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PubMed1986

Are the effects of gestational stress on motor development and cerebellar cholinesterase activity mediated prenatally?

Prenatal random noise and light stress retards early motor development in the rat. To determine whether this delay is pre- or postnatally mediated and whether the developing cerebellum may play a role in the delay, rats were subjected to this form of stress and their offspring were fostered or cross-fostered onto control rats and vice versa. Their motor development was assessed by a series of behavioral tests between birth and day 10 of life. Prenatally stressed pups (Eo), whether reared by stressed (Em) or control mothers (Cm), showed a retardation in motor development. However, stressed pups matured earlier when reared by a control mother than by a stressed dam. Control pups (Co) raised by stressed mothers showed normal behavioral development. Cerebellar cholinesterase activity, which has been shown to undergo characteristic alterations with normal maturation, did not differ between stressed and control pups at birth. However, on day 10, cholinesterase activity was lower in EmCo than in CmCo pups, whereas that in CmEo and EmEo pups did not differ significantly from controls. It is concluded that three effects of random noise and light stress during pregnancy may be distinguished: (1) A prenatal effect as expressed by a delay in motor development, (2) a postnatal (rearing) effect on motor development and (3) a rearing effect expressed as a decrease in cerebellar ChE activity.

Animals↗
PubMed2005

[Prolonged succinylcholine-induced apnoea associated with cholinesterase silent plasma variant].

Mivacurium and succinylcholine are short-acting neuromuscular blocking drugs. The duration of their action depends on their rapid hydrolysis by plasma cholinesterase or butyrylcholinesterase. More than thirty genetic variants of this enzyme have been described but the atypical variant is the most frequently involved in prolonged apnoea following the administration of these two myorelaxants. We present one case of patient who presented a five hours long apnoea associated with null cholinesterase activity and detection of a butyrylcholinesterase silent variant (Sil-1, 1 for 100,000 persons in population) after sequencing.

Aged↗
PubMed2006

[Butyrylcholinesterase deficiency: how to analyse the cholinesterase activity in small children?].

We report the case of a prolonged neuromuscular blockade in an 18-month-old age girl following administration of a usual dose of succinylcholine. The diagnosis was highly suggested by the clinical history while cholinesterase activity was included in adult normal values but below values of a personal series of 41 small children. The familial analysis of dibucaine and fluoride number confirmed the hypothesis of an atypical variant (AA phenotype). The cholinesterase activity is higher in small children than in adult and has to be analysed according to the age.

Age Factors↗
PubMed2006

Analysis of cholinesterase binding to a carnitine-modified EQCM sensor.

A sensor for cholinesterases (ChEs) has been developed by binding carnitine via 1,6-diaminohexane to a mixed monolayer of 11-mercaptoundecanoic acid/11-mercapto-1-undecanol on the surface of a gold-coated quartz crystal. Catalytically active and organophosphate-inhibited acetyl- and butyryl-cholinesterases of different origins were tested for their binding ability to D- and L-carnitine, respectively. The binding constants were calculated by using a one-to-one binding model. Additionally, the activity of the immobilized ChE was monitored and the operational stability was investigated amperometrically.

Animals↗
PubMed2006

Cholinesterase inhibitors: SAR and enzyme inhibitory activity of 3-[omega-(benzylmethylamino)alkoxy]xanthen-9-ones.

In this work, we further investigated a previously introduced class of cholinesterase inhibitors. The removal of the carbamic function from the lead compound xanthostigmine led to a reversible cholinesterase inhibitors 3. Some new 3-[omega-(benzylmethylamino)alkoxy]xanthen-9-one analogs were designed, synthesized, and evaluated for their inhibitory activity against both acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE). The length of the alkoxy chain of compound 3 was increased and different substituents were introduced. From the IC(50) values, it clearly appears that the carbamic residue is crucial to obtain highly potent AChE inhibitors. On the other hand, peculiarity of these compounds is the high selectivity toward BuChE with respect to AChE, being compound 12 the most selective one (6000-fold). The development of selective BuChE inhibitors may be of great interest to clarify the physiological role of this enzyme and to provide novel therapeutics for various diseases.

Acetylcholinesterase↗
PubMed2005

Monitoring cholinesterases to detect pesticide exposure.

Progress toward a standard blood cholinesterase assay to assess pesticide exposures in the agricultural workplace and to identify possible victims of chemical warfare agents is discussed. Examples given are drawn from collaborations with clinical laboratories in California and the Department of Defense Cholinesterase Reference Laboratory (CRL).

