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

Plasma sodium, potassium, bicarbonate, calcium, magnesium, pseudocholinesterase, amylase and alkaline phosphatase were estimated in 43 cases of country-liquor poisoning and 29 normal controls. In the poisoned subjects, plasma potassium, magnesium and amylase levels were elevated, while plasma bicarbonate levels were diminished; and plasma pseudocholinesterase and alkaline phosphatase were not affected. Plasma calcium and pseudocholinesterase were elevated in poisoned patients who recovered; however, these were diminished in fatal cases. Plasma bicarbonate and amylase were affected depending upon the severity of poisoning.
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PMID:Plasma electrolytes and enzymes in country liquor poisoning. 715 40

The innervation of human lower respiratory tract was studied with special emphasis on airways with sodium-potassium glyoxylic acid (SPG) and acetylcholinesterase (AChE) methods to demonstrate catecholamine-containing and acetylcholinesterase-containing nerve fibers. AChE-method revealed a rich network of cholinesterase positive nerves both inside the bronchial glands where they run around and between the acini, and the airway smooth muscle from secondary bronchi to terminal bronchioli. No AChE-positive fibers were found in connection with the blood vessels or within the epithelium of bronchi or bonchioli. The AChE-positive nerve fibers in bronchial smooth muscle greatly outnumbered those containing catecholamine. The SPG-method revealed the presence of adrenergic nerves from the level of secondary bronchi to that of terminal bronchioli. These nerve fibers were most abundant in bronchial glands, where their amount was equal and distribution similar to those of AChE-containing nerve fibers. Outside the glands adrenergic fibers were constantly seen in connection with the bronchial blood vessels in connective tissues surrounding bronchi. A few nerve fibers were also present in airway smooth muscle from the secondary bronchi to terminal bronchioli.
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PMID:Catecholamine- and acetylcholinesterase-containing nerves in human lower respiratory tract. 716 Nov 45

To prevent crash-related death and injury among spray pilots, a program including pre-crash, crash and post-crash stages of intervention for aircraft, physical environment, and pilots and ground crews was proposed in accordance with a matrix of options derived from road crash epidemiology. In addition to the dangers of fixed obstacles, low-altitude runs, and heavy work schedules, work hazards included combined exposures to noise, vibration, G forces, heat stress, pesticides, and dehydration. Together, these exposures were believed to have produced slight, but crucial decreases in pilot performance, alertness and skill. For aircraft, the major pre-crash measure was cockpit air cooling, with filter technologies to prevent in-flight pesticide exposure. Crash and post-crash design changes to reduce energy transfers to the pilot's body (thermal, kinetic) were the most important recommendations, because absolute prevention of the crash event was unlikely. For the environment, pre-crash recommendations included marking fixed obstacles, such as power and telephone lines, but preferably their elimination. Other measures included drainage pits with sodium hydroxide points to neutralize parathion and prevent dispersion of parathion-containing mists. Pilot pre-crash measures (more fluid intake, biological monitoring--EMG, urinary alkyl phosphate, cholinesterase testing) required special organizational arrangements. Systematic application of options from the foregoing matrix suggest that the high risk of death and injury from aerial spraying is unnecessary.
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PMID:Death and injury in aerial spraying: pre-crash, crash, and post-crash prevention strategies. 721 90

Five differential inhibitors of plasma cholinesterase have been compared using benzoylcholine as substrate. None of the inhibitors (dibucaine, NaF, NaBr, NaCl, or pancuronium dibutyryloxy bromide) could be used singly to resolve all the variants. Better resolution was obtained when two inhibitors were used in conjunction. Clear differentiation of all six genotypes was obtained only with the combined use of pancuronium dibutyryloxy bromide and sodium fluoride. The limitations of some of the parameters are discussed.
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PMID:A comparison of some methods of phenotyping the plasma cholinesterase variants using benzoylcholine as substrate. 725 66

