Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of the acetylated derivative of HC-3 (acetylsecohemicholinium; AcHC-3) have been studied at cholinergic nerve terminals and compared with the effects of the parent compound. AcHC-3 blocked neuromuscular transmission in nerve-muscle preparations; it was shown to be less effective than HC-3 in producing a pre-junctional block in the rat diaphragm but was more effective than HC-3 in eliciting a post-junctional blocking effect in the chick biventer muscle. On the frog rectus abdominis muscle AcHC-3 caused a substantial potentiation of the contractures elicited by acetylcholine but did not by itself cause a contracture of the muscle. AcHC-3 inhibited the synthesis of acetylcholine by cholinergic nerve ending particles and inhibited the uptake of [14C]choline into brain synaptosomal fractions to a similar extent to HC-3. AcHC-3 was shown to be a substrate for cholinesterase enzymes although the rate of hydrolysis was much less than the rate of hydrolysis of acetylcholine. It is concluded that AcHC-3 is effective in inhibiting cholinergic transmission and this action is exerted by the open chain (seco) compound and is not due to the hydrolysis of the AcHC-3 by cholinesterases to form the active HC-3 molecule.
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PMID:Some pharmacological actions of acetylsecohemicholinium. 2 42

The effects of pyridostigmine pretreatment on the neuromuscular blockade produced by soman in anaesthetized, atropinized animals have been studied on the soleus and anterior tibialis muscle (rhesus monkeys, cats and rabbits) and the gastrocnemius muscle (guinea-pigs and rats). Pyridostigmine pretreatment produced a complete recovery of neuromuscular function following blockade by soman; the rate of recovery was similar in all the species, suggesting a common mechanism of action. In the absence of pyridostigmine or if pyridostigmine was delayed until after blockade by soman, there was no recovery of neuromuscular function. Detailed studies in the guinea-pig showed that the recovery of neuromuscular function was related to the dose of soman and to the degree of carbamoylation of blood cholinesterase at the time of nerve agent challenge, i.e. to the dose of pyridostigmine and the time interval between the administration of pyridostigmine and soman. It is suggested that the effectiveness of pyridostigmine pretreatment is due to the carbamoylation of a portion of the tissue acetylcholinesterase, which protects it against irreversible inhibition by soman: after poisoning spontaneous decarbamoylation produces sufficient free acetylcholinesterase to restore normal function.
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PMID:Effectiveness of pyridostigmine in reversing neuromuscular blockade produced by soman. 2 7

The effect of physostigmine has been studied on cholinesterase in homogenates of chick biventer cervicis muscles and on the contractile responses of the intact muscles to acetylcholine and carbachol. The concentration of physostigmine required to produce the maximum increase in sensitivity to acetylcholine almost completely inhibited the cholinesterase in muscle homogenates. This concentration of physostigmine had no effect on muscle contractures elicited by carbachol. By taking account of the combined effects of acetylcholine diffusion and enzymic hydrolysis, a quantitative theoretical relationship has been derived between the level of cholinesterase activity in cylindrical muscles and the fractional occupancy of the acetylcholine receptors in these muscles in the presence of different concentrations of exogenous acetylcholine. This theory attributes the thousand-fold increase in sensitivity to exogenous acetylcholine produced by anticholinesterases in chick biventer cervicis muscles largely to an alteration in acetylcholine concentration gradient within the muscle and accounts satisfactorily for the shift in the dose-response curve for acetylcholine which occurs after treatment of the muscles with various concentrations of physostigmine.
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PMID:The relationship between cholinesterase inhibition in the chick biventer cervicis muscle and its sensitivity to exogenous acetylcholine. 2 8

Acetic acid was found to repress cholinesterase synthesis in the cells of Arthrobacter simplex var. cholinesterasus even at very low concentrations (0.1%). The repression is very stable. It is not eliminated by glucose or an organic acid of the Krebs cycle being added to the medium with acetic acid. The combination of acetic and butyric acids decreases the repression but does not eliminate it. The kinetics of cholinesterase synthesis was different in the cells grown on the medium with acetic acid and the cells cultivated on the medium with acetic acid and glucose, then washed and transferred to a fresh growth medium with glucose and acetylcholine as the sources of carbon.
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PMID:[Acetic acid, a catabolite repressor of cholinesterase synthesis by an Arthrobacter simplex culture]. 2 5