Animals↗
PubMed2005

A case with cholinesterase inhibitor responsive asymmetric posterior cortical atrophy.

A 55-year-old right-handed woman presented initially with mild amnestic and depressive episodes but slowly developed progressive neurobehavioral symptoms, indicative of posterior cortical atrophy in ensuing years. A more detailed neurobehavioral test suggested predominant right temporo-parietal dysfunction with executive functional deficits. SPECT and MRI findings revealed right unilateral temporo-parietal involvement. Cholinesterase inhibitor administration led to amelioration of symptoms. We suggest that cases of posterior cortical atrophy or visual variant of Alzheimer's disease may be responsive to cholinesterase inhibitor therapy; however, the observation in a single case should be confirmed on larger populations in a clinical trial design with placebo control.

Apraxias↗
PubMed2006

Current understanding of the application of pyridinium oximes as cholinesterase reactivators in treatment of organophosphate poisoning.

This paper reviews the mechanisms of interaction of organophosphorus compounds with cholinesterases and clinical signs of acute poisoning. Further, we describe the current understanding of the mechanisms of action of pyridinium oximes pralidoxime (PAM-2), trimedoxime (TMB-4), obidoxime (LüH-6, Toxogonin), HI-6 and HLö-7 which are used as cholinesterase reactivators in the treatment of poisoning with organophosphorus compounds. We also review the most important literature data related to the efficacy of these oximes in the treatment of poisoning with warfare nerve agents soman, sarin, tabun, VX and cyclosarin and organophosphorus insecticides. Finally, we discuss the criteria for selection of oximes intended for further development as antidotes in poisoning with organophosphorus compounds and auto-injectors for their application in urgent situations.

Animals↗
PubMed2005

Association with the cholinergic precursor choline alphoscerate and the cholinesterase inhibitor rivastigmine: an approach for enhancing cholinergic neurotransmission.

The effects of association of cholinergic precursors choline or choline alphoscerate with the cholinesterase inhibitor rivastigmine on acetylcholine levels and [(3)H]hemicholinium-3 binding were assessed in rat frontal cortex, hippocampus and striatum. Acetylcholine immunoreactivity was also evaluated in cerebrocortical cholinergic fibers by immunohistochemistry. Choline alphoscerate or rivastigmine, but not choline increased acetylcholine levels as well as [(3)H]hemicholinium-3 binding used as a marker of high affinity cholinergic transporter. The association of choline alphoscerate with rivastigmine dose-dependently increased both acetylcholine levels and [(3)H]hemicholinium-3 binding. Rivastigmine alone or in association with either choline or choline alphoscerate decreased acetylcholinesterase (AChE), whereas choline or choline alphoscerate alone did not affect AChE activity. Choline alphoscerate or rivastigmine alone or in association, but not choline increased acetylcholine immunoreactivity in nerve fibers supplying cerebral cortex. These data suggest that combination of a suitable precursor of brain acetylcholine such as choline alphoscerate and of a cholinesterase inhibitor may represent an association worthwhile of being further investigated as a cholinergic replacement therapy in pathologies characterized by altered cholinergic neurotransmission.

Acetylcholine↗
PubMed2005

Mefloquine inhibits cholinesterases at the mouse neuromuscular junction.

Mefloquine is effective against drug-resistant Plasmodium falciparum. This property, along with its unique pharmacokinetic profile, makes mefloquine a widely prescribed antimalarial drug. However, mefloquine has neurologic effects which offset its therapeutic advantages. Cellular actions underlying mefloquine's neurologic effects are poorly understood. Here, we demonstrate that mefloquine inhibits human recombinant acetylcholinesterase. To explore the consequences of this action, we investigated mefloquine's actions at a model cholinergic synapse, the mouse neuromuscular junction. Sharp electrode recording was used to record miniature endplate potentials (mepps) in the Triangularis sterni muscle. Within 30 min of exposure to 10 microM mefloquine, mepps were altered in three ways: 10-90% rise time, 90-10% decay time and amplitude significantly increased. Mepp decay time increased linearly with mefloquine concentration. Pretreatment of muscles with the cholinesterase inhibitor physostigmine (3 microM) precluded the mefloquine-induced prolongation of mepp decay. Mefloquine also prolonged mepps at endplates of acetylcholinesterase knock-out mice. Since the selective butyrylcholinesterase inhibitor iso-OMPA (100 microM) also prolonged mepp decay at the neuromuscular junction of acetylcholinesterase knock-out mice, mefloquine inhibition of this enzyme is physiologically relevant. The non-selective anti-cholinesterase action can contribute to the neurologic effects of mefloquine.

