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Serum cholinesterase was estimated in eight male and 18 female children, 4 to 12 years old, admitted to the paediatric ward of the Gadjah Mada University Hospital, Yogyakarta, with dengue haemorrhagic fever. The mean serum cholinesterase activity was low, i.e., 0.299 +/- 0.036 deltapH/hour (mean +/- s.e.m.).
Content of organophosphorous inhibitors (with the structure RO/CH3/P/O/SC2H4SC2H5) of cholinesterase as well as their hydrophobic properties (distribution coefficient in hexan/water system) were studied in subcellular fractions of rat brain. Relative content of organophosphorous inhibitors was distinctly decreased in supermicrosomal fraction with increase of hydrophobic properties of the fraction. Nuclear and mitochondrial fractions contained the more hydrophobic substances in relatively higher amount. When homogenate of supermicrosomal fraction was incubated at 37 degrees, own brain cholinesterase was not depressed by organophosphorous inhibitors, containing in the fraction at low concentration. The phenomenon exhibits that content of free organophosphorous inhibitors is distinctly lower in the subcellular fractions studied than amount of the inhibitors, extracted with chloroform.
The Dutch aquatic environment was monitored from September 1969 to December 1975 for organochlorine pesticides and their metabolites, cholinesterase inhibitors, and aromatic amines. The 1,492 samples analyzed included surface water, rainwater, groundwater, and drinking water. The highest concentrations of hexachlorobenzene (HCB) and alpha- and beta-benzene hexachloride (BHC) were found in the Rhine River and its tributaries. Concentrations of the compounds in the Dutch part of the Rhine River decreased downstream. Other organochlorine pesticides and their metabolites, heptachlor, heptachlor epoxide, aldrin, dieldrin, endrin alpha- and beta-endosulfan, and sigmaDDT were detected occasionally, but only in low concentrations. Cholinesterase inhibitors and aromatic amines were always present in the Rhine River and its tributaries.
Plasma cholenesterase is classified among blood markers whose genetic variation in man was discovered during past years. To look broadly at the characteristics of this system two main fields are now well established: geographical hematology and pharmacogenetics. In the present work the results of the study of that enzyme are reported in 2 400 individuals belonging to distinct Pyrenean communities. On geographical hematology the data obtained show the existence of a genetic polymorphism, the extent of which has a significant variation in the different areas. The E1a gene reaches the highest frequency (7.7%) in the central part of the Pyrénées (Lux Saint-Sauveur Valley): the rate decreases in Toulouse (3%) and in the Basques (2.3%). The E1s allele was found in the Basques with a frequency of 2.13% value which gives a peculiar feature to this group when compared to other Pyrenean populations. The E1f gene was seldom discovered in the samples studied. These data fill a gap in mapping the distribution of blood markers in France. On pharmacogenetics, the gene frequencies observed at the E1 locus were used for the likelihood of findings genotypes with a sensitivity to suxamethonium or other chemicals. Such a sensitivity cannot be underestimated in some groups (central part of Pyrénées, Basques). In medical practice a molecular abnormality of cholinesterase may be detected after apnea due to suxamethonium administration during anesthesia or in some cases of toxic syndromes induced by chemical compounds (agricultural or industrial products), inhibition of Cholinesterase.
Reduced plasma cholinesterase activity results in prolongation of the neuromuscolar block caused by succinylcholine and in prolonged apnoea. Cyclophosphamide administration, even at low dose, causes a prolonged fall of serum cholinesterase levels. This effect induced to take the necessary precautions in patients submitted to preoperative chemotherapy.
ChE activity was studied in a series of 193 patients of different classes of chronic hepatitis. CAH and much more cirrhosis showed a mean value significantly lower than normal controls. In CAH, no difference was found between HBsAg positive and HBsAg negative cases. Alcoholic cirrhotics had serum cholinesterase levels more lowered than non alcoholic patients. Finally, the follow-up of serum cholinesterase levels could be useful in assessing the prognosis of cirrhotic patients.
Since the chromatographic separation of cholinesterase (ChE) by Malström in 1956 many investigator studied ChE isozyme, Harris divided five spots by two dimensional paper electrophoresis and starchgel electrophoresis, and referred as C1 C2 C3 C4. Clinically, Juul separated ChE 12 bands by polyacrylamidegel electrophoresis. We separated ChE as five bands using polyacrylamidegel electrophoresis, revealing fusion and deformity of the band. Takahashi et al reported separation of band using acetyl and butyrylthiocholine as substrate. They found abnormal band in liver cirrhosis, however they have thought it acetyl cholinesterase. Hada et al revealed a defect of band II in liver cirrhosis. They investigated ChE isozyme using affinity electrophoresis with Concanavalin A (Con A) and wheat germ agglutinin (WGA). They found disappearance of band 2, Con A and WGA containing agarose gel electrophoresis seem to be useful method in differentiating liver cirrhosis from chronic hepatitis. The number of isozyme fraction exhibited a species related variations in laboratory animals. Rats, hamsters guinea pigs, rabbits, dogs, monkeys, pigs, horses and quails have 4, 3, 4, 3-5, 3, 3, 4 and 3 isozyme bands, respectively.
