural workers with a history of exposure to organophosphate pesticides were followed up to evaluate the utility of sequential postexposure cholinesterase analyses to confirm organophosphate intoxication in the absence of baseline cholinesterase values. Three or more cholinergic symptoms were reported by 50 of the 72 patients. Initial plasma and red blood cell cholinesterase values of 45 of the workers were above the lower limit of the laboratory normal range. Follow-up examinations, including cholinesterase analyses, were conducted on 57 patients. When final postexposure cholinesterase determinations were taken as estimates of individual normal baseline values, the plasma and red blood cell activity of the three groups was shown to have been inhibited. The data support the use of sequential postexposure plasma cholinesterase analyses to confirm the diagnosis of organophosphate-induced illness in the absence of baseline values.

Adolescent↗
PubMed1980

Serum cholinesterase activity in patients with malaria infection.

Serum cholinesterase activities were determined in 87 patients of both sexes with P. falciparum malaria in comparison to those of 80 blood donors. Patients with acute P. falciparum malaria had significantly lower serum cholinesterase activity than those of the control group. After treatment, their serum cholinesterase levels returned to the normal level. Serum albumin concentration also showed the same pattern and had a direct relationship to those of serum cholinesterase levels. These findings indicated that malarial parasites had some effect on the liver cells which resulted in impaired hepatic synthesis of serum cholinesterase and albumin concentrations. This result therefore add new information that there was a disturbance of enzyme cholinesterase among many liver enzymes that have been shown to be altered during an acute malarial attack.

Adolescent↗
PubMedDate not supplied

[Effect of substituted thiobutinylic esters of phosphorus thio acids and their saturated analogs on cholinesterases of different origins].

Studies have been made of the effect of organophosphorus inhibitors (OPI) containing butynilic group in the detectable part of the molecule, and of their saturated analogues on cholinesterases from different species of mammals and arthropods. In all cases without a single exception, acetylene compounds exhibited higher anticholinesterase effect than saturated ones. The value of "acetylene effect" varied to a great extent and depended on both the structure of OPI and the source of cholinesterase, these data indicating the existence of differences in the structure of the active site in cholinesterases investigated. The acetylene effect was always higher in ethylmercapto-substituted OPI than in chloride-substituted ones. Among thiophosphates, the highest (7,600) effect was found for cholinesterase of the spider mite in the case of dimethyl esters. Among thiophosphonates, exceptionally high (38,000) effect was noted for cholinesterase from the head of the domestic fly when methylthiophosphonates were compared. In this pair of compounds, the inhibitory constant k2 for the cholinesterase of the fly by acetylene derivative was equal to 1.1 . 10(9).

Acetylcholinesterase↗
PubMed2005

Serum acetyl cholinesterase as a biomarker of arsenic induced neurotoxicity in sprague-dawley rats.

Arsenic is an environmental toxicant, and one of the major mechanisms by which it exerts its toxic effect is through an impairment of cellular respiration by inhibition of various mitochondrial enzymes, and the uncoupling of oxidative phosphorylation. Most toxicity of arsenic results from its ability to interact with sulfhydryl groups of proteins and enzymes, and to substitute phosphorus in a variety of biochemical reactions. Most toxicity of arsenic results from its ability to interact with sulfhydryl groups of proteins and enzymes, and to substitute phosphorus in a variety of biochemical reactions. Recent studies have pointed out that arsenic toxicity is associated with the formation of reactive oxygen species, which may cause severe injury/damage to the nervous system. The main objective of this study was to conduct biochemical analysis to determine the effect of arsenic trioxide on the activity of acetyl cholinesterase; a critical important nervous system enzyme that hydrolyzes the neurotransmitter acetylcholine. Four groups of six male rats each weighing an average 60 +/- 2 g were used in this study. Arsenic trioxide was intraperitoneally administered to the rats at the doses of 5, 10, 15, 20mg/kg body weight (BW), one dose per 24 hour given for five days. A control group was also made of 6 animals injected with distilled water without chemical. Following anaesthesia, blood specimens were immediately collected using heparinized syringes, and acetyl cholinesterase detection and quantification were performed in serum samples by spectrophotometry. Arsenic trioxide exposure significantly decreased the activity of cholinesterase in the Sprague-Dawley rats. Acetyl cholinesterase activities of 6895 +/- 822, 5697 +/- 468, 5069 +/- 624, 4054 +/- 980, and 3158 +/- 648 U/L were recorded for 0, 5, 10, 15, and 20 mg/kg, respectively; indicating a gradual decrease in acetyl cholinesterase activity with increasing doses of arsenic. These findings indicate that acetyl cholinesterase is a candidate biomarker for arsenic-induced neurotoxicity in Sprague-Dawley rats.