PC12, a clonal line of rat pheochromocytoma, synthesizes, stores, and secretes dopamine and acetylcholine. The cells take up choline by a saturable process and rapidly convert the accumulated choline to acetylcholine. This choline transport has a Km of 12 microM, is Na+ and energy independent, and is relatively insensitive to hemicholinium-3 (IC50 approximately 50 microM). Different ionic conditions can modulate the choline transport. Uptake was increased by pretreatment with 55 mM K+ whereas it was decreased in the presence of 55 mM K+. Choline uptake had similar characteristics in PC12 cells that had been induced to extend neurites by treatment with nerve growth factor. In undifferentiated PC12 cells, storage of newly synthesized acetylcholine was found in bound and free compartments as evidenced from subcellular fractionation. The free pool had a faster turnover rate. Most of the newly synthesized acetylcholine was rapidly degraded in the absence of a cholinesterase inhibitor while continuous incubation with labeled choline resulted in a slow incorporation of newly labeled acetylcholine into a bound pool. The accumulation of acetylcholine in the bound pool, but not acetylcholine synthesis, was inhibited by each of several agents that are known to interfere with the generation or maintenance of proton electrochemical gradients. The newly synthesized acetylcholine could be released from PC12 cells by incubation of the cells with 55 mM K+. These properties indicate that PC12 cells are a good system for studying acetylcholine metabolism by secretory cells.
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PMID:Choline and acetylcholine metabolism in PC12 secretory cells. 728 37

The anti-cholinesterase factor from Naja naja atra venom was purified by means of successive column chromatography on Sephadex G-75, carboxymethyl-cellulose and hydroxyapatite. The purified anti-cholinesterase factor was homogeneous by sodium dodecyl sulfate polyacrylamide gel electrophoresis. The molecular weight was estimated to be approx. 50 000. The isoelectric point was determined to be 6.8. This factor was found to be the first cholinesterase inhibitor protein. We have called this anti-cholinesterase factor atramine.
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PMID:Purification and characterization of anti-cholinesterase factor from the venom of Naja naja atra. 739 18

Some patients present prolonged apnea following the administration of succinylcholine because of substantial portion of plasma cholinesterase (the enzyme responsible for the hydrolysis of this muscle relaxant) is present as an atypical variant. Up to the present four types of cholinesterase genes are known which combination can cause apnea to a greater or less extent. Silent homozygous EsEs present apnea of greatest duration due to the complete absence of cholinesterase activity. The case reported belongs to a family of four members and is an example of this extremely uncommon genetic variant, with a frequency of 1/170.000. To determine total cholinesterase activity genetic typing of the whole family was carried out utilizing the spectrophotometric technique of Szasz and Knedel with butirylthiocholine iodide as substrate. Inhibition studies were performed using benzoylcholine and dibucaine, sodium fluoride, scholine, and sodium chloride as inhibitors.
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PMID:[A rare case of silent cholinesterase genetic variant (author's transl)]. 743 39

The effects of intracerebroventricular (i.c.v.) injection of physostigmine and hemicholinium-3 (HC-3) on reflex bradycardia and tachycardia have been studied in unanesthetized rats. The reflex increases and decreases in heart rate were elicited by i.v. injection of norepinephrine and sodium nitroprusside, respectively. Physostigmine (5-10 micrograms) increased basal mean arterial pressure (MAP), reduced basal heart rate (HR), enhanced the reflex bradycardia and reduced reflex tachycardia. Physostigmine did not modify either the pressor effect of norepinephrine, the depressor effect of sodium nitroprusside or the responsiveness of peripheral muscarinic receptors. Pretreatment (i.c.v.) with atropine (0.3 micrograms) completely abolished the effect of physostigmine on MAP, HR, reflex bradycardia and reflex tachycardia. Pretreatment (i.c.v.) with mecamylamine (50 micrograms) did not modify the effect of the cholinesterase inhibitor on MAP, HR and reflex tachycardia, but inverted its effect on reflex bradycardia. Injection of HC-3 (20 micrograms i.c.v.) did not modify MAP, but reduced HR and inhibited both reflex bradycardia and reflex tachycardia. The HC-3 bradycardic effect started within minutes and lasted for about 1 hr, while the depressor effect on the reflexes began only after 15 min and continued for several hours. In addition, i.c.v. pretreatment with HC-3 completely abolished all the effects of physostigmine on MAP, HR, reflex bradycardia and reflex tachycardia. These results suggest that brain acetylcholine has a modulatory effect on baroreceptor reflexes. This modulation operates through muscarinic receptors in reflex tachycardia and through both muscarinic and nicotinic receptors in reflex bradycardia.
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PMID:Modulatory effect of brain acetylcholine on reflex-induced bradycardia and tachycardia in conscious rats. 744 97

