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 characteristics and clinical usefulness for aspartate aminotransferase (AST) isoenzyme including apo- and holo-type enzymes were reviewed. The activation effect on mitochondrial- and cytosolic-AST (mAST and cAST) was compared in the presence of PALP, to sera of various diseases such non-alcoholic liver-, heart-, renal, and alcoholic liver diseases. A higher activation by PALP was described on both AST in the sera with ischemic heart disease than liver disease. Significantly higher apo and holo type of serum mAST were found even in patients with alcoholic fatty liver in the early stage of alcoholic liver injury than those in the normal. The mitochondrial injury relates to onset and progression of cellular necrosis so that differential measurement of apo and holo type activities of serum mAST might be useful for early prediction of necrotic diseases.
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PMID:[Aspartate aminotransferase]. 760 69

The effects of alcohol consumption on serum concentrations of apolipoproteins (apo) A-I, C-III, B, and E and of lipoproteins (Lp) A-I, A-I:A-II, C-III, C-III:B, and (a) were studied in 132 healthy subjects, including 55 low drinkers of alcohol (<20 g/day), 36 moderate drinkers (20-50 g/day), and 41 heavy drinkers (>50 g/day), and in 97 hospitalized alcoholic patients (> 100 g/day) without severe liver disease (especially functional insufficiency), before and after 21 days of withdrawal treatment. Serum concentrations of apo A-I, LpA-I, LpA-I:A-II, apo C-III, and LpC-III significantly (P </= 0.01) increased with alcohol intake (mean +/- SE in low drinkers vs in alcoholics)--1.45 +/- 0.03 vs 1.78 +/- 0.05 g/L; 0.45 +/- 0.02 vs 0.56 +/- 0.02 g/L; 0.99 +/- 0.02 vs 1.22 +/- 0.04 g/L; 27.6 +/- 1.5 vs 39.7 +/- 1.7 mg/L; and 8.4 +/- 0.9 vs 24.7 +/- 1.7 mg/L, respectively-whereas apo B and LpC-III:B concentrations tended to decrease--1.20 +/- 0.04 vs 1.06 +/- 0.04 g/L and 19.3 +/- 1.2 vs 14.9 +/- 1.0 mg/L, respectively. No significant difference between these four types of alcohol consumption was noticed for cholesterol, triglycerides, apo E, and Lp(a). After withdrawal, the concentrations of serum apo A-I, apo C-III, LpA-I, LpA-I:A-II, and LpC-III decreased significantly (P </= 0.01), reaching values comparable with those in low drinkers; concentrations of triglycerides, apo B, apo E, and Lp(a) rose; and cholesterol concentration was unaffected. In multiple regression analysis, after adjustment for serum concentrations of albumin, aspartate aminotransferase, and gamma-glutamyltransferase and for the Quetelet index, alcohol consumption remained positively correlated to apo A-I, LpA-I:A-II, apo C-III, and LpC-III concentrations. Study of other determinants of serum apo and lipoprotein concentrations suggests that alcohol-related variations in some of them, especially apo A-I, might depend on the metabolic ability of the liver to synthesize proteins and on induction phenomena. Finally, although the increase of antiatherogenic apo- and lipoproteins and the decrease of those known to be atherogenic were generally marked in alcoholics, alcohol-related modifications of these markers were very limited in our sample of French healthy men. We conclude, therefore, that moderate alcohol consumption (20-50 g/day) is unlikely to protect against ischemic heart disease through an effect on the proteins measured in this study.
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PMID:Changes in serum apolipoprotein and lipoprotein profile induced by chronic alcohol consumption and withdrawal: determinant effect on heart disease? 885 52

A number of simple clinical and laboratory variables were analysed in a group of patients with chronic heart failure to evaluate their prognostic significance. Five hundred and fifty-two patients were followed for a maximum of 13 years with a total exposure time to death or censored survival of 1148 years. Of the clinical variables, diuretic dose and NYHA class were related to mortality (P < 0.01), and ischaemic heart disease was associated with a worse prognosis than other aetiologies (P < 0.05). Of the laboratory variables, abnormalities of liver function tests including bilirubin (P < 0.01), aspartate transaminase (P < 0.005), gamma glutamyl transpeptidase (P < 0.005) and alkaline phosphatase (P < 0.01) were all related to mortality as was plasma urate (P < 0.01). Multivariate survival analysis of all variables showed aspartate transaminase (chi 2 17.36, P < 0.001) accounted for the greatest variance followed by serum bilirubin (chi 2 14.35, P < 0.005). Thus, abnormalities in liver function tests have prognostic importance in chronic heart failure.
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PMID:The importance of abnormalities of liver function tests in predicting mortality in chronic heart failure. 888 55

