Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

We have evaluated the effect of acute administration of pyridostigmine bromide, a cholinesterase inhibitor, on the GHRH-induced GH rise in 11 obese children and in 8 age-matched controls. The GH response to GHRH (hpGRF 1-40, 1 microgram/kg iv), evaluated both as maximum GH peak and as integrated area under the curve, was significantly lower in the obese children than in the controls. Pretreatment with pyridostigmine bromide (60 mg orally 60 min before the GHRH injection) significantly increased both baseline GH levels and the GH response to GHRH in all the obese subjects, so that their mean baseline GH, peak GH levels and integrated area under the curve after pyridostigmine bromide plus GHRH were similar to those of the control children after GHRH. Also in control children pyridostigmine bromide increased (though not significantly) baseline GH levels. and caused a significant augmentation of the GH response to GHRH. Mean peak GH levels and mean integrated area under the curve after pyridostigmine bromide plus GHRH were significantly higher in the controls than in the obese children given the same treatment. Mean baseline Sm-C levels were significantly higher in the obese than in control children. These data show that enhancement of cholinergic neurotransmission, likely in the hypothalamus, counteracts the blunted GH response to GHRH present in the obese children, and that in simple obesity the potential of the pituitary to make a secretory response to a direct GH secretagogue is preserved.
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PMID:Pyridostigmine counteracts the blunted growth hormone response to growth hormone-releasing hormone of obese children. 249 49

To determine if alterations in muscle morphology occur after subchronic oral administration of pyridostigmine bromide, rats were fed 90 mg/kg continuously in meal and examined at 1, 2, 4, 7, and 15 days. Within the first day, cholinesterase activity was reduced by 87% and remained inhibited by 74-91% for the entire course of the feeding. Light microscopy demonstrated that by the first day approximately 1 in 100 myofibers was shrunken and contained centralized nuclei. Electron microscopic examination showed that while presynaptic areas of neuromuscular junctions were relatively unaffected by this dose, postsynaptic areas invariably showed maximal changes. Ultrastructural alterations included disruption of myofilaments, mitochondrial changes consistent with accumulation of calcium, and nuclear alterations. These effects appeared not to be cumulative and were greatly diminished by 15 days even under constant drug administration and inhibition of cholinesterase activity. We conclude that subchronic feeding of pyridostigmine bromide induces primarily myopathic rather than neurogenic changes in the diaphragm and that some mechanism of accommodation may be activated that minimizes continued muscle injury.
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PMID:Myopathic changes in diaphragm of rats fed pyridostigmine bromide subchronically. 276 51

The effect of chemical modification on the pseudocholinesterase and aryl acylamidase activities of purified human serum pseudocholinesterase was examined in the absence and presence of butyrylcholine iodide, the substrate of pseudocholinesterase. Modification by 2-hydroxy-5-nitrobenzyl bromide, N-bromosuccinimide, diethylpyrocarbonate and trinitrobenzenesulfonic acid caused a parallel inactivation of both pseudocholinesterase and aryl acylamidase activities that could be prevented by butyrylcholine iodide. With phenylglyoxal and 2,4-pentanedione as modifiers there was a selective activation of pseudocholinesterase alone with no effect on aryl acylamidase. This activation could be prevented by butyrylcholine iodide. N-Ethylmaleimide and p-hydroxy-mercuribenzoate when used for modification did not have any effect on the enzyme activities. The results suggested essential tryptophan, lysine and histidine residues at a common catalytic site for pseudocholinesterase and aryl acylamidase and an arginine residue (or residues) exclusively for pseudocholinesterase. The use of N-acetylimidazole, tetranitromethane and acetic anhydride as modifiers indicated a biphasic change in both pseudocholinesterase and aryl acylamidase activities. At low concentrations of the modifiers a stimulation in activities and at high concentrations an inactivation was observed. Butyrylcholine iodide or propionylcholine chloride selectively protected the inactivation phase without affecting the activation phase. Protection by the substrates at the inactivation phase resulted in not only a reversal of the enzyme inactivation but also an activation. Spectral studies and hydroxylamine treatment showed that tyrosine residues were modified during the activation phase. The results suggested that the modified tyrosine residues responsible for the activation were not involved in the active site of pseudocholinesterase or aryl acylamidase and that they were more amenable for modification in comparison to the residues responsible for inactivation. Two reversible inhibitors of pseudocholinesterase, namely ethopropazine and imipramine, were used as protectors during modification. Unlike the substrate butyrylcholine iodide, these inhibitors could not protect against the inactivation resulting from modification by 2-hydroxy-5-nitrobenzyl bromide, N-bromosuccinimide and trinitrobenzenesulfonic acid. But they could protect against the activation of pseudocholinesterase and aryl acylamidase by low concentrations of N-acetylimidazole and acetic anhydride thereby suggesting that the binding site of these inhibitors involves the non-active-site tyrosine residues.
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PMID:Chemical modification of the bifunctional human serum pseudocholinesterase. Effect on the pseudocholinesterase and aryl acylamidase activities. 286 42