The authors describe a case of prolonged neuromuscular blockade following suxamethonlum in a patient with a normal cholinesterase activity and dibucaine number > or = 75%. In this case a peripheral nerve stimulator and capnography allowed neuromuscular blockade evaluation and fresh frozen plasma infusion led to a normal recovery from suxamethonium neuromuscular blockade. This report suggests a case of abnormal cholinesterase activity described as "silent variant".
A rapid method is described for the quantitative determination of cholinesterase activity in large batches of blood and brain samples. The technique is an adaptation of the Ellman procedure for a 96-well microtiter plate reader. Ten samples can be analyzed simultaneously in 5 min, with all calculations, including statistical analysis, done automatically. The method detection limit is 0.1 microM/mL/min for blood and 0.1 microM/g/min for brain samples. The procedure has been applied to the routine analyses of samples presented to the veterinary diagnostic laboratory. Method performance, quality control, and normal ranges of cholinesterase activity in livestock and other animals are described.
In toto analysis of cholinesterase activity in the cephalic extremity of 9- to 14-day old mouse embryo permits to define four different stages. Stage 1 corresponds to activity in the cephalic neural crest-derived cells. Stage 2 is characterized by activity in the proximal part of both first branchial arches and in the oculomotor blastemata. Stage 3 corresponds to a decrease of the activity, which appears in the area of fusion of several facial processes. Stage 4 corresponds to activity in nervous and muscular blastemata. Cholinesterase activity is thus chronologically varying and implies several differentiating cell populations.
Initial stages of animal poisoning with phosphacole and carbophos are accompanied by growth of erythrocytes in size and considerable changes of their surface shape, which disappear in 15 min--4 hrs regardless of the remaining cholinesterase activity inhibition. The phenomenon of erythrocytes' deformation is reproducible in in vitro experiments under the conditions of simultaneous inhibition of cholinesterase activity and exposure to acetylcholine with concentration of 1 x 10(-8) M and higher.
I present the general pattern relationship between (a) plasma fibrinogen and cholinesterase activity and (b) plasma fibrinogen and hemoglobin, in 250 and 310 hospitalized adults, respectively. Although responses of cholinesterase were often unrelated to fibrinogen, when its activity in plasma was depressed, above-normal fibrinogen concentrations were present in about 90% of the subjects. Further, despite the observed independence of hemoglobin and fibrinogen concentrations, whenever frank anemia was present (hemoglobin less than 110 to 120 g/liter), hyperfibrinogenemia was also present in about 75-85% of such anemic patients. Thus, these studies affirm that fibrinogen determination would be an appropriate component of tests on hospital admission and also that hyperfibrinogenemia is a very sensitive "acute phase" reactant, and an important reaction for gauging the course of numerous disorders.
Cetyltrimethyl ammonium and cetylpyridinium, both being cationic detergents, have been studied for their effect on the catalytic activity of horse blood serum cholinesterase (BuHChE) in reactions of hydrolysis of carbonic acid esters. It is shown that the detergents tested are reversible competitive inhibitors of the reaction of butyryl cholinesterase hydrolysis of butyryl choline, a specific cationic substrate, but in this case they activate enzymic hydrolysis of alpha-naphthylacetate, a nonspecific neutral substrate. Values of constants, describing enzyme binding with a detergent, are estimated both by the degree of inhibition of enzymatic hydrolysis of butyryl choline and by the degree of activation of enzymatic hydrolysis of alpha-naphthylacetate and are practically equal. An assumption is made that in both cases the same complex of BuHChE with a molecule of the detergent is formed. The enzyme, as a constituent of such a complex, possesses different substrate specificity as compared with the initial one.
