Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The blood esterase mediating the hydrolysis of esmolol was characterized in several different species including man. In contrast to most ester-containing drugs, hydrolysis of esmolol was mediated by an esterase in the cytosol of red blood cells (RBC) in man and dogs and not in plasma or RBC membrane. Species differences in the esterase activity existed. Guinea pig and rat blood esterase activities were much greater than those in the dog followed by those in man. In addition, the esterase activity in rat and guinea pig blood was localized in plasma and not in RBC. Purified human serum cholinesterase, human RBC membrane acetylcholinesterase, human hemoglobin, human carbonic anhydrases A and B, and human and dog serum albumin were all inactive against esmolol. Esmolol esterase activity in human and dog blood was inhibited by sodium fluoride, EDTA, and p-hydroxymercuribenzoate, but not by echothiophate, eserine, and acetazolamide. In contrast, echothiophate and sodium fluoride, but not eserine, inhibited the esterase activity in rat and guinea pig plasma. Metabolic interaction studies indicated that acetylcholine, succinylcholine, procaine, and chloroprocaine did not interfere with the metabolism of esmolol by human and dog blood. Based on the results, it appeared that an arylesterase in human and dog RBC cytosol mediated the hydrolysis of esmolol while an aliphatic esterase mediated the hydrolysis of esmolol in guinea pig and rat plasma.
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PMID:Biochemical properties of blood esmolol esterase. 286 4

The effects of t-butylhydroperoxide (tBHP), its alkoxyl radical (tBuO.) and its peroxyl radical (tBuOO.) in model systems and on red blood cells were studied. Glyceraldehyde-3-phosphate dehydrogenase was strongly inhibited by tBHP via a direct reaction of the hydroperoxide with an essential sulfhydryl group in the enzyme molecule. Several other enzymes were unaffected by tBHP. Alcohol dehydrogenase was strongly inhibited by tBuO. but was much less sensitive to tBuOO.. Lysozyme, lactate dehydrogenase and trypsin, on the other hand, were very sensitive to the peroxyl and not, or much less, to the alkoxyl radical, whereas acetylcholinesterase was very sensitive to both radicals. tBuOO. caused covalent binding of tryptophan, tyrosine, histidine and methionine to serum albumin. The corresponding alkoxyl radical was ineffective in this respect. Conversely, tBuO. caused peroxidation of linolenic acid, whereas tBuOO. did not. Incubation of human erythrocytes with tBHP caused lipid peroxidation and K+ leakage. Both effects were caused by tBHP-derived radicals generated in a reaction of the hydroperoxide with hemoglobin. With radical scavengers it was possible to dissociate tBHP-induced lipid peroxidation and K+ leakage, demonstrating that these two processes are not causally related. Experimental results indicate that tBuO. causes lipid peroxidation, whereas tBuOO. is responsible for K+ leakage.
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PMID:Inhibition of enzymes and oxidative damage of red blood cells induced by t-butylhydroperoxide-derived radicals. 293 Jul 85

Biochemical and hemodynamic changes were assessed in 13 dogs subjected to sub-coronary valvular aortic stenosis and chronic protein-calorie malnutrition (PCM). Red blood cell, hemoglobin, serum albumin, free fatty acids, blood glucose, cholinesterase and blood amino acid levels were measured. The dynamic geometry of the left ventricle (LV) was assessed with chronically implanted sonomicrometric piezoelectric crystals. Cardiac function was evaluated by mean velocity of circumferential fiber shortening (mean VcF) and the relationship between LV end-systolic pressure (LVESP) or LV wall stress (LVWst) and LV end-systolic diameter (LVESD). The following results were obtained: A decrease in body weight and increases in free fatty acids and 3-Methylhistidine were observed following long-term PCM. Mean VcF was not depressed in dogs subjected to PCM. The relationship between LVESP or LVWst and LVESD shifted downward and to the right after PCM, indicating reduced myocardial contractility. These findings suggest that the left ventricle in hypertrophied dog hearts subjected to PCM retains normal pump function, despite a low state in the myocardium.
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PMID:Biochemical and hemodynamic changes in the hypertrophied dog heart subjected to chronic protein-calorie malnutrition. 295 29