Three patients with chronic obstructive lung disease (COPD) and myasthenia gravis whose pulmonary symptoms were worsened by therapy with cholinesterase inhibitors were improved by inhaled ipratropium bromide. Two had increases in FEV1 (19 percent, 35 percent) and specific conductance (106 percent, 81 percent) and reductions in dyspnea. The third had no change in airflow with ipratropium, but improved due to decreased bronchial secretions which had limited the use of cholinesterase inhibitors. In contrast, beta agonist bronchodilators had no effect in any of these patients. This experience suggests that ipratropium may be the bronchodilator drug of choice in patients with obstructive lung disease aggravated by cholinesterase inhibitors.
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PMID:Ipratropium in patients with COPD receiving cholinesterase inhibitors. 296 27

It is known that in normal subjects repeated administration of the growth hormone-releasing factor (GRF) induces a state of partial refractoriness of the somatotropes to GRF. Studies were conducted to verify whether the cholinergic system plays a role in the mechanism(s) underlying the reduced GH responsiveness to the neuropeptide. In five healthy men, the GH response to three consecutive injections of GRF (50 micrograms iv), administered at 2 h intervals, was considerably blunted after the second and third GRF bolus. Administration of the inhibitor of cholinesterase, pyridostigmine bromide (120 mg orally) 30 min before the second GRF bolus, not only restored but greatly potentiated the GH responsiveness to the second GRF bolus. The GH response to the third GRF bolus was not apparently influenced by pre-treatment with pyridostigmine. These data reinforce the view that cholinergic neurotransmission plays an important role in the control of GH secretion in human.
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PMID:Potentiation of cholinergic tone by pyridostigmine bromide re-instates and potentiates the growth hormone responsiveness to intermittent administration of growth hormone-releasing factor in man. 302 Aug 50

Electron microscopical localization of non-specific cholinesterase activity was studied in the encapsulated part of rat hindlimb muscle spindles. After incubation of the muscle tissue in a medium containing butyrylthiocholine bromide as substrate and BW284c51 as the specific inhibitor of acetylcholinesterase, a distinct electron-dense precipitate corresponding to non-specific cholinesterase activity was found along the whole length of muscle spindles. The richest source of non-specific cholinesterase activity were the motor end-plates present in the polar and juxtaequatorial regions. Much smaller amounts of reaction deposits were found at the secondary sensory terminals in the juxtaequatorial zones. The primary sensory terminals in the equatorial zone contained only low amounts of the reaction product. A fine homogeneous reaction product was localized in the narrow spaces between Schwann cell processes or in gaps between the Schwann cell, and axonal and muscle membranes. A granular precipitate was localized on the basal lamina in the synapse region of motor terminals or covering Schwann cell processes and sensory terminals with adjacent intrafusal muscle fibres. Our results suggest that most of non-specific cholinesterase in muscle spindles is synthesized by the Schwann cells; but a small amount can also be synthesized by fibroblast-like cells forming the inner capsule of muscle spindles. Non-specific cholinesterase thus coexists with acetylcholinesterase at motor end-plates, but is single at sensory terminals. The function of non-specific cholinesterase in sensory receptors is still not clear. It seems most probable that non-specific cholinesterase in muscle spindles may play a role in the maintenance of the external milieu around nerve endings, especially in the sensory region.
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PMID:Ultrastructural localization of non-specific cholinesterase activity in rat muscle spindles. 312 47

