Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism of the protein leak from exercised muscle remains obscure, but may be related to depletion of intracellular high-energy phosphate and/or to mechanical disruption. The high levels of creatine kinase (CK) and other muscle proteins found in plasma for several days after marathon running, especially downhill running, are due to protein efflux from skeletal muscle. There is no evidence that marathon running damages the healthy, well-perfused myocardium, despite the fact that the plasma levels of total creatine kinase (CK), the isoenzyme CK-MB, CK-MB/total CK (%), myoglobin, aspartate transaminase, lactate dehydrogenase and tropomyosin may be the same as after myocardial infarction. These indices must be interpreted with the greatest caution when found in anyone who habitually undertakes strenuous exercise, especially if they have done so within the previous week.
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PMID:Plasma creatine kinase after the marathon--a diagnostic dilemma. 652 95

The relationship between histologically determined infarct size and release or peak levels of circulating cardiac enzymes and myosin light chain 2 (LC2) was studied. Myocardial infarction was produced by ligating the left anterior descending coronary artery in 18 conscious closed-chest dogs. Creatine phosphokinase (CPK), cytosolic and mitochondrial isozymes of aspartate transaminase (sAST and mAST) in the plasma, and LC2 in the serum were measured serially until 10 days after infarction, when infarct size was determined histologically [range 4.0-38.8% of the left ventricular weight (%LV)]. Infarct size correlated most closely with LC2 release (r = 0.82, P less than 0.001) and less closely with peak sAST (r = 0.59, P less than 0.01), peak mAST (r = 0.49, P less than 0.05), peak CPK (r = 0.22), and CPK release (r = 0.14). The correlation between infarct size and CPK release was improved by limiting the analysis to the dogs with infarct size of less than 20% LV (n = 11, r = 0.53, P less than 0.1). Because, among cardiac enzymes and LC2, CPK activity decayed most rapidly in the lymph fluid when incubated in vitro, degeneration of CPK in the lymph stream may contribute to the nonlinear relationship between infarct size and CPK release.
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PMID:Evaluation of methods for estimating infarct size by myosin LC2: comparison with cardiac enzymes. 661 89

Enzyme kinetics for creatine kinase (CK), CK-MB, aspartate aminotransferase (AST), and lactate dehydrogenase (LD) in serum were followed in 14 patients who had suffered acute myocardial infarction and who were given intracoronary streptokinase shortly (mean 4.9 h, SD 2.6 h) after onset of symptoms. In the 10 patients for whom thrombolysis was successful, CK activity peaked earlier (12.8 vs 21.6 h) and at higher values (3548 vs 2436 U/L) than in the four patients for whom the treatment was unsuccessful. The mean maximum rate of increase in CK was threefold greater in the former group (574 vs 169 U/L per hour), but the total amount of CK released into the circulation and the fractional disappearance rates were similar for both groups. The profiles for AST and CK-MB for successfully treated patients closely resembled those for CK. LD, however, peaked significantly later than CK (25.7 vs 12.8 h). Early peaking of CK or CK-MB after nonsurgical reperfusion can be potentially useful as a noninvasive in vitro index to the success of therapy of myocardial infarction with thrombolytic agents.
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PMID:Activities of some enzymes in serum after therapy with intracoronary streptokinase in acute myocardial infarction. 671 33