Thyroid function was studied in 40 patients with chronic heart failure. Thyroid antibodies and microsome antibodies were negative in all cases. Serum T4, and T3 concentrations showed significant inverse correlation with cardiothoracic ratio, mean right atrial pressure, pulmonary artery systolic pressure, and peripheral venous pressure. Serum T4, T3 concentrations showed significant correlation with PaO2, serum albumin, and serum cholinesterase. Serum TSH concentrations increased with increasing cardiothoracic ratio. Histological examinations showed fibrosis and atrophy of the thyroid gland in 2 cases. These findings suggest the possible development of primary hypothyroidism as a result of chronic heart failure.
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PMID:Primary hypothyroidism in severe chronic heart failure. 296 70

The in vivo effect of dimethoate and deltamethrin on body and organ weights, serum proteins and on plasma acetylcholinesterase (AChE), aromatic esterase and ATPase were examined in growing male rabbits throughout five months period. Both compounds had no significant effect on body weight; however, adrenal, testis & pituitary weights decreased (P less than 0.01); the liver and spleen weights increased (P less than 0.01) in a dose dependent manner. Serum total proteins and globulin decreased (P less than 0.01) in a dose dependent trend, while serum albumin was not greatly affected. AChE activity was increased (P less than 0.01) after 1 month of treatment with the two doses of dimethoate and deltamethrin; thereafter, AChE activity showed 40% inhibition of the control level. The activity of aromatic esterase increased markedly after the first month, then declined gradually until the fifth month. High dose of dimethoate markedly inhibited this enzyme particularly after the 5th month of treatment. Both doses of deltamethrin increased ATPase activity after the first month of treatment, then the ATPase activity was normal. Dimethoate inhibited ATPase particularly at the end of treatment in a dose dependent manner.
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PMID:In vivo chronic effect of dimethoate and deltamethrin on rabbits. 297 91

We describe a case of liver cirrhosis lacking the expected increase in serum thyroxin (T4)-binding globulin (TBG) despite abrupt, severe increases in aspartate and alanine aminotransferases (ASAT and ALAT) in serum. Sequential change in serum T4, triiodothyronine (T3), and TBG concentrations were also measured retrospectively in serum of 10 hospitalized patients with acute viral hepatitis. Although their mean T4 and TBG concentrations significantly exceeded those in 40 normal subjects (P less than 0.002 and P less than 0.001, respectively), these values were within the normal reference intervals in five patients. ASAT and ALAT concentrations were not significantly different in patients with increased TBG and patients with normal TBG, whereas mean concentrations of serum albumin and cholinesterase and mean prothrombin times (in percent) in the former group were significantly higher than those in the latter group (P less than 0.05, P less than 0.05, and P less than 0.001, respectively). For 60 samples with increased ASAT and ALAT, TBG and albumin or cholinesterase correlated significantly (r = 0.49, P less than 0.001 and r = 0.50, P less than 0.001, respectively), but not TBG and ASAT or ALAT. Collectively, these results suggest that the increase in serum TBG in acute hepatitis may reflect its synthesis in regenerating hepatocytes rather than a simple leakage from damaged hepatocytes.
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PMID:Are increases in thyroxin-binding globulin in patients with acute hepatitis ascribable to synthesis by regenerating hepatocytes? 312 18

A previous study of cholinergic development indicated a possible trophic relationship between the olfactory bulb and its afferents from the basal forebrain (Large et al., J. Neurochem., 46 (1986) 671-680). To examine this possibility further, cultured embryonic basal forebrain neurons from rat were used as a test system for trophic factor activity hypothesized to be present in olfactory bulb. Basal forebrain neurons grown in defined medium typically died within 2-3 days. However, survival and differentiation were strikingly enhanced by soluble extracts of olfactory bulb tissue. This trophic effect was noticeable with 2 micrograms/ml olfactory bulb protein, and plateaued at 100 micrograms/ml. The activity was heat- and trypsin-sensitive, non-dialyzable, stable in the cold, resistant to NGF antiserum, and approximately 100-150 kDa in size. Nerve growth factor, bovine serum albumin, laminin and extracts from heart did not mimic the activity. Long-term growth (21 days) in the presence of olfactory bulb proteins resulted in extensive neurite production, formation of thick neurite fascicles, and aggregation of cells. Some glia were present, as evidenced by the presence of glial fibrillary acidic protein, and large numbers of cells were positive for neuron-specific enolase and true acetylcholinesterase. Trophic activity was also present in medium conditioned by olfactory bulb slices, implying secretion of active factors.
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PMID:Soluble proteins from rat olfactory bulb promote the survival and differentiation of cultured basal forebrain neurons. 340 3

