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 guanase, aspartate aminotransferase, alanine aminotransferase, creatine phosphokinase and hydroxybutyrate dehydrogenase activities were measured in 290 blood samples from 96 consecutive patients admitted to a Coronary Care Unit. Elevated serum guanase activities (greater than 2 U/l) were found in 19 patients (20%). The magnitude and frequency of these elevations did not negate the value of guanase as a "liver function test", since all cases with raised guanase also had abnormal serum alanine aminotransferase activities. This fact, together with other information in the literature, indicated that elevated serum guanase activity following myocardial infarction was consequent upon some degree of sub-clinical hepatic necrosis. Caution must be exercised when serum asparate aminotransferase is used as an index of heart muscle necrosis unless guanase or some other "liver specific" enzyme is known to be normal, or unless creatine phosphokinase or hydroxybutyrate dehydrogenase activities are elevated.
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PMID:Serum guanase activities after myocardial infarction. 117 93

A method is described in which the extent of myocardial infarction in man is assessed by mathematical analysis of the rise in plasma enzyme levels after infarction. Five enzymes are used in this study: lactate dehydrogenase (LDH); alpha-hydroxybutyrate dehydrogenase (alpha-HBDH); aspartate aminotransferase (GOT); creatine phosphokinase (CPK); and phosphohexoseisomerase (PHI). It is shown that a reasonable assessment of the total enzyme release, reflecting the extent of the infarcted area, can be made when a sufficient number of blood samples are taken after infarction. This could provide a method by which to judge therapeutic effects of intervention in the course of a myocardial infarction, as demonstrated in this study by the assessment of the effect of urokinase on the enzyme release after an infarct.
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PMID:Quantitation of infarct size in man by means of plasma enzyme levels. 119 41

Biochemical variables have been measured in a group of volunteers during and after a long-distance run. Plasma glucose levels remained relatively constant and a significant decrease in plasma bicarbonate was noted. Plasma sodium, chloride, total protein, albumin and calcium showed significant increased of an order compatible with water losses occurring during the run. Plasma potassium, urea, creatinine, uric acid, phosphate and bilirubin all show much more marked and variable increases. The plasma enzymes alkaline phosphatase, lactate dehydrogenase, aspartate aminotransferase and creatine kinase likewise increased significantly throughout the run. Whilst most constituents showed a tendency to return to normal at 20-30 hours after the run, gross increases were observed for aspartate aminotransferase and creatine kinase.
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PMID:The effect of long-distance running on some biochemical variables. 119 11

The behavior of the mitochondrial and cytoplasmic fractions of aspartate aminotransferase (AAT) (E.C. 2.6.1.1) has been quantitatively evaluated in the serum of patients with acute myocardial infarction. For this purpose a new electrophoretic procedure on Cellogel strips with spectrophotometric evaluation has been used. An increase of the mitochondrial fraction of AAT has been observed in the very early phase of myocardial infarction (i.e., 6 hr after the onset of symptoms). The serum increase of the mitochondrial AAT precedes those of other enzymes, including creatine phosphokinase.
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PMID:Cytoplasmic and mitochondrial fractions of serum aspartate aminotransferase in the early phase of myocardial infarction. 122 46

The effect of continuous removal of thoracic duct lymph on plasma activities of creatine phosphokinase (PCK), glutamic-oxaloacetic transaminase (PAST); and lactic dehydrogenase (PLDH), uas examined in pentobarbital-anaesthetised dogs over a 5.5-hour period. PCK and PAST declined relative to levels in control dogs while PLDH was unaltered. Lymph/plasma (L/P) ratios for AST and CPK were greater, and for LDH less, than the L/P ratio for total protein. It was concluded that PCK, and to some extent PAST, are normally maintained by introduction of enzyme, escaping from the intracellular compartment, into the circulating blood via the lymphatic system. PLDH and PAST appear to be maintained principally by introduction of enzyme directly from the intracellular to the plasma compartment.
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PMID:Plasma enzyme levels in the anaesthetised dog during drainage of thoracic duct lymph. 124 97

Seventeen patients who had been admitted to hospital for wasp/bee sting were studied. Mild pyrexia was encountered in 7 patients, rash/urticaria in 3, angioneurotic oedema in 2, oliguria in 2, microscopic haematuria and albuminuria in 3, transient hypotension in 1. However, there were frequent elevations of serum glutamic-oxaloacetic transaminase (9 out of 17 patients), serum creatine phosphokinase (14 out of 17 patients) and serum lactate dehydrogenase (8 out of 14 patients), indicating presence of damage to muscle fibres. This was confirmed by the histological findings of a muscle-biopsy from the most severe case. Elevation of serum glutamic-pyruvic transaminase was found in 6, and elevation of serum isocitrate dehydrogenase in 5 out of 14 patients, suggesting presence of liver damage. The above enzyme elevations appeared short-lived except in the clinically most severe patient (case 9) who developed acute tubular necrosis. All patients except the latter suffered no clinical sequelae and there was no correlation between their clinical condition and the presence or degree of elevations of serum enzymes.
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PMID:Elevated serum enzymes in patients with wasp/bee sting and their clinical significance. 124 43

