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)

A 74-year-old man with myxedema and hypothermia had increased activities in plasma of creatine kinase (CK; EC 2.7.3.2), aspartate aminotransferase (AST; EC 2.6.1.1), and lactate dehydrogenase (LD; EC 1.1.1.27) and increased proportions of CK-MB (up to 20% of total CK) and LD1 isoenzymes, but no clinical or investigational evidence of associated myocardial infarction. This case illustrates that plasma enzyme activity and isoenzyme profiles in such clinical settings should be interpreted with caution, because increases in CK-MB and LD1 may relate to myxedema coma or hypothermia (or both) rather than to myocardial infarction.
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PMID:Cardiac enzyme changes in myxedema coma. 382 11

We used an RIA and inhibition of enzyme activity to monitor the changes in mass and catalytic concentrations of the aspartate aminotransferase (EC 2.6.1.1;AST) isoenzymes in serum after myocardial infarction. Cytosolic (c-AST) and mitochondrial (m-AST) forms of AST were present in sera from all 38 of our patients. Although the immunological and catalytic concentrations of both isoenzymes correlated well with the size of the infarct, c-AST gave a better measure than did m-AST. About 20% of the total enzyme activity at peak activity was from the mitochondrial isoenzyme. Both isoenzyme activities peak at very nearly the same time, but m-AST has the longer half-life. Immunological evidence of the mitochondrial isoenzyme can be detected in serum for at least eight days after the infarct. The presence of left ventricular failure produces greater serum isoenzyme activities than in those without failure.
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PMID:Changes in mass and catalytic activity concentrations of aspartate aminotransferase isoenzymes in serum after a myocardial infarction. 394 92

A prospective follow-up study was carried out to investigate the impact of a health education program and other factors related to patient's social background and severity of heart attack on stopping smoking after heart attack. The study consisted of male patients below the age of 65 years, who had suffered a heart attack between April 1 and September 30, 1977, living in two provinces of eastern Finland, North Karelia and Kuopio. Of the patients who smoked before the heart attack, 102 responded to both the 6- and the 12-month follow-up postal survey. Of these 102 patients, 25 stopped smoking within 12 months after the heart attack, while 77 continued to smoke. Continuing smoking was most strongly associated with working and unemployment before heart attack, maximum serum aspartate aminotransferase (GOT) concentration and subjective recovery after the heart attack. The quitting rate among men in the program area was 1.2-fold (p = 0.012) compared with the reference area men, after making allowance for the seven most confounding factors in the multivariate analysis. This observation indicates that either the community-based primary program or the secondary prevention program in North Karelia succeeded in dissuading patients from smoking after heart attack.
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PMID:Impact of a health education program and other factors on stopping smoking after heart attack. 402 64

The induction of myocardial infarction in rats by ligation of the left-anterior coronary artery was confirmed by measurement of increased plasma levels of creatine kinase, aspartate aminotransferase and lactate dehydrogenase. Using this model system it has been established that intravenous administration of 125I-labelled hyaluronidase to rats resulted in a preferential uptake of the enzyme by damaged myocardium as compared to normal heart tissue.
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PMID:Preferential uptake of intravenously administered hyaluronidase (Hyalosidase) by damaged rat myocardium. 402 52

The mortality rate from myocardial infarction is disproportionately high in diabetic patients. One explanation for this may be that diabetic patients incur more extensive myocardial necrosis. This possibility was examined in a three part study. Firstly, peak serum aspartate aminotransferase concentrations of all diabetic and non-diabetic patients admitted with myocardial infarction over a 16 year period were compared retrospectively. Secondly, peak aspartate aminotransferase concentrations in a series of diabetic patients and controls matched by age and sex were examined retrospectively. Thirdly, creatine kinase MB release and electrocardiographic measures of infarct size were investigated prospectively in a case/control study. Although cardiac failure and death were more common in the diabetic groups, there were no significant differences in estimates of infarct size between diabetic and non-diabetic patients in any of the studies. Therefore, the high case fatality rate amongst diabetic patients is not caused by increased myocardial damage. Presumably survival is prejudiced by factors operating before the infarction.
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PMID:Myocardial infarct size and mortality in diabetic patients. 405 87

The levels of creatine kinase, hydroxybutyric dehydrogenase, and aspartate transaminase have been serially measured in the serum of patients undergoing surgery. Serum enzyme levels often rose to a range commonly found after myocardial infarction but fell to normal within 5-10 days. Raised serum enzyme levels have no diagnostic significance in a case of postoperative chest pain until after the fifth postoperative day, but may be significant thereafter.
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PMID:Serum enzyme levels in diagnosis of postoperative myocardial infarction. 507 12