(-)-N1-Benzylnorphysostigmine (4), prepared from synthetic (-)-O-methyl-N1-noreseroline (1) by N-benzylation, ether cleavage, and reaction of (-)-N1-benzylnoreseroline (3) with methyl isocyanate, was the intermediate used to prepare the title compounds. Catalytic debenzylation of 4 afforded (-)-N1-norphysostigmine (5), and (-)-eseramine (6) was obtained by reaction of 5 with methyl isocyanate. Reductive N-methylation of 5 gave (-)-physostigmine (9) while reaction of 5 with allyl bromide and phenethyl bromide afforded carbamates 7 and 8, respectively. Data on the in vitro potencies (IC50) and activities of certain of these compounds (4-8) as inhibitors of electric eel acetyl cholinesterase are reported. (-)-N1-Norphysostigmine (5) was found to be similarly potent against AChE as (-)-physostigmine (9).
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PMID:Synthesis and anticholinesterase activity of (-)-N1-norphysostigmine, (-)-eseramine, and other N(1)-substituted analogues of (-)-physostigmine. 319 22

An estimate of the amplitude of respiratory sinus arrhythmia (V) has been proposed as a noninvasive measure of parasympathetic activity. This experiment monitored V in response to a subclinical dose of pyridostigmine bromide (PYR) and a pharmacological challenge of atropine sulfate (ATR). Twelve male rhesus macaques received 200 micrograms/kg of PYR 30 min prior to an injection of 0, 14, 44, or 140 micrograms/kg ATR. The decrease in V after both the 44 and 140 micrograms/kg ATR doses was similar to the response to ATR alone in a previous experiment. The 14 micrograms/kg dose of ATR did not significantly decrease V in this experiment, which is in contrast with the large decrease of V after ATR alone in a previous experiment. Neither drug affected respiration. The dose of ATR which would be effective in causing a 30% decrease of V in the presence of PYR was estimated to be 18.3 micrograms/kg of ATR. This is twice the dose of ATR calculated to have the same effect without PYR. The attenuated response of V after a pharmacological challenge of ATR may be used to quantify the latent muscarinic effects from exposure to anticholinesterase agents. The attenuated response to ATR may also be useful for evaluating the return of normal cholinergic function after disruption by cholinesterase inhibitors.
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PMID:Quantifying the altered cardiac response to atropine following pyridostigmine in rhesus macaques. 324 15

The effects on vision of ingestion of the anticholinesterase pyridostigmine bromide (60 mg), assessed from pharmacokinetic data to provide at least 20% inhibition of blood cholinesterase over the 1 1/2-4 1/2 h experimental period, was compared with 60 mg lactose in a double-blind crossover protocol. Contrast sensitivity to stationary oscilloscope-generated gratings of 3-40 c/deg showed a small but significant increase of 7% which was consistent with a small reduction in pupil diameter, surmised to cause a small improvement in optical quality. This reduction in pupil diameter was, however, overshadowed by a larger though still non-significant reduction on the second visit to the laboratory compared with the first. Contrast sensitivities to laser interference fringes observed in the Maxwellian view, by which the effects of the optical media are essentially bypassed, thus providing an entirely neural assessment, were unchanged after pyridostigmine. It is concluded that pyridostigmine may be given as a prophylactic in anticipation of exposure to an organophosphorus anticholinesterase without a deleterious effect on stationary visual function.
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PMID:The effects of ingestion of 60 mg pyridostigmine bromide on contrast sensitivity in man. 341 Apr 84

The effect of ethidium bromide (3,8-diamino-5-ethyl-6-phenyl-phenanthridinium bromide) on the activity of purified horse serum butyrylcholinesterase in vitro has been studied. Ethidium bromide is a middle reversible inhibitor with complex mixed competitive-noncompetitive inhibition kinetics. The inhibitor is bound to the anionic site of the enzyme surface.
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PMID:Inhibition of the butyrylcholinesterase by ethidium bromide. 344 3


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