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

Discriminant analysis was used to discriminate between Reye syndrome (RS) patients and non-RS cases based either on conventional blood chemistry data obtained upon admission, or on the activities of hepatic mitochondrial enzymes in biopsy or necropsy tissue. The control group for blood chemistry measurements contained children with upper respiratory tract infections, varicella, etc. who did not develop RS, as well as healthy children. Subjects with no liver disorder (e.g., accidental death, sudden infant death, etc.) or with non-RS liver disorders were used as controls for hepatic enzyme studies. Hepatic damage indicators (aspartate aminotransferase, AST; alanine aminotransferase, ALT; and bilirubin) correctly classified 86-96% of non-RS cases and 61-71% of RS. By contrast, AST and ALT had little prognostic value (63% overall correct). Ammonia effectively classified favorable outcome cases (95% correct) but not unfavorable (14% correct). However, when ammonia was included with stage of coma information 88% of the favorable and 85% of the unfavorable outcome cases were correctly classified. Discriminant analysis of hepatic enzymes (glutamate dehydrogenase and monoamine oxidase activity) for a RS and a non-RS group correctly classified 80% of non-RS and 95% of RS specimens. The function was suitable for the direct evaluation of RS-like mitochondrial enzyme changes in rat liver.
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PMID:Prognosis and diagnosis of Reye syndrome by discriminant analysis. 404 46

Twenty-three patients underwent cardiac surgery for valve replacement, valve reconstruction, aorto-coronary bypass grafting, aneurysmectomy or combinations of these. Excised cardiac tissue was obtained from left ventricular (LV) papillary muscle (17 patients), LV outflow tract (3 patients), or LV aneurysms (3 patients). A total of 34 myocardial samples, collected from excised cardiac tissue, were analysed for creatine kinase (CK), CK-isoenzymes, cytoplasmic and mitochondrial isoenzymes of aspartate aminotransferase (cAST and mAST, respectively), and lactate dehydrogenase (LDH) isoenzymes. Myocardial CK activity correlated positively with preoperative LV ejection fraction (p less than 0.001), negatively with the preoperatively measured extent of LV wall motion abnormalities (p less than 0.001), and negatively with preoperative LVEDP (p less than 0.02). Myocardial CK activity was negatively correlated with preoperative validity class (p less than 0.005). However, no correlation existed between myocardial CK activity and postoperative validity. Excluding the biopsies from LV aneurysms, myocardial CK activity was positively correlated with the fraction H-subunits in LDH (p = 0.02), and was negatively correlated with the fraction mAST in total AST (p less than 0.005). While cAST activity was proportional to CK activity in the biopsies from VL papillary muscle and LV outflow tract, mAST activity declined only with 2.4 +/- 1.2% per 10% fall of CK. The increase of mAST/cAST ratio with decreasing CK, together with the decrease of LDH-H/LDH and CK-M/CK ratios with decreasing CK, indicated the presence of an adaptation process in a myocardium with low CK activity rather than a process of necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparative study on enzymatic data from myocardial biopsies and cardiac function in patients who underwent cardiac surgery. 608 15

Over the period of two years, the blood serum of dairy cows from three localities was examined repeatedly for the activities of aspartate aminotransferase (EC 2.6.1.1) (AST), alanine aminotransferase (EC 2.6.1.2) (ALT) and gammaglutamyltransferase (EC 2.3.2.1) (GMT). First examinations were performed two to four weeks before the expected term of delivery, the repeated examinations between the sixth and eighth week after delivery. The results obtained were used to calculate AST/ALT and GMT/ALT indexes in the studied group of animals (n = 12). As found out, the decrease in these indexes or the equality of values from the sixth to the eighth week after delivery, as compared with the period of two to four weeks prior to delivery, were connected with the clinically detectable disturbances of puerperium, i. e. inflammable discharge from the reproductive organs of dairy cows; this was observed even in the cases when the enzymatic activity was within the references standards.
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PMID:[Development of aspartate aminotransferase, alanine and gamma-glutamyltransferase in the blood serum of dairy cows during the last month of pregnancy and the puerperium in relation to liver function]. 613 81

Serum alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), 5'nucleotidase (5'NT), sorbitol dehydrogenase (SDH), and aspartate transaminase activities were measured in 10 clinically healthy foals, 10 yearlings, and 10 two-year-old Quarter Horses. Enzyme activities in foals at 0.5 to 3 days, 2 to 3 weeks, and 5 to 7 weeks of age were compared with enzyme activities from yearling and 2-year-old horses. Multivariate analyses of variance revealed significantly higher enzyme values in foals (P less than 0.002). This increase was mainly a result of higher ALP and GGT activities, with lesser effects due to higher SDH and 5'NT activities. Standard deviations for ALP and GGT were also larger in foals than in adult horses. The wide variation of ALP and GGT activities may limit their usefulness in the diagnosis of hepatic disease in foals. Standard deviations for serum AST, SDH, and 5'NT activities were smaller. These enzymes may be indicators of hepatobiliary disease in foals. The high serum enzyme activities in healthy foals may reflect a physiologic difference between foals and adult horses. Relative hepatic mass (as a percentage of body weight) and enzyme activity per gram of hepatic tissue are high in young animals, indicating that the high serum enzyme activities in foals are due partly to a high rate of enzyme production and release.
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PMID:Effect of age on liver enzyme activities in serum of healthy quarter horses. 614 23