The serum creatine kinase (CK), aspartate transaminase (AST), lactic dehydrogenase (LD) and alpha-hydroxybutyric dehydrogenase (HBD) were determined before and 3, 6, 18, and 36 hours after cardiac catheterization and angiocardiography in 56 consecutive patients with ischaemic heart disease. Five of these patients whose serum enzyme levels were higher than normal before the procedure were excluded from the study. Forty-one of the remaining 51 patients had left ventriculography and also selective coronary arteriography. In these 41 patients (groups 1 and 2--see below), the mean serum CK levels increased after the procedure to exceed the upper limit of normal at every study interval. The mean serum AST, LD, and HBD levels generally remained within the normal range at all study intervals, though serum AST increased abnormally in 9 of the 41 patients (22%) and serum LD and HBD each increased above the normal limit in 2 of 41 patients (4.9%). In 24 patients (group 1) whose coronary arteriograms showed insignificant coronary narrowing (less than 75%) in any of the three major coronary arteries, the increase in serum CK was significantly higher than in 17 patients (group 2) with greater than 75% narrowings in at least one of the three major coronary arteries. However, the degree of serum CK elevation observed during the postangiographic period was much lower than that in another group of 30 consecutive patients with acute myocardial infarction. In 10 patients (group 3) who had the same procedure as groups 1 and 2 except without the selective coronary arteriography, the serum enzyme levels showed no noticeable increase after the procedure. The difference in postangiographic serum CK elevation between patients with and without selective coronary arteriography and the difference between group 1 (without significant coronory narrowing) and group 2 (with significant narrowing) strongly suggest that the raised serum CK levels represent some form of myocardial damage caused by the coronary arteriography, which, however, is different at least in degree from that of acute myocardial infarction.
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PMID:Significance of serum enzyme changes after cardiac catheterization and selective coronary arteriography. 125 4

Serum levels of lactate dehydrogenase, creatine kinase, and glutamate oxaloacetate transaminase show initial elevations within 12 hr of exposure to 2,000 rads of gamma-radiation to the thoracic region of rats. Significant decreases in heart muscle homogenate levels of these enzymes parallel initial elevations in the serum and may suggest that enhanced leakage of enzymes is a consequence of radiation injury to heart muscle. Insignificant alterations in mitochondrial glutamate oxaloacetate transaminase levels after exposure indicate that in vivo injury to the mitochondria from therapeutic levels of gamma-radiation is questionable. The results support the contention that ionizing radiation instigates alterations in the dynamic permeability of membranes, allowing leakage of biologically active material out of the injured cell.
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PMID:Radiation-induced enzyme efflux from rat heart: sedentary animals. 125 84

Intramuscular injections of digoxin, bumetanide, pentazocine or isotonic sodium chloride have been given to 39 patients. We followed the serum concentrations of creatine kinase (CK), aspartate aminotransferase (ASAT), lactate dehydrogenase (LDH) and LDH isoenzymes for 4 days. Ten patients receiving 500 mug digoxin showed a significant rise in CK, which lasted for 48 hours, and 6 of them had CK values exceeding the upper normal limit. Pentazocine in a dose of 30 mg given to 9 patients caused a significant rise in CK and LDH isoenzyme 1, but in no case did the level exceed the upper normal limit. No rise in ASAT or total LDH was found after digoxin and pentazocine injections. No changes in enzymes were discovered after bumetanide or isotonic sodium chloride. In the diagnostic evaluation of acute myocardial infarction, a moderate rise in CK must be assessed with caution when the patients have received i.m. injections of drugs with osmolarity and pH outside the physiological limits.
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PMID:The effect on serum enzymes of intramuscular injections of digoxin, bumetanide, pentazocine and isotonic sodium chloride. 126 67

Ten children, three girls and seven boys, aged 4-10 years, were admitted with benign acute childhood myositis during spring and winter months (March 1988 to March 1990). They presented with an acute onset of symmetrical calf muscle pain and tenderness, weakness and inability to walk a few days after a flu-like illness. All had raised serum creatine kinase and a normal erythrocyte sedimentation rate, and the majority had low peripheral white blood cell counts with relative lymphocytosis. Serum aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase were found to be raised in four patients. Virological studies performed in six children gave negative results. Full clinical recovery was achieved within 1-7 days. One child developed a second episode. These ten cases of benign acute childhood myositis are the first to be reported from this region.
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PMID:Benign acute childhood myositis in Kuwait. 128 48


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