Paraoxon (O,O-diethyl O-p-nitrophenyl phosphate) is the neurotoxic metabolite of the insecticide parathion (O,O-diethyl O-p-nitrophenyl phosphorothioate). The effects of organophosphorus compounds on peripheral synapses have been attributed to inhibition of cholinesterase and to direct actions on muscarinic and nicotinic receptors, but less is known about the actions of organophosphorus compounds, including paraoxon, in the central nervous system. We investigated initially the effects of paraoxon on spontaneous transmitter release by recording miniature postsynaptic currents (MPSCs) from cultured rat hippocampal neurons using the whole-cell mode of the patch-clamp technique. Paraoxon (0.3 microM) in the presence of tetrodotoxin (0.3 microM) and atropine (1 microM) caused a significant increase in the frequency of gamma-aminobutyric acid- and glutamate-mediated MPSCs, but did not change the peak amplitudes or decay-time constants of these MPSCs. In contrast, application of nicotinic agonists or antagonists did not change the MPSC frequency. The presynaptic effect of paraoxon shown here was not mediated by actions on muscarinic or nicotinic receptors, or by elevated acetylcholine levels secondary to inhibition of cholinesterase. In addition, agonists were applied to assess the postsynaptic effects of paraoxon on excitatory and inhibitory amino acid receptors. Paraoxon (30 microM-1 mM) blocked the ion channels of glycine, gamma-aminobutyric acidA, N-methyl-D-aspartic acid and nicotinic acetylcholine receptors, but not the ion channels of kalnate- and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptors. The combined effects of paraoxon on spontaneous transmitter release and on the functions of several ligand-gated receptors may constitute mechanisms relevant to the neurotoxicity of paraoxon.
The effects of somatosensory stimulation on the regional cerebral blood flow (rCBF) response were studied in unanesthetized monkeys before and after treatment with scopolamine and three cognitive enhancers (physostigmine, E2020 and tacrine) that inhibit cholinesterase, using 15O-labeled water and high-resolution positron emission tomography. Under control conditions, somatosensory stimulation induced a significant increase in the rCBF response in the contralateral somatosensory cortex of monkey brain. Intravenous administration of scopolamine (50 microg/kg) resulted in abolishment of the rCBF response to stimulation. The rCBF response abolished by pretreatment with scopolamine was recovered by administration of physostigmine (1 or 10 microg/kg), E2020 (10 or 100 microg/kg) or tacrine (100 or 1000 microg/kg), in a dose-dependent manner. The effect of E2020 (100 microg/kg) on the rCBF response lasted for >4 hr, whereas the effects of physostigmine and tacrine were of shorter duration. These findings suggest that these compounds reversed the scopolamine-abolished rCBF response to somatosensory stimulation via enhancement of cholinergic neurotransmission, which was mainly induced by cholinesterase inhibition.
The effects of NIK-247 on cholinesterase, scopolamine-induced amnesia and spontaneous movement were examined and compared with those of the well-known cholinesterase inhibitors tacrine and E-2020. NIK-247, tacrine and E-2020 all strongly inhibited acetylcholinesterase (AChE) in human red blood cells (IC50s = 1.0 x 10(-6), 2.9 x 10(-7) and 3.7 x 10(-8) M, respectively). In addition, NIK-247 and tacrine, but not E-2020, strongly inhibited butyrylcholinestrase (BuChE) in human serum. All three drugs produced mixed inhibition of AChE activity. Moreover, the inhibitory effect of NIK-247 on AChE was reversible. All compounds at 0.1-1 mg/kg p.o. significantly improved the amnesia induced by scopolamine (0.5 mg/kg s.c.) in rats performing a passive avoidance task. The three compounds at 1 and 3 mg/kg p.o. did not significantly decrease spontaneous movement by rats. These findings suggest that NIK-247 at a low dose (0.1-1 mg/kg p.o.) improves scopolamine-induced amnesia but does not affect spontaneous movement. The findings suggest that NIK-247 may be a useful drug for the treatment of Alzheimer's disease.
The presynaptic and antidote activity of various combinations of cholinesterase reactivators and that of muscarinic antagonist were compare it was show that the mechanism of the antidote effect of some cholinesterase reactivators in poisoning with organophosphorous compounds, in addition to restoring the activity of the enzyme, includes the effect of counteraction to the effect of muscarinic antagonists in increased acetylcholine secretion into the synaptic cleft. The expression of this effect depends on the presynaptic activity of the reactivator and on the selectivity of muscarinic antagonist. It is suggested that the type relation of the presynaptic muscarin receptors in the cerebral hemispheres and the brain stem is different and that the probability of the functional value of the ligand presynaptic interaction for the protection from organophosphorous compounds is higher in the brain higher in the brain stem than in the cerebral hemispheres of rats.
Cerebrospinal fluid cholinesterase activity was determined in 5 species of domestic animals. Suitable samples of cerebrospinal fluid could be obtained repeatedly from sheep, calves, and dogs without killing, but not from pigs and rabbits. The cholinesterase activity among erythrocytes, plasma, and cerebrospinal fluid of these species was also compared statistically.