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PubMedDate not supplied

[Experimental data on a new cholinesterase reactivator from the group of thiohydroximic esters].

Experimental data on the effectiveness of p-brombenzothiohydroximic S-diethylaminoethylate (diethyxime) -a new cholinesterase reactivator - are presented. The diethyximetoxicity with its single and multiple administration to animals was studied. The drug is shown to display a marked antidotal action when used in a dosage range of 490-10 mg/kg. Diethyxime is shown capable of restoring the activity of cholinesterase inhibited by dimethyldichlorovenylphosphate, of preventing the neuro-muscular block of the impulses conduction and of normalizing the function of the cardiovascular system. The drug is less toxic than is presently employed reactivator diproxime and it does not produce any side-effects on a number of organs and systems of the organism with its multiple administration to worm-blooded animals.

Animals↗

PubMedDate not supplied

The effect of adrenaline on acetylcholine synthesis, choline acetylase and cholinesterase activity.

The effect of adrenaline on acetylcholine synthesis, choline acetylase and cholinesterase activity. Acta Physiol. Pol. 1975, 26 (1): 45-54. The purpose of the study was to assess the participation of adrenaline in the processes of acetylcholine synthesis and breakdown in white rats. After intraperitoneal administration of adrenaline the content of acetylcholine in the tissues (brain, stomach, sciatic nerve, lumbar spinal cord) initially, slightly decreased, increased in the 30th, 60th, and 120th min, and then fell again below the initial value after 240 min. The rise in acetylcholine tissue content after administration of adrenaline seems to be due to its increased synthesis. This was also confirmed by in vitro investigations. The fall in the tissue acetylcholine content was associated with reduced synthesis of acetylcholine in the cerebral cortex. The increase in acetylcholine synthesis in the brain tissue after adrenaline given in vitro and in vivo does not seem to be caused by activation of choline acetylase. The activity of cholinesterase in the brain was not changed after adrenaline administered in vivo and in vitro.

Abdominal Muscles↗

PubMed1976

[Changes in the acetylcholine--cholinesterase system in the dynamics of experimental boltulin poisoning].

A study was made of the effect of botulin, type B, on the acetylcholine-cholinesterase system. High doses of the toxin increased the level of acetylcholine in the peripheral blood nervous system, as well as in the central nervous system. Injection of DLM of the toxin results in elevation of the acetylcholine level in the peripheral nervous system. Cholinesterase activity was practically unchanged.

Acetylcholine↗

PubMed2002

Recovery of plasmatic cholinesterase activity in a neotropical fish Prochilodus lineatus (Pisces, Curimatidae) exposed to organophosphorous pesticides.

The objective was to determine the plasmatic enzyme cholinesterase recovery, after being inhibited by an organophosphorous in juveniles of Prochilodus lineatus. Fish were exposed 12 h to a sublethal concentration of 1 mg/l of monocrotophos, and immediately placing in clean water during 12, 24, 48 and 96 h to detoxification. After this period, blood was extracted and plasma were used for the quantification of cholinesterase. The results showed a enzymatic inhibition of 91.9%, 55.1%, 50.4% and 33.4% with 12, 24, 48 and 96 h of recovery, respectively. The enzymatic activity spreads to be normalized with the course of hours and the degree of inhibition obtained initially was very high and sustained in the first 48 h.

Adaptation, Physiological↗

PubMed2000

[Participation of a distant cholinergic mechanism in the response of the vascular bed to intoxication by organophosphorus inhibitors of cholinesterase].

Poisoning with phosphacol causes dose--dependent decrease of blood flow speed in small vessels of mesoappendix. Administration of LD50 of phosphacole results in blood stagnation, simultaneous blood pressure fall, which leads to death of part of the animals. Electron microscopic study revealed the presence of acetyl and buthyryl cholinesterase in endotheliocytes of mesoappendicular capillaries, the activity of which was completely suppressed by administration of LD50 of phosphacol. 0,0-dimethyl-0 (2,2-dichlorvinyl) phosphate LD10 caused the damage of endotheliocyte surface. It was suggested that endothelial cholino-receptors that are activated through the rise of redundant acetyl-choline level in blood on the background of cholinesterase inhibition participate in the mechanism of pathological reactions described. Such variant of toxic effect was characterized as distant.

Acetylcholine↗

PubMed1976

Plasma cholinesterase variants - an unexpectedly high incidence of the silent allele.

The silent allele is one of the rarer plasma cholinesterase variants. In a series of 9 South African families with an inherited abnormal cholinesterase, the silent allele occurs in 5. In 2 it is the only abnormal allele present while in 3 it occurs with the 'atypical' (dibucaine-resistant) form. Identification of the single silent allele requires full family studies, since its inhibition characteristics are those of the other allele present, normal or abnormal.

Adolescent↗

PubMed1992

Effectiveness of alpha 2-adrenergic receptor stimulation in reducing the central toxicity following cholinesterase inhibition.