Acetylcholinesterase↗
PubMed2003

Making connections: cholinesterase-domain proteins in the CNS.

Recent studies have highlighted novel functions of a group of cell adhesion molecules during nervous system development. Members of this protein family are characterized by an extracellular domain with sequence homology to cholinesterases and include the neuroligins, synaptic cell adhesion molecules recently implicated in autism, and neurotactin, a cell surface receptor involved in axonal pathfinding. Although these proteins have a structural organization similar to the enzyme acetylcholinesterase, the cholinesterase domain lacks enzymatic activity and functions as a protein-protein interaction motif. This protein family provides a striking example of how the function of a catalytically active domain has evolved to mediate receptor-ligand interactions that regulate morphogenetic processes during development of the nervous system.

Acetylcholinesterase↗
PubMed2003

The cholinesterase inhibitor DFP facilitates the expression of paradoxical sleep (PS) propensity in rats subjected to short-term PS deprivation.

Short-term paradoxical sleep (PS) deprivation was used to examine the effects of chronic exposure to subtoxic doses of the cholinesterase inhibitor diisopropylfluorophosphate (DFP) on PS regulation. Rats were injected once daily with DFP (0.2 mg/kg per day; s.c.) for 11 consecutive days; control rats received a daily injection of oil vehicle. The experiment was conducted on the 10th and 11th days of treatment, when brain cholinesterase inhibition induced by DFP exposure was maximal. On the 10th day, an 8-h baseline recording was carried out. On the 11th day, a 6-h PS deprivation was carried out by manually awaking rats each time they showed polygraphic signs of PS; recordings were then continued for another 2 h to examine recovery sleep. During deprivation, though they slept less than controls, DFP-treated rats made more attempts to enter PS. After deprivation, their PS rebound had an overall amount comparable to that of the controls, but its time course was shortened: whereas PS elevation was manifested through the 2 h of recovery in the control group, it occurred only during the first hour in the DFP group. These results demonstrate that chronic, low-level DFP exposure facilitated the expression of the PS propensity that accumulated as a result of PS deprivation: it enhanced the tendency for PS during deprivation; it accelerated the rate of compensatory PS expression after deprivation. They support the hypothesis that DFP promotes PS initiation by increasing cholinergic transmission.

Animals↗
PubMed1992

Mechanized assay of serum cholinesterase by specific colorimetric detection of released acid.

An automated assay method has been developed for the measurement of serum cholinesterase activity. The samples were prepared by an automated liquid handling unit and incubated for 9.7 min at 30 degrees C, followed by automatic injection into a colorimetric flow injection determination system for acetic acid liberated from acetylcholine by cholinesterase catalytic activity. The coloration reaction employed is based upon the formation of 2-nitrophenylhydrazide utilizing a water-soluble carbodiimide and has a high selectivity for carboxylic acids. The coefficients of variation of the proposed method were 2.4% for within-run analysis (n = 14) and 2.6% for between-run analysis (n = 6). Sera of 55 hospitalized patients were analyzed and the values obtained correlated well with an automated differential pH method (gamma = 0.989).

Acetates↗
PubMed1975

Relationship between serum cholinesterase and low density lipoproteins in children with nephrotic syndrome.

1. A significant increase in the activity of serum cholinesterase and concentration of dextran sulphate precipitable lipoproteins, cholesterol and triglycerides was observed in sixteen children with a diagnosis of nephrotic syndrome when compared with the values obtained in 22 other normal children of comparable ages. 2. In 7 children with nephrotic syndrome serum concentrations of beta-lipoprotein and cholinesterase were markedly higher in the acute stage compared to the convalescent stage. A working hypothesis is proposed to explain the hyperlipoproteinemia in nephrotic syndrome.

Child↗
PubMed1985

Depression of serum cholinesterase activity as an indicator for insecticide exposure--consideration of the analytical and biological variations.