Urinary kallikrein excretion was found as compared with 22 normal subjects (0.88 +/- 0.05 mumol/min/day) to be significantly reduced in 15 cirrhotics without ascites (0.42 +/- 0.04; p less than 0.01) and in 23 cirrhotics with ascites (0.15 +/- 0.02; p less than 0.01), and further, showed a significant difference between the two groups (p less than 0.01), but did not significantly change in 14 patients with chronic active hepatitis. Urinary kallikrein excretion in cirrhotics showed a positive correlation with serum albumin, indocyanine green disappearance rate, cholinesterase, and prothrombin, and an inverse correlation with bilirubin. After indomethacin administration to 13 cirrhotics with ascites, not only plasma renin activity and plasma aldosterone decreased significantly (p less than 0.01), but urinary kallikrein excretion also showed a small but statistically significant decrease (p less than 0.05). These results suggest that urinary kallikrein excretion decreases almost parallel to the severity of liver damage and is mediated via prostaglandins or the renin-angiotensin-aldosterone system, which may be involved in the reduction of renal blood flow in patients with liver cirrhosis.
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PMID:Urinary kallikrein excretion in chronic liver disease and effect of indomethacin. 351 May 29

Plasma fibronectin (FN) has been measured by immunonephelometric method in 100 cirrhotic patients and compared with that of 77 normal subjects and with that of 57 patients suffering from liver disorders different from cirrhosis. Both, compensated and decompensated cirrhotics had lower plasma FN than controls (31.14 +/- 11.42 and 20.88 +/- 10.43 respectively vs 40.13 +/- 8.58 mg/dl; rho less than 0.02 and rho less than 0.001). FN in ascitic patients was lower than in non-ascitic (rho less than 0.001). These differences were not due to different weight or age of patients. It appears, therefore, that FN parallels in cirrhosis the grade of liver function impairment. No significant difference has been noted between plasma FN of patients with liver diseases different from cirrhosis and control subjects. In cirrhosis, a positive relation has been observed among FN and other parameters of liver function such as serum albumin, cholinesterase activity, fibrinogen and prothrombin time. Plasma FN has a low sensitivity but a high specificity and a good positive predictive value in distinguishing normals and patients with liver disorders different from cirrhosis. This diagnostic value is similar to that of serum albumin.
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PMID:Plasma fibronectin in liver cirrhosis and its diagnostic value. 353 10

This study was undertaken to examine the influence of hospitalization on the nutritional status of cancer patients. We examined 126 patients consecutively admitted to the Istituto Nazionale Tumori of Milan. At admission, all patients underwent standard evaluations, including actual weight, percentage weight loss, arm circumference, triceps skinfold, serum proteins, serum albumin, total iron binding capacity, cholinesterase and peripheral lymphocytes. Finally, from all patients a 24-h dietary recall was obtained, in order to calculate calorie and protein intake. All the patients underwent another evaluation after 1 week of hospitalization; after 2 weeks only 37 of them were evaluated again, since some were operated, some were treated with radio-chemotherapy, some were discharged or had died. Results showed that after one week of hospitalization some variables were significantly altered, such as arm circumference in male patients, serum proteins, cholinesterase, total iron binding capacity, peripheral lymphocytes, calorie and protein intake. A significant weight loss was seen after 2 weeks. The reduced calorie and protein assumption was correlated with depletion of some of the nutritional variables (body weight, arm circumference in males, total iron binding capacity, serum albumin, cholinesterase, lymphocytes). Our data show that hospitalization plays an important role in deterioration of nutritional status in our patient population, and this problem is generally overlooked by the clinicians primarily involved in the care of cancer patients.
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PMID:Impact of hospitalization on the nutritional status of cancer patients. 366 Apr 76


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