Previous studies in this laboratory have demonstrated that the centrally-acting alpha 2-adrenergic agonist clonidine can offer significant protection against both the acute and chronic toxicity following irreversible cholinesterase inactivation with soman. The purpose of this study was to estimate the contribution of central mechanisms to soman toxicity in a rat model; and to determine the effectiveness of clonidine and a series of related agonists to offer protection against the acute and chronic manifestations of this toxicity. To investigate the central component of soman toxicity, animals were pretreated with the peripherally selective reversible cholinesterase inhibitor pyridostigmine, a standard protective agent. Pyridostigmine pretreatment resulted in significant improvement in survival following soman administration. However, pyridostigmine was not able to inhibit the signs of central soman toxicity, including convulsive behavior. Clonidine and several related drugs produced both a further reduction in lethality and a significant reduction in the central signs of soman toxicity. Signs of delayed toxicity to soman were apparent in rats surviving 48 h after administration as measured in open-field locomotor monitoring. Again, pyridostigmine did not offer protection against such delayed toxicity. When clonidine was included in the regimen, however, significant improvement in performance in this measure was observed. These results are consistent with our earlier findings of significant protection provided by clonidine and related drugs against acute and chronic manifestations of soman toxicity and provide further evidence that 1) central toxicity is an important contributor to soman's actions, and 2) stimulation of central alpha 2-adrenergic receptors limits the expression of this central toxicity.

Adrenergic alpha-Agonists↗

PubMed1992

Silent cholinesterase gene: three homozygotes in a small Caucasian population.

Three sera, showing only a 2-3% of the usual cholinesterase activity and belonging to two families of 800 Caucasian inhabitants of the same small town, were classified as type II silent cholinesterase genes by polyacrylamide slab gel electrophoresis, dibucaine and fluoride number and by their specific activity with acetyl- butyryl- or propionyl-thiocholine.

Blood Protein Electrophoresis↗

PubMed1977

[Cholinesterases and arylesterase in the umbilical cord, the placenta, and the amniotic membrane, in the female at term].

Cholinesterasic activity of umbilical cord (tissue), completely bloodless, is exclusively due to pseudocholinesterase. Cholinesterase is more active in placenta than in cord; it is an acetylcholinesterase at 80 per cent. Both forms coexist, about equally, in amniotic membrane. A considerable arylesterasic activity is proved in cord, placenta and membrane, the greatest activity being in placenta. Comparing the greater activity in maternal plasma and cord blood's plasma to the very weak activity in amniotic fluid, it is possible to think that cork, membrane, placenta and also amniotic fluid pseudocholinesterase and arylesterase, come from plasma. On the contrary, placental acetylcholinesterase seems original and probably is the source of this enzyme activity in amniotic fluid.

Acetylcholinesterase↗

PubMed2003

[Cholinergic deficiency syndrome as an indicator for the cholinesterase inhibitors].

Cholinesterase inhibitors are licensed for the treatment of dementia in Alzheimer's disease. In clinical practice, these drugs have little effect on the cognitive symptoms of dementia. Several studies report a beneficial effect of cholinesterase inhibitors on neuropsychiatric symptoms. We hypothesise that symptoms such as the impairment of attention and concentration, anxiety, restlessness and hallucinations, delineate a specific central cholinergic deficiency syndrome. It is postulated that this syndrome crosses boundaries of nosological entities and occurs in various neurodegenerative diseases. Symptoms resulting from cholinergic deficiency might be a much better target for treatment than cognitive deficits.

Acetylcholinesterase↗

PubMedDate not supplied

[Neuropsychological sequelae of acute poisoning by pesticides containing cholinesterase inhibitors].

In recent years a number of studies have drawn attention to the possible neuropsychological sequelae stemming from acute poisoning by certain substances, namely cholinesterase inhibitors. These chemicals, carbamates and organophosphorates (OP), have been used in industry, for washing cattle, as insecticides and even as chemical agents in terrorist attacks and in wars. Nowadays, they are widely used as a pesticide and this is particularly so in regions such as the west of Almeria. The intensive farming in greenhouses carried out in this area, together with the conditions in which these products are used and handled, leads to a relatively high number of cases of poisoning. Yet this is not an isolated fact; the first clinical study to describe cases of poisoning by these substances in workers was published back in 1955. Some of the neurotoxic sequelae deriving from such intoxications are well defined: acute cholinergic syndrome, intermediate syndrome and delayed polyneuropathy provoked by OP (OPIDN). Several studies have been carried out over the past few decades to measure the long term neuropsychological disorders produced by acute poisoning by these substances, and findings suggest that both cholinesterase inhibition and other biochemical phenomena can have permanent neurotoxic consequences. This communication aims to bring some order to the data offered by the different studies by analysing and verifying the evaluation protocols followed, the results of the neurophysiological and neurocognitive biochemical measurements, the type of poisoning and the time elapsed since they occurred, so that they can be summarised and taken as guidelines for possible work to be carried out in the future.

Animals↗

PubMed2003

Report on blood cholinesterase among vegetable growers.