We studied the effects on 25 analytes of duration of contact of serum with non-anticoagulated blood and of temperature. Serum was separated after blood was allowed to stand, for 0, 2, 4, 6, 8, 24, or 48 h at 4, 23, or 30 degrees C. Results obtained for bilirubin, albumin, zinc sulfate turbidity, thymol turbidity, cholinesterase (EC 3.1.1.8), alkaline phosphatase (EC 3.1.3.1), leucine aminopeptidase (EC 3.4.11.1), amylase (EC 3.2.1.2), total cholesterol, triglycerides, beta-lipoprotein, serum urea nitrogen, creatinine, uric acid, and gamma-glutamyltransferase (EC 2.3.2.2) were not influenced by storage at 4, 24, or 30 degrees C for as long as 48 h. Negligible differences were seen for potassium in sera in contact with cells as long as 24 h at 23 degrees C and for inorganic phosphorus after 48 h at 4 degrees C. However, at 4 degrees C we noted an increase at 8 h, a slight decrease at 30 degrees C. Statistically significant changes were seen for total protein and calcium after 48 h at 30 degrees C; for aspartate aminotransferase (EC 2.6.1.1), and alanine aminotransferase (EC 2.6.1.2), between 8 and 24 h at 23 degrees C and as soon as 6 h at 30 degrees C; for lactate dehydrogenase (EC 1.1.1.27) after 8 h at 30 degrees C and between 8 and 24 h at 23 degrees C; for glucose at 24, 4, or 2 h of storage at 4, 23, or 30 degrees C, respectively; for inorganic phosphorus after 48 h at 23 degrees C or 8 h at 30 degrees C; for potassium after 4 h at 4 degrees C or 24 h at 30 degrees C; and for sodium after 48 h at 4 degrees C or 6 h at 23 or 30 degrees C.
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PMID:Serum-constituents analyses: effect of duration and temperature of storage of clotted blood. 744 20

Endogenous digitalis-like factor (EDLF), an inhibitor of membrane Na+/K(+)-ATPase, is discussed to be involved in the pathogenesis of cirrhogenic portal hypertension, ascites formation and development of functional hepatorenal failure. Therefore, we investigated the serum content of this mediator in patients with liver cirrhosis Child-Pugh stage A, B, and C (n = 27) by means of enzyme immunoassay with a specific digoxin antibody. Furthermore, a correlation analysis was performed in order to find out correlations between signs of cell injury, cholestasis, synthetic cell function, ascites formation, and hepatorenal failure. Our results demonstrate that EDLF is significantly elevated in Child C cirrhosis (0.61 +/- 0.15 ng/ml) in comparison to Child A cirrhosis (0.013 +/- 0.2 ng/ml) and is also higher than in Child B cirrhosis (0.23 +/- 0.25 ng/ml). In patients without ascites EDLF (0.056 +/- 0.19 ng/ml) differs significantly from that of patients with non-complicated ascites (0.156 +/- 0.176 ng/ml) and from that of patients with therapy refractory ascites (0.66 +/- 0.17 ng/ml) or hepatorenal failure (1.56 ng/ml). There are no correlations between EDLF and renal function. Significant correlations were demonstrated for cholestasis (serum bilirubin), synthesis function (serum protein, Quick's value, cholinesterase, fibrinogen, albumin), and the degree of portasystemic encephalopathy (number connection test). We conclude that EDLF may act as a mediator in the process of progressive portal hypertension and its complications due to cirrhosis. This process of progression is caused by the inhibition of Na+/K(+)-ATPase, vasoconstriction, and endothelin secretion.
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PMID:[Endogenous digitalis-like factor in liver cirrhosis and cholestasis]. 748 6


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