Serum activity of the mitochondrial isoenzyme of aspartate aminotransferase (mAST) was measured with an immunological method in 74 subjects. Fourty-six were chronic alcoholics with (30) or without (16) obvious alcoholic liver disease; 28 were nonalcoholic controls among whom 14 had acute or chronic viral hepatitis, the remaining 14 being healthy individuals. Mean mAST activity was much higher in all the alcoholic subjects, with or without liver disease, 10.4 and 1.95 units per liter, respectively, than in the healthy controls (0.43, p less than 0.001). The mean mAST to total AST ratio was similar in the healthy controls and in the patients with viral hepatitis (2.98 and 3.19%, NS), whereas it was about 4 times higher in the alcoholics with a sensitivity which reached 93% in the patients with alcoholic liver disease and 100% in those without. Both gamma-glutamyl transpeptidase and glutamate dehydrogenase serum activities were far less sensitive and specific. As almost all chronic alcoholics had similar abnormal values of mAST/total AST ratio, this leads to question whether "normal" liver may really exist in any of such subjects.
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PMID:Serum activity of mitochondrial aspartate aminotransferase: a sensitive marker of alcoholism with or without alcoholic hepatitis. 614 99

Human myocardium with focal myocytolysis (vacuolar degeneration, colliquative myocytolysis) was examined by routine light microscopy and by immunoperoxidase staining techniques for creatine kinase (CK) M and B, myoglobin, lactate dehydrogenase (H4)(LDH-1), and aspartate aminotransferase (AST, GOT). Sections of myocardium were selected from autopsy and surgical specimens from patients with and without clinical morphologic evidence of ischemic heart disease. Areas of coagulation necrosis showed loss of enzyme staining, while both normal and myocytolytic cells stained darkly. These results indicate that fibers with myocytolysis retain enzymes and other proteins, indicating sarcolemmal integrity, which is not present in fibers with coagulation necrosis. The implication of these findings is that fibers with myocytolysis are viable; thus, myocytolysis may be a reversible form of myocardial alteration that does not necessarily lead to cell death and eventual myocardial fibrosis.
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PMID:Myocytolysis (vacuolar degeneration) of myocardium: immunohistochemical evidence of viability. 620 21

A sensitive and specific sandwich enzyme immunoassay (EIA) for human cytosolic aspartate aminotransferase (c-AST) has been developed. Serum was incubated with anti-c-AST antibody-coated polystyrene beads, and further incubated with anti-c-AST antibody-peroxidase conjugate. The peroxidase activity bound to the polystyrene bead was proportional to the amount of c-AST. The method allows measurement of serum c-AST ranging from 50-2,000 micrograms/l. No cross-reactivity with m-AST or other serum components was observed. Recovery, within-day precision, and day-to-day precision were good. The levels of c-AST obtained by the proposed EIA were compared with those based on enzyme activity. The results suggest that there is a considerable excess of immunologically active but catalytically inactive c-AST in normal and patient's sera, and that variable specific activities of c-AST are may be found in sera from different individuals.
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PMID:Enzyme immunoassay of human cytosolic aspartate aminotransferase. 639 41

Acute treatment with sodium selenite effectively reduces bromobenzene hepatotoxicity in male, Sprague-Dawley rats. Hepatocellular damage was ameliorated as shown by marked decreases in plasma alanine and aspartate aminotransferase (ALT and AST) activities. A single dose of selenite (12.5 or 30 mumol Se/kg, ip) was administered to rats at 4, 24, 48, or 72 hr before injection of bromobenzene (7.5 mmol/kg, ip). Plasma ALT and AST activities and hepatic glutathione (GSH) content were measured 24 hr after bromobenzene treatment. As the length of time of selenite pretreatment increased, the extent of reduction of bromobenzene-induced elevation in plasma enzyme activities by selenite was enhanced, and generally, in a dose-related manner with optimal protection occurring in rats pretreated 72 hr prior with selenite. However, depletion of liver GSH by bromobenzene was not affected by selenite treatment. Hepatic GSH levels and GSH detoxication enzyme activities were measured at various intervals in rats treated with selenite alone. Selenite increased hepatic GSH content 20 to 25% at both 24 and 48 hr after injection, with a return to GSH control levels at 72 hr. Selenite treatment produced slight decreases in GSH peroxidase activity but did not alter GSH S-transferase activity. These studies suggest that the reduction of bromobenzene hepatotoxicity by selenite does not involve alterations in the activity of hepatic GSH detoxication enzymes; however, the data suggest that factors in addition to selenite-induced changes in hepatic glutathione levels are also involved.
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PMID:Selenite-induced protection of bromobenzene hepatotoxicity in male rats. 671 Apr 76


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