One hundred and forty-one randomly selected surgical patients, aged 35 years or over, were studied preoperatively, followed through their operative procedures, and reassessed during the first post-operative week for evidence of myocardial ischaemia associated with surgical operations under general anaesthesia. Of these patients 38% were found to have preoperative clinical evidence of heart disease, hypertension, or diabetes; 45% had abnormal preoperative E.C.G. patterns.Three patients experienced myocardial infarction during or within 36 hours of operation, all of the occult type; all were in the preoperative abnormal groups. Non-specific postoperative E.C.G. changes were equally common in the groups of patients with normal or abnormal preoperative electrocardiograms.A relationship existed between a rise in serum lactic dehydrogenase (L.D.H.) concentration and the field of the operation, but the diagnosis of infarction was not confused provided serum L.D.H. isoenzyme patterns and a rise in serum aspartate aminotransferase (S.G.O.T.) levels were consistent with the diagnosis.
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PMID:Myocardial infarction following surgical operations. 572 23

Fifty consecutive patients undergoing coronary artery bypass grafting for chronic stable angina were assessed by serial electrocardiography, preoperative and postoperative myocardial scanning with technetium-99m pyrophosphate, gated radionuclide ventriculography, and serial measurement of creatine kinase, aspartate aminotransferase, urea stable lactic dehydrogenase, and creatine kinase isoenzyme (MB) to assess the incidence of perioperative myocardial infarction and identify the most appropriate diagnostic techniques. The correlation between myocardial scanning and the measurement of peak enzyme and isoenzyme activity was excellent in the diagnosis of perioperative infarction, although electrocardiography proved less helpful. There appeared to be no advantage in measuring creatine kinase MB rather than the more routinely measured enzymes. There were two deaths and evidence of myocardial infarction in five other patients, an incidence of 14%. Perioperative infarction was associated with a significant reduction in resting ejection fraction in two cases. In those patients without evidence of perioperative infarction the mean increase in ejection fraction of 7.8% was statistically significant.
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PMID:Myocardial infarction related to coronary artery bypass graft surgery. 632 26

We utilized immunoperoxidase methods to study the distribution of both cytosolic or soluble(s) and mitochondrial (m) aspartate aminotransferase (AspAT) in normal, ischemic, and necrotic myocardium. Human myocardium was obtained from autopsy (n = 9) and surgery (n = 6). Cardiac tissue from 26 dogs with experimental myocardial infarction induced by closed-chest balloon occlusion and four dogs with myocardial ischemia without necrosis induced by a 50% reduction in left main coronary artery flow for 3 hours were studied. Duration of occlusion was 45 minutes (n = 1), 3 hours (n = 11), 5 to 6 hours (n = 10), or 15 to 24 hours (n = 4). Highly purified m- and s-AspAT and specific antibodies were prepared in our laboratory. In all cases, control experiments were performed. Microscopically normal human and dog myocardium uniformly stained for m- and s-AspAT. Necrotic myocardium from patients with infarcts showed markedly reduced immunostaining. In those dogs with myocardial necrosis, all dogs with coronary occlusion of 5 to 24 hours, and eight of 11 dogs with 3-hour occlusions, immunostaining was significantly reduced for both s- and m-AspAT in regions confirmed to be necrotic by triphenyl tetrazolium chloride and hematoxylin and eosin staining. Myocardial necrosis was confirmed in the 3-hour infarcts by electron microscopy. In the four dogs with a 50% reduction in left main flow for 3 hours, and one dog with a 45-minute coronary occlusion, ischemia was demonstrated by glycogen loss in period acid-Schiff-stained sections but there was no evidence of necrosis by electron microscopy or triphenyl tetrazolium chloride staining and there was no loss of immunostaining evident for s- or m-AspAT. Thus, s- and m-AspAT were visualized in normal and ischemic myocardium with decreased staining in necrotic tissue using immunoperoxidase techniques. Loss of both s- and m-AspAT can be demonstrated in human myocardium and in experimental canine myocardium as early as 3 hours after coronary occlusion and appears to be specific for irreversible myocardial injury. No depletion of isoenzyme can be detected by immunohistochemical techniques in tissue that is ischemic but not necrotic. Furthermore, by these immunoperoxidase techniques, loss of s- and m-AspAT from necrotic myocardium appears to be simultaneous.
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PMID:Distribution of cytosolic and mitochondrial aspartate aminotransferase in normal, ischemic, and necrotic myocardium. An immunohistochemical study. 638 75

Aminotransferases are ubiquitous enzymes of mammalian cells and several are of important diagnostic use. The application of aspartate aminotransferase activity measurements in serum from individuals suffering from myocardial infarction brought about a new dimension in clinical laboratory testing in the 1950s. This review focuses on measurement techniques for aspartate aminotransferase and their application (a subsequent article will review other aminotransferases). Assay techniques measuring enzyme activity are direct spectrophotometric measurements, manometric techniques, assays using dye substances, coupled enzyme techniques, and radiometric procedures. Of these procedures, the one employing malate dehydrogenase and NADH is the most important and is covered in particular detail. The estimation of the mitochondrial isoenzyme of aspartate aminotransferase is also of clinical interest, in particular for estimating severity of disease or in specific applications (e.g., chronic alcoholism). Methods reviewed for estimation of this enzyme are electrophoresis, chromatography, differential kinetic behavior, and immunochemical separation. Determination of the enzyme protein by techniques independent of its catalytic activity are also reviewed.
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PMID:Measurement of aminotransferases: Part 1. Aspartate aminotransferase. 639 17


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