Interest has recently been shown in the use of serum cholinesterase levels as a marker for chronic organophosphate insecticide exposure. Interpretation of the results must, however, take into account both long-term biological and analytical variations. The intraindividual variation of serum cholinesterase activity for 12 laboratory workers was 4.3%. The variation was much smaller than the interindividual variation of the whole population (20%). Based on the homogeneity of the intraindividual variance, it is possible to show the level of minimal decrease in enzyme activity which constitutes a departure from "normal".

Analysis of Variance↗
PubMed1986

Evaluation of a new method for cholinesterase determination.

We report the evaluation of a new commercially available assay system for determination of the catalytic activity of serum cholinesterase (EC 3.1.1.8) and application of the method to a centrifugal fast analyzer. Serum cholinesterase activity is determined at 30 degrees C using para-hydroxybenzoylcholine as substrate. This reaction is coupled to a second reaction using para-hydroxybenzoate hydroxylase (EC 1.14.13.2) as coupling enzyme. Enzyme activity is measured kinetically by monitoring the decrease in absorbance at 340 nm of NADPH in the second reaction. The procedure is precise and the results obtained from normal and pathological sera show good correlation with those obtained by the alternative procedures employing propionylthiocholine, butyrylthiocholine and benzoylcholine as substrates. The reference range for 700 healthy subjects was estimated to be 140-345 U/L (95% central range, determined non-parametrically), with significant difference between males and females (155-353 U/L for men and 134-323 U/L for women, p less than 0.001).

Acetylcholinesterase↗
PubMed1985

[Affinity electrophoresis in polyacrylamide gel. Influence of the concentration in the gel on the apparent affinity of cholinesterase for an anionic ligand site].

Affinity electrophoresis of three purified molecular forms of human plasma cholinesterase (monomer C1, dimer C3, tetramer C4) was carried out in polyacrylamide gels at various total acrylamide concentrations ranging from 3.48 to 9% in a discontinuous buffer system. A water-soluble linear copolymer supporting procainamide, a ligand of the anionic site of cholinesterase, was physically entrapped at various concentrations within the gel network. The combined effects of gel concentration and ligand concentration on the affinity pattern of the three molecular forms were studied. It was found that gel concentration influences the apparent binding activity of their anionic site: The apparent strength of interaction varied with the gel concentration: the denser the gel was, the higher the apparent affinity. The ligand-induced isomerization process was also depending on the gel concentration: the ligand concentration from which each zone is splitting into two moving zones decreased as the total gel concentration increased. These results show that the electrophoretic matrix plays an important role in the affinity process in affinity electrophoresis presumably by controlling kinetic effects: kinetics of protein-ligand complex formation and dissociation reactions, and mass transfer kinetics.

Butyrylcholinesterase↗
PubMed2001

Viral neuroinvasion as a marker for BBB integrity following exposure to cholinesterase inhibitors.

Exposure to the nerve agent soman, an irreversible cholinesterase (ChE) inhibitor, results in changes in blood-brain barrier permeability attributed to its seizure-induced activity. However, smaller BBB changes may be independent of convulsions. Such minor injury may escape detection. A nonneuroinvasive neurovirulent Sindbis virus strain (SVN) was used as a marker for BBB permeability. Peripheral inoculation of mice with 2 x 10(3) plaque forming units (PFU) caused up to 10(5) PFU/ml viremia after 24 hours with no signs of central nervous system (CNS) infection and with no virus detected in brain tissue. Intra-cerebral injection of as low as 1-5 PFU of the same virus caused CNS infection, exhibited 5-7 days later as hind limb paralysis and death. Soman (0.1-0.7 of the LD50) was administered at peak viremia (1 day following peripheral inoculation). Sublethal soman exposure at as low as 0.1 LD50 resulted in CNS infection 6-8 days following inoculation in 30-40% of the mice. High virus titer were recorded in brain tissue of sick mice while no virus was detected in healthy mice subjected to the same treatment. No changes in the level of viremia or changes in viral traits were observed in the infected mice. The reversible anticholinesterases physostigmine (0.2 mg/kg, s.c.) and pyridostigmine (0.4 mg/kg, i.m.) injected at a dose equal to 0.1 LD50, induced similar results. Thus, both central and peripheral anticholinesterases (anti-ChEs) induce changes in BBB permeability sufficient to allow, at least in some of the mice, the invasion of this otherwise noninvasive but highly neurovirulent virus. This BBB change is probably due to the presence of cholinesterases in the capillary wall. SVN brain invasion served here as a highly sensitive and reliable marker for BBB integrity.

Alphavirus Infections↗