Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum mitochondrial glutamic-oxaloacetic transaminase activity was determined in 83 patients with various liver diseases and 10 healthy adults. 1) The average of mitochondrial glutamic-oxaloacetic transaminase value was 1.2 mU in healthy adults, 8.3 mU in patients with acute hepatitis, 13.7 mU in patients with post-transfusion hepatitis, 5.0 mU in patients with persistent hepatitis, 4.5 mU in patients with chronic inactive hepatitis, 9.6 mU in patients with chronic active hepatitis, 5.6 mU in liver cirrhosis, and 295 mU in a patient with fulminant hepatitis. 2) While one patient with acute hepatitis showed the highest value in the group of 29 mU, one patient with fulminant hepatitis showed an extremely high value of 295 mU, revealing an obvious difference between them. 3) One patient with fresh myocardial infarction also showed an extremely high value of 110 mU.
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PMID:Clinical significance of mitochondrial glutamic-oxaloacetic transaminase in serum of patients with liver disease. 21 85

In a consecutive series of 25 coronary bypass operations, the postoperative serum activity levels of total creatine kinase (CK) and its more heart-specific isoenzyme CK-MB were examined and related to the levels of aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT) and thermostable lactate dehydrogenase (LD-T), to electrocardiographic (ECG) findings and to surgical characteristics. Detectable CK-MB activity was found in all patients, usually appearing while the operation was still in progress. Peak CK-MB occurred earlier than peak total CK. There was no ECG evidence of myocardial infarction in any patient. The degree of postoperative CK-MB elevation, however, correlated to the duration of extracorporeal circulation (ECC) and aortic cross-clamping (AC). After 120 min of ECC and 70 min of AC, release of CK-MB, as well as of the other enzymes studied, increased considerably. There was a significant correlation between high CK-MB activity and high early postoperative activities of total CK, ASAT and LD-T. When CK-MB determinations are not available, ASAT is preferable to total CK or LD-T in the early evaluation of operative myocardial injury. From the fourth postoperative day, only LD-T is informative in this respect; a second rise of ASAT and ALAT is probably of hepatic origin.
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PMID:Serum enzymes with special reference to CK-MB following coronary bypass surgery. 31 43

A radioimmunoassay for quantitation of serum myoglobin in healthy individuals and patients with different diseases is described. Purified myoglobin was labelled by an 125I-labelled ester (N-succinimidyl 3-(-4 hydroxy, 5-[125I]iodophenyl) propionate), a commercially available antiserum was used, and the antigen-antibody complex was precipitated with polyethylene glycol 6000. The rapid assay can be performed within 1 h at 37 degrees C with a detection limit of 45 micrograms/l. Prolonged incubation at 4 degrees C for 18 or 72 h gives a detection limit of 6 and 2 micrograms/l, respectively. The mean coefficient of variation of the routine assay was 11%. In healthy human subjects a significant difference in mean serum myoglobin concentration was found between 43 women (34 +/- 17 micrograms/l) and 51 mean 47 +/- 15 micrograms/l). In twenty patients admitted to hospital with the clinical diagnosis acute myocardial infarction, the serum myoglobin concentration profiles were in close agreement with the final diagnosis. In three patients with myocardial infarction serum samples were taken every 2 h after the acute episode, and serum myoglobin levels were compared with the levels of creatine kinase, lactate dehydrogenase, aspartate aminotransferase and creatine kinase isoenzyme-MB.
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PMID:Rapid and sensitive radioimmunoassays for human myoglobin. 53 83

Myoglobin and the enzymatic activity of creatine phosphokinase CK), MB-isoenzyme of CK (CK-MB), aspartate aminotransferase (GOT), alanine aminotransferase (GPT) and lactic acid dehydrogenase (LDH) were serially determined in 10 patients with acute myocardial infarction. Additionally the same parameters were assessed in 5 patients with angina pectoris for 24 hours after bicycle ergometry. 10 in-patients served as controls. Myoglobin was determined by radioimmunoassay and the other enzyme activities according to the current kinetic methods. Comparison of myoglobin with the enzymatic parameters showed that the myoglobin peak occurs 5.6 hours after the beginning of the sampling period, i.e. 7.3 hours earlier than CK and CK-MB and 11.6 hours earlier than GOT. In analogy to this finding the descending limb of the myoglobin curve was significantly earlier at a level of one third of the peak value, i.e. 8.2 hours earlier than CK-MB, 18.8 hours earlier than CK and 27.3 hours earlier than GOT. No signs of myocardial necrosis in terms of myoglobin or enzymatic activity could be detected after bicycle ergometry. It is concluded that myoglobin is a more sensitive parameter for assessment of the acute phase in patients with myocardial infarction than the usualy enzymatic parameters.
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PMID:[Plasma myoglobin level as a course criterium in patients with acute myocardial infarct]. 53 58

Aspartate aminotransferase activity was measured in plasma, in liver and in heart mitochondrial and cytoplasmic preparations from rats immediately after death and after a post-mortem interval of 15 h. No significant stimulation of activity on addition of pyridoxal 5-phosphate to the assay medium could be demonstrated in any preparations obtained immediately after death. Significant stimulation occurred in both cytoplasmic and mitochondrial preparations of liver and myocardium after a 15-h post-mortem interval, but not in plasma stored for the same period. It appears, therefore, that variations in the intracellular saturation of apoenzyme with coenzyme cannot account for the observed differences in activation of aspartate aminotransferase by pyridoxal 5-phosphate in sera from patients with myocardial infarction and liver disease. Changes in degree of saturation of apoenzyme seem to occur intracellularly after cell death or injury and before release into the circulation.
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PMID:The changes in activation of intracellular aspartate aminotransferase by pyridoxal 5-phosphate after cell death. 63 4