Mitochondrial and cytoplasmic isoenzymes of aspartate aminotransferase (AST) were studied in the sera of 42 patients following acute myocardial infarction and compared to creatine kinase (CK), lactate dehydrogenase (LDH) and alanine aminotransferase (ALT). Mitochondrial AST( ASTm ) was detected in 93% (39/42) of patients. Maximum recorded ASTm activity was 59.5 +/- 8.8 U/l and was found 39.4 +/- 3.5 hours after the onset of symptoms (chest pain) of myocardial infarction. In contrast the maximum recorded cytoplasmic AST ( ASTc ) activity was greater (327 +/- 23 U/l) and it occurred earlier (33.5 +/- 2.2 hours) after onset of infarction compared to ASTm . ASTm correlated significantly (p less than 0.05) with ASTc , LDH and ALT but not with total CK or CK-MB. ASTc correlated significantly (p less than 0.05) with total CK, CK-MB and LDH but not ALT. Maximum recorded ASTm activity was significantly associated with the clinical assessment of left ventricular failure ( Killip classification) but not with ventricular arrhythmias. In a subset of 15 patients evaluated with invasive hemodynamic measurements of cardiac output and pulmonary capillary wedge pressure. ASTm correlated significantly (p less than 0.05) and better than CK-MB with the hemodynamic assessment of left ventricular dysfunction. Thus ASTSm can be readily identified in sera of patients after acute myocardial infarction and may be of value in the evaluation of patients with acute myocardial infarction.
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PMID:Mitochondrial and cytoplasmic isoenzymes of aspartate aminotransferase in sera of patients after myocardial infarction. 672 62

Fifty consecutive patients, 25 undergoing aortic valve replacement and 25 mitral valve replacement, were studied by serial electrocardiography, preoperative and postoperative technetium-99m pyrophosphate radionuclide scanning, and serial measurement of enzymes (creatine kinase, aspartate aminotransferase, urea stable lactic dehydrogenase) and the MB isoenzyme of creatine kinase to define the incidence of preoperative myocardial infarction and to identify the most appropriate diagnostic techniques. The use of myocardial scanning and measurement of peak enzyme activity proved to be accurate indicators of myocardial infarction, but the electrocardiogram was of limited value. The measurement of creatine kinase MB isoenzyme had no diagnostic advantage over that of the other enzymes. There were two deaths in the series, one due to acute pancreatitis after aortic valve replacement and the other due to myocardial injury after mitral valve replacement. There were four non-fatal myocardial infarctions after aortic valve replacement, giving an incidence of 16%, and none after mitral valve replacement, giving an incidence of 4%.
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PMID:Myocardial infarction related to valve replacement surgery. 673 91

The possibility of predicting myocardial infarct size from early enzyme measurements was studied using a physiological two compartment distribution model. Based on this the time dependent appearance function in plasma was calculated for creatine kinase, aspartate aminotransferase, and lactate dehydrogenase in 29 patients suffering from acute myocardial infarction. On average, the appearance function of the three enzymes started four hours after the onset of symptoms, and the maximum was reached after 12 hours for creatine kinase, 13 hours for aspartate aminotransferase, and 22 hours for lactate dehydrogenase. The cumulated appearance function was used as an acceptable estimate of infarct size. The prediction of infarct size from defined points of the appearance function curve for each of the three enzymes was attempted according to a set schedule during the first 25 hours after the onset of myocardial infarction. The prediction using creatine kinase was superior to the other enzymes. Even so, a reliable prediction could only be established at the very earliest from nine hours and this is too late, as irreversible loss of myocardium occurs rapidly after the onset of symptoms. This, together with the fact that other models have unacceptable variability of the prediction, lead to the conclusion that enzymatic predictive models are of no practical value in clinical intervention studies to reduce infarct size.
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PMID:Limitation of enzymatic models for predicting myocardial infarct size. 686 May 13

Diagnosis of injury to the myocardium is facilitated by information on the activities of creatine kinase (EC 2.7.3.2) MB isoenzyme (CK-MB) and lactate dehydrogenase (EC 1.1.1.27) isoenzyme 1 in serum, thee isoenzymes being present in higher activities in the myocardium than in other tissues or in normal serum. The temporal relationships of these isoenzymes, total creatine kinase, total lactate dehydrogenase, and aspartate aminotransferase (EC 2.6.1.1) are highly sensitive and specific for acute injury to the heart, particularly acute myocardial infarction. Chronic heart diseases, electric cardioversion for heart rhythm disturbances, coronary catheterization, and exercise usually do not produce increases of CK-MB, although abnormal aspartate aminotransferase, creatine kinase, lactate dehydrogenase, and lactate dehydrogenase isoenzyme 1 activities are seen in some individuals. Many other causes of increased activities of these enzymes and isoenzymes in serum are unrelated to injury to the heart. Because CK-MB is present in the skeletal muscle in low activities, substantial injury to skeletal muscle can increase CK-MB activities in the blood to abnormal values. Pulmonary embolism can mimic myocardial infarction in its clinical presentation. In patients with an accurately known time of onset of symptoms and serial enzyme analysis every 12 h during the first 48 h, acute myocardial infarction can be distinguished from pulmonary embolism by determinations of creatine kinase, CK-MB, aspartate aminotransferase, and lactate dehydrogenase isoenzyme 1 in serum.
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PMID:Serum enzymes and isoenzymes in the diagnosis and differential diagnosis of myocardial ischemia and necrosis. 699 25