We report our study on serum cholinesterase in vegetable growers, a risk occupation in a rural area of Thailand. In this study, 70 subjects (35 vegetable growers and 35 controls) were studied. The mean blood cholinesterase level in vegetable growers (17.7 +/- 7.0 U/ml) was significantly lower than that of the control group (24.7 +/- 12.4 U/ml) (p=0.01).

Agriculture↗

PubMed2004

Treating autistic spectrum disorders in children: utility of the cholinesterase inhibitor rivastigmine tartrate.

Rivastigmine tartrate is a dual-action cholinesterase inhibitor shown to improve language, cognition, and global functioning in patients with Alzheimer's disease, likely via increased availability of cerebral acetylcholine. Because cholinergic receptor abnormalities can contribute to the neuropathology of autistic spectrum disorders, rivastigmine tartrate could prove to be an effective therapy for affected children. Observations of improved behavior and language output from prior open-label and double-blind treatment of autistic children with donepezil, another cholinesterase inhibitor, prompted this 12-week open-label study with rivastigmine tartrate of 32 autistic patients. Therapeutic indices were the Childhood Autistic Rating Scale, Gardner's Expressive and Receptive One-Word Picture Vocabulary tests, and the Conners' Parent Rating Scale. Testing administered at baseline, 6 weeks, and 12 weeks showed gains in both expressive speech and overall autistic behavior over baseline. These improvements were statistically significant and supported the hypothesis that treatment with cholinergic enhancing drugs in autistic spectrum disorders yields positive therapeutic effects.

Acetylcholine↗

PubMed2003

Effect of fenvalerate technical grade on acetyl cholinesterase activity in Indian bullfrog Haplobatrachus tigerinus (Daudin).

Indian bullfrog Haplobatrachus tigerinus (Daudin) was exposed to sublethal dose (1/3 of LC50 I.E. 1.166 mg/kg) of fenvalerate technical grade and the effect was studied on the specific activity of acetyl cholinesterase in the different tissues of frog viz., brain, muscle, liver, kidney and testis at different time periods viz., 3,6, 12, 24, 48 and 72 hours. The inhibition of specific activity of acetyl cholinesterase was in the order of kidney > brain > muscle > liver > testis. A significant inhibition was noticed in kidney at 12 hours (-64.33%) and no effect was noticed at 3 hours in testis (+0.67%). The AChE activity was inhibited in first three hours of administration of fenvalerate in all the tissue tested. The inhibition continued upto 6 hours or 2 hours in different tissue but the recovery was started by 24 hours and almost completed by 72 hours.

Acetylcholinesterase↗

PubMed2004

Serum cholinesterase inhibition by omeprazole and lansoprazole.

Omeprazole inhibited human and rat serum cholinesterase by approximately 5 to 60% over the 0.5 to 50 mg/L (1.4-140 microM) concentration range. In contrast lansoprazole only produced 20-30% inhibition at the highest concentration of 10 mg/L (29 microM). Thus omeprazole but not lansoprazole is likely to potentiate the effect of succinylcholine at human clinical concentrations by inhibiting its hydrolysis in vivo by serum cholinesterases.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMedDate not supplied

[Comparative study of enzymatic activity of cholinesterases of different origin in thionaphthylacetate hydrolysis reactions].

A comparative determination of kinetic parameters V and Km in the reaction of hydrolysis thionaphthylacetate and well known substrate acetylthiocholine by choline esterases from different sources was conducted. It is shown that butyrylcholine esterases hydrolyze thionaphthylacetate with velocity comparable with that of hydrolysis of acetylthiocholine, while acetylcholine esterases and propionylcholine esterases hydrolyze this substrate several times slower than acetylthiocholine. The values of Km in the reactions of hydrolysis of thionaphthylacetate for all studied cholinesterases is an order higher than for acetylthiocholine except cholinesterase of blood serum of fish. This value for the latter enzyme is practically equal.

Acetylthiocholine↗

PubMed2006

[Cholinesterase inhibitors in dementia: the precarious balance between efficacy and safety].

Cholinesterase inhibitors are widely prescribed in patients with Alzheimer's disease. Recently it has become clear that using these medications increases the risk of serious adverse events like cardiac arrhythmias, and some studies report a much-increased mortality in the treatment group on comparison with the placebo group. In the light of the at best, modest, treatment effects, we advocate that the safety of cholinesterase inhibitors should be the subject of continuing, intense scrutiny. Efforts should be made to delineate the profile of a true 'cholinergic deficiency syndrome', in order to be able to prescribe these medications to a group of patients in whom the benefits outweigh the risks.

Alzheimer Disease↗

PubMedDate not supplied

[Heavy water (D2O) as a protective protein containing medium. Example: human cholinesterase].

Looking for a possible protective effect of heavy water on proteins, cholinesterase and lactate dehydrogenase in combination with D2O and further protective substances were exposed to a temperature of 60 degrees C (for 10 min) and about 45 degrees C (for several days). In combination with glycerine there resulted an additive protective effect; with NaCl and/or albumin being added the individual effects raised to a higher level. In the cold D2O protects cholinesterase only against acid denaturation, but in combination with warmth also against basic denaturation.

Cholinesterases↗