Acetylcholinesterase↗
PubMed2000

Serial neuro-electrophysiological studies in acute organophosphate poisoning--correlation with clinical findings, serum cholinesterase levels and atropine dosages.

OBJECTIVES AND METHODS: A prospective evaluation of the correlation between the serial clinical findings, serum cholinesterase levels, electrodiagnostic abnormalities and the daily atropine requirement was undertaken in 29 patients with confirmed acute organophosphate poisoning (OPP). RESULTS: Clinical weakness conforming to the pattern found in 'Intermediate Syndrome' was noted in 19 patients (65.55%). It was associated with all types of organophosphate compounds and occurred in all patients in whom the serum cholinesterase on admission was less than 200 units. Three types of electrodiagnostic abnormalities were noted: single supramaximal electrical stimulus induced repetitive response, a decrement--increment response to 30 Hz repetitive nerve stimulation (RNS) and a decremental responses to 30 Hz RNS. The 30 Hz decremental response correlated best with the presence of clinically detectable weakness (sensitivity = 61.72%; specificity = 81.54%; positive predictive value = 73.91%; negative predictive value = 71.62%). Time trends evaluation revealed that the peak daily atropine dosages were given at a mean of 1.76 +/- 0.83 days in comparison to a mean nadir of serum cholinesterase of 2.48 +/- 1.97 days and a mean nadir of 9:1 ratio of 2.65 +/- 1.76 days. The 2-tailed correlation coefficient analysis and simple regression analysis revealed a positive correlation between serum cholinesterase levels and the 9:1 ratios (correlation coefficient: 0.59). A negative correlation was observed between the 9:1 ratios and the daily atropine requirement (correlation coefficient: -0.57) and between serum cholinesterase levels and daily atropine requirement (correlation coefficient: -0.49). CONCLUSIONS: At admission, level of serum cholinesterase of less than 200 units is a predictor and the 30 Hz RNS decremental response could be a useful marker for the 'Intermediate Syndrome'.

Acetylcholinesterase↗
PubMed1985

Assessment of exposure to organophosphate insecticides during spraying in Haiti: monitoring of urinary metabolites and blood cholinesterase levels.

Measurement of blood cholinesterase activity and of the urinary metabolites of fenitrothion (p-nitrocresol) and malathion (monocarboxylic acid) was used to assess the exposure to these insecticides of workers in the Haitian malaria control programme and of residents in the sprayed houses. Cholinesterase activity was significantly reduced at the end of the working week in 3 out of 28 fenitrothion workers. Urinary levels of p-nitrocresol (PNC) in the spraymen ranged from 2.2 to 25.2 mg/l. In fenitrothion workers who had no direct contact with spraying (weighers and supervisors), the cholinesterase activity remained >/= 75% of the normal control value, and the urinary PNC levels were relatively low. Urinary malathion monocarboxylic acid (MCA) levels at the end of the working week ranged between 1.1 and 5.3 mg/l in workers using malathion and their blood cholinesterase activity remained essentially normal. In both groups of workers the cholinesterase levels improved and the urinary excretion of metabolites decreased after 2 days of rest from the spraying operations. In the residents of the sprayed houses, low concentrations of PNC and MCA were detected in the urine 1 day after spraying and measurable but reduced levels were still present after 7 days. In all these cases the cholinesterase activity remained >/= 75% of the normal control value.

Carboxylic Acids↗
PubMedDate not supplied

In vitro protection of plasma cholinesterases by metoclopramide from inhibition by mipafox.

Metoclopramide (MCP) is a dopamine receptor antagonist and serotonin receptor agonist widely used as an antiemetic and gastric prokinetic drug. In addition MCP is a reversible inhibitor of cholinesterases from human central nervous system and blood. Metoclopramide may have a cholinesterase protective effect against inhibition by organophosphates. The purpose of the study was to quantify in vitro, by means of the IC(50) shift, the extent of MCP conferred protection, using mipafox (MPFX) as an inhibitor. Mipafox is a neuropathic organophosphate. Cholinesterase activities (with acetylthiocholine [ChE-A] and butyrylthiocholine [ChE-B] as substrates) in human plasma were measured photometrically in the presence of different MPFX concentrations and the IC(50) was calculated. Determinations were repeated in the presence of increasing MCP concentrations. It appears that the shift induced by the presence of MCP increases with the MCP concentration in a linear manner. In the presence of a clinically easily achievable plasma concentration of 1 micro M MCP, the IC(50) of MPFX for cholinesterase 'shifts' by a factor of ca. 3-6. The protective effect of MCP on cholinesterase could be of practical relevance in the treatment of organophosphate poisoning. We conclude that in vivo testing of MCP as an organophosphate protective agent is warranted.

Cholinesterase Inhibitors↗