Fifty-three consecutive patients, mean age 63 years, undergoing either peripheral vascular reconstructive surgery (n = 40) or lobectomy for bronchial carcinoma (n = 13) were examined pre- and postoperatively with conventional electrocardiogram (ECG), vectorcardiogram (VCG) and estimation of serum levels of aspartate aminotransferase, alanine aminotransferase, total lactic dehydrogenase and the heat-stable fraction of lactic dehydrogenase for the diagnosis of per/postoperative myocardial infarction (MI). Six patients (11%) developed signs of acute MI. In 2 patients whose ECG showed only unspecific changes, the VCG was decisive for the diagnosis. The serum enzyme values alone were of limited value in the diagnosis of per/postoperative MI.
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PMID:Vectorcardiography in the diagnosis of postoperative myocardial infarction. 708 Aug 62

We investigated the relation between haptoglobin (Hp) phenotypes and serum levels of various biochemical markers after myocardial infarction in 496 patients. In 122 subjects selected on the basis of short delays until hospitalization, patients with Hp 2-2 had higher cumulated creatine kinase activity than patients with Hp 1-1, or Hp 2-1 (P less than 0.05), as well as higher myoglobin concentrations (P less than 0.02) 12 to 28 hours after admission. Comparison of serum enzyme activities in the remaining 374 patients confirmed that Hp 2-2 patients had significantly higher total creatine kinase, creatine kinase isoenzyme MB fraction, aspartate aminotransferase, and lactate dehydrogenase peak levels. Complications of left ventricular failure were more frequent in these patients (P = 0.05). Our results suggest that Hp 2-2 patients have more severe myocardial infarctions than Hp 1-1 and Hp 2-1 patients, However, no difference in the distribution of haptoglobin phenotype was found between patients who had a myocardial infarction and healthy subjects, indicating that Hp 2-2 does not predispose to the occurrence of infarction.
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PMID:Effect of the haptoglobin phenotype on the size of a myocardial infarct. 709 7

The aspartate aminotransferase activity with and without pyridoxal 5'-phosphate supplementation was examined in mitochondrial and cytoplasmic preparations from fresh human heart and liver samples. The apoenzyme was fully saturated in all cases. Liver cell damage was produced by ischaemia and carbon tetrachloride poisoning in two groups of rabbits. The activity of aspartate aminotransferase with and without pyridoxal 5'-phosphate was measured in the plasma and in cytoplasmic and mitochondrial preparations from both groups. After carbon tetrachloride poisoning the enzyme activity in the plasma increased within 2 h but was not enhanced by pyridoxal 5'-phosphate. Following ischaemia, plasma enzyme activity only increased between 4 and 8 h and was progressively stimulated by pyridoxal 5'-phosphate. Up to 15 h after carbon tetrachloride poisoning the liver cytoplasmic and mitochondrial apo-enzyme remained fully saturated with co-enzyme. In contrast, a pronounced loss of co-enzyme occurred in both fractions of the ischaemic group. These result suggest that the type of injury and not necessarily the organ affected could determine the degree of activation of aspartate aminotransferase by pyridoxal 5'-phosphate observed in human myocardial infarction and liver disease.
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PMID:Changes in activation of aspartate aminotransferase by pyridoxal 5'-phosphate after experimental liver damage in rabbits. 710 22


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