The total and free acetylcholine (Ach) and cholinesterase (CHE) content of adult Setaria cervi were estimated. The Ach was estimated by bioassay on rectus abdominis muscle of frog and the CHE by measuring the drop in pH following incubation of worm homogenate with Ach chloride. The free and total Ach contents (4.0 +/- 0.57 and 6.0 +/- 0.48 microgram/g wet weight of worms respectively) were as high as found in mammalian brain cortex. The cholinesterase activity was found to be 5.57 +/- 0.6 units/g wet weight of worms. It is possible that there may exist a well developed system responsible for the synthesis, storage, release and destruction of Ach and that Ach may be acting as an excitatory neurohormone in S. cervi.
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PMID:Acetylcholine: a possible neurotransmitter in Setaria cervi. 2 90

The in vitro effect of ten benzodiazepine derivatives on the cholinesterases of human plasma and red cells was determined. Flurazepam, temazepam, lorazepam, flunitrazepam and diazepam had an inhibitory effect on plasma cholinesterase of 60--90 per cent and, with the exception of lorazepam, an inhibitory effect of 40--50 per cent on red cell cholinesterase. Clonazepam, oxazepam, chlordiazepoxide, nitrazepam and bromazepam had comparatively minor effects on both enzymes
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PMID:Effect of benzodiazepine derivatives on human blood cholinesterase in vitro. 2 27

A diagnostic dip-stick for measuring pseudocholinesterase activity has been assessed by 4 participants and compared with a standard spectrophotometric method. Duplicate dip-stick estimations (measured in kU/l) corresponded closely, and concurrence between participants was good. The dip-stick estimate of cholinesterase was consistently lower than the spectrophotometric value; the magnitude of this deviation depended on the absolute enzyme activity. With enzyme activities of up to 1 kU/l the dip-stick value was 1 unit lower. Between 1 and 4 kU/l the dip-stick estimate compared well with the spectrophotometric value. From 5 to 7 kU/l and beyond 7 kU/l the negative deviation recorded by the dip-stick increased to 2 units or more. Normal enzyme activity is 3 - 6 kU/l. Over the 1 - 4 kU/l range the method is most accurate, thus negative deviation below 1 kU/l or above 4 kU/l is generally diagnostically irrelevant. On the basis of cost, convenience, speed and accuracy this method will suffice in the absence of sophisticated assay facilities.
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PMID:Assessment of a diagnostic dip-stick for assaying plasma or serum pseudocholinesterase activity. 2 48

The anticholinesterase (antiChE) activity of haloperidol, droperidol and trifluperidol was studied by employing dog plasma as a cholinesterase source and changes in arterial blood pressure, elecited by a mixture of acetylcholine (Ach) and dog plasma with or without those drugs, as an indicator of their antiChE activity. When butyrophenones were present in concentrations of 0.5 up to 5 X 10(-4)M in plasma containing Ach the hypotensive effect of the latter was preserved. Such findings provide experimental evidence that butyrophenones may exert antiChE activity.
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PMID:Anticholinesterase activity of some butyrophenones. 3 Apr 21

Following intravenous administration of the cholinesterase reactivator HS-6 (30 mg/kg), blood pressure fell (up to 50 mmHg) and maximal blood levels of HS-6 reached 242 microgram/ml. HS-6 attenuated the pressor response resulting from carotid occlusion and the depressor effect of vagal stimulation. Doses of HS-6 below those used to protect against soman in different animal species (10--30 mumol/kg) progressively blocked the ganglion-stimulating effects of nicotine and dimethylphenylpiperazinium but not the pressor effect following adrenaline, a pattern similar to that produced by hexamethonium but only 1/84 as potent. HS-6, like hexamethonium and mecamylamine, progressively blocked the contraction of the nictitating membrane of the cat resulting from preganglionic stimulation. The results indicate that HS-6 possesses ganglion-blocking properties at doses likely to be used in the protection against soman poisoning. The ganglion-blocking properties of the drug may be a factor in the beneficial effects of HS-6.
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PMID:The ganglionic blocking properties of the cholinesterase reactivator, HS-6. 3 May 27

Psychotropic drugs such as the phenothiazine neuroleptics and tricyclic antidepressants are known to cause electrocardiographic abnormalities as well as a central anticholinergic syndrome. Physostigmine is known to reverse the central muscarinic anticholinergic manifestations by inhibition of the enzyme cholinesterase. An unusual case of trifluoperazine overdose, in which the patient presented with cardiac arrhythmias and a central anticholinergic syndrome, is presented. Treatment with physostigmine reversed the central anticholinergic syndrome as well as the electrocardiographic abnormalities. Effects of phenothiazines on altering cardiac status are also discussed.
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PMID:Physostigmine for cardiac and neurologic manifestations of phenothiazine poisoning. 3 May 64


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