Serum m-AST (mitochondrial isoenzyme of AST) activity in patients with acute myocardial infarction was determined quantitatively by a new immunological technique which is sensitive and easily available. All 31 patients with acute myocardial infarction showed abnormally high levels of serum m-AST (more than 5 KU/ml); the mean serum m-AST activity attained its peak (42.0 +/- 4.9 KU/ml) on the first day after the onset of infarction 5 hours later than that of serum t-AST (total AST) activity in 15 patients whose peak m- and t-AST activities were identified clearly. The individual peak m-AST activity correlated with the total CK released (r = 0.83, n = 15), indicating that the release of m-AST also reflects the infarct size. The ratio of serum m-AST/t-AST increased following myocardial infarction and showed the maximal value (average 25.7%) on the third to seventh day after onset. This ratio in the patients with acute myocardial ifarction was also greater than that in patients with liver disease or with heart failure from causes other than acute myocardial infarction. In the patients who had the additional complication of heart failure and/or cardiogenic shock the ratio was also greater than that is the patients without these hazards. These results indicate that the ratio of serum m-AST/t-AST reflects the severity of the myocardial cellular damage in acute myocardial infarction.
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PMID:Immunological determination of serum m-AST activity in patients with acute myocardial infarction. 71 64

The prognostic effect of the peak level of serum creatine kinase (CK) and aspartate transaminase (AST), estimated daily for 3--5 days after acute myocardial infarction, was studied in 560 patients who survived the first day in hospital. In a subgroup of 54 patients, peak enzyme levels correlated well with the cumulated CK release (r = 0.90 with peak CK, r = 0.74 with peak AST), thus reflecting the extent of myocardial necrosis. Total mortality within a year after infarction was not significantly different in the lower three quintiles of peak serum enzyme level, but increased from 15.5% to 27.9% (p less than 0.001) when peak CK level exceeded eight times the upper limit of normal (8 X N) and form 13.1% to 34.8% (p less than 0.001) when peak AST level exceeded five time the upper limit of normal (5 X N). The effect of high enzyme levels was more marked in patients with a prior history of myocardial infarction; mortality increased from 14.7% for first infarctions to 18.2% for recurrent infarctions, with peak CK greater than 8 X N, and from 27.0% for first infarctions to 38.0% for recurrent infarctions with peak CK greater than 8 X N. Early mortality was more significantly affected (p less than 0.0001) than late mortality (p less than 0.05). In hospital survivors, late deaths from cardiac decompensation were three times (p less than 0.05) more frequent in the high enzyme group as in the low enzyme group, but the number of sudden deaths was unaffected. These findings have important implications for studies of reduction of myocardial infarct size.
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PMID:Enzymatic indices of myocardial necrosis: influence on short- and long-term prognosis after myocardial infarction. 75 3

Two-hundred consecutive patients thought to have suffered a myocardial infarction were admitted to a randomised, double-blind controlled trial of oxygen or air administered by MC mask throughout the first 24 hours in hospital. Forty-three patients in whom myocardial infarction was not subsequently confirmed were excluded from the analysis. The remaining air and oxygen groups were comparable except for a significantly higher PaO2 and serum aspartate aminotransferase level in the oxygen group. There was no significant difference in mortality, incidence of arrhythmias, use of analgesics, or systolic time intervals between the two groups, although a higher incidence of sinus tachycardia was found in those given oxygen. There appears to be no evidence of benefit from the routine administration of oxygen in uncomplicated myocardial infarction.
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PMID:Controlled trial of oxygen in uncomplicated myocardial infarction. 77 7

In a group of 113 consecutive patients taken into a coronary care unit on suspicion of acute myocardial infarction, blood samples were taken every 6 h and the following enzyme activities were measured: creatine kinase (S-CK), aspartate aminotransferase (S-ASAT), alanine aminotransferase (S-ALAT) and lactate dehydrogenase (S-LD). All measurements were made according to the Recommendations of the Scandinavian Committee on Enzymes. On all patients S-CK B subunit activity was determined by immunoinhibition with a specific anti CK M-subunit inhibitory antibody. At peak values of the respective total enzyme activities CK and LD isoenzymes were further qualitatively estimated by electrophoresis. The data indicate that even serial determinations of total CK, ASAT, ALAT and LD activities in serum do not provide the information required for a conclusive diagnosis of myocardial infarction in the individual case. In contrast, the positive predictive value (PV) of S-CK B was found to be 1.0 and the negative predictive value was 0.98. S-CK MB showed a PV pos. of 1.0 and also a PV neg. of 1.0. Electrophoretic determination of S-LD isoenzymes was slightly poorer with a PV pos. of 0.96 and PV neg. of 0.98. S-CK, total activity with nearly 9 per cent false positives had a positive predictive value of only 0.91, but a negative one of 1.0.
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PMID:Creatine kinase B-subunit activity in human serum. II. Evaluation of s-ck b-subunit activity in the diagnosis of acute myocardial infarction. 88 49

Serum creatine kinase, aspartate transaminase, and hydroxybutyrate dehydrogenase activities were abnormal in 76, 50, and 28% respectively of 50 patients studied within 26 hours of surgery. No patient showed clinical evidence of myocardial infarction. Creatine kinase MB isoenzyme elevation, and lactate dehydrogenase LD1 activity greater than LD2 (LD) greater than LD2) were infrequent (6 and 10% respectively). No patient showed the combination of transient MB isoenzyme elevation and LD1 greater than LD2, although their rare association without infarction after surgery is to be anticipated.
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PMID:Serum enzymes and isoenzymes after surgery. 92 Dec 11


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