Angiotensin-converting enzyme (ACE) inhibitors have proven to be effective in the reduction of ischemia/reperfusion damage after myocardial ischemia. Whether this favorable effect can be related to other models of ischemia and reperfusion has not yet been investigated. Therefore, we studied in a model of syngeneic liver transplantation in the rat the effect of recipient enalapril treatment on postischemic liver injury. Untreated animals served as the control group. Treatment with enalapril was started 5 minutes before reperfusion by intravenous infusion of enalapril at a dosage of 5 mg/kg/h. By means of in vivo microscopy, the sinusoidal perfusion rate and leukocyte adherence in sinusoids and postsinusoidal venules were analyzed during 45 to 60 minutes of reperfusion. Liver function was monitored by measuring bile output over a period of 60 minutes. Analysis of coagulation factors (prothrombin time, factor V, fibrinogen) and liver enzymes (alanine transaminase [ALT], aspartate transaminase [AST]) served for the evaluation of organ dysfunction and damage secondary to ischemia/reperfusion injury. The sinusoidal perfusion rate was significantly improved by enalapril treatment (94.7% [1.0] vs. 75.3% [3.8]; mean [SEM]; P = .005). In addition, leukocyte-sticking in both liver sinusoids and postsinusoidal venules was remarkably reduced in enalapril-treated animals as compared with controls (stickers/lobule: 21.0 [3.3] vs. 59.2 [2.1]; P = .0004; stickers/mm2 venular surface: 20.5 [4.7] vs. 110.3 [18.1]; P = .0004). Moreover, bile output was increased (1.13 [0.35] vs. 0.43 [0.18] g bile/60 min x 100 g liver; P = .06). Values for PT (22.5% [2.1] vs. 9.7% [1.8]; P = .005), factor V 99.4% [9.5] vs. 49.5% [8.5]; P = .007), and fibrinogen (64.1% [7.7] vs. 12.8% [3.2]; P = .001) were significantly improved, paralleled by a remarkable reduction in serum ALT (1,428 U/L [190] vs. 2,315 [248]; P = .02). Our data show for the first time that ACE inhibition in the liver recipient by enalapril attenuates hepatic ischemia/reperfusion damage after experimental liver transplantation. Our results may offer a novel approach to reduce ischemia/reperfusion injury in clinical liver transplantation.
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PMID:Angiotensin-converting enzyme inhibition by enalapril: a novel approach to reduce ischemia/reperfusion damage after experimental liver transplantation. 904 13

Perioperative myocardial infarction as well as other major cardiac events induced by myocardial ischemia during and after a more complex or long-lasting operation represents a permanent threat for a successful outcome. High number of cardiac ischemic events especially following major vascular surgery and in elder subjects requires early, sensitive and specific diagnostic markers. This review paper presents conventional as well as novel biochemical methods fulfilling the above mentioned criteria. Until now used estimations of traditional enzyme activities (aspartate aminotransferase and lactate dehydrogenase) are either entirely discarded or subsequently lose their importance (i.e. activities of total creatine kinase and its MB-isoenzyme) an instead modern methods that estimate the amounts of specific cardiac proteins--troponins T and I, constituents of myocardial contractile apparatus--released from ischemized heart are used. Patient's monitoring by means of these cardiac markers allows an early, rapid and reliable estimation of perioperative myocardial infarction enabling possible to arrange an immediate effective treatment. Recently the myocardial regulatory protein troponin I is considered the most specific cardiac marker the plasma level of which does not increase in acute damage and chronic diseases of skeletal muscles, nor in chronic renal failure. (Ref. 52.)
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PMID:[Biochemical markers of perioperative myocardial infarct in non-cardiac surgery]. 1057 43

This study aims at developing per- and postopertive surveillance of the myocardium and focuses on ischemic damage following cardioplegic heart arrest. Levels of troponin T and total aspartate aminotransferase (ASAT) were analyzed in the myocardial interstitium of 10 patients with ischemic heart disease (IHD) who underwent coronary bypass surgery and in 12 patients with nonischemic heart disease (N-IHD) who underwent valvular surgery. Fluid from the myocardial interstitium of the anterior and the lateral wall of the heart was sampled by microdialysis probes that were implanted during surgery and extracted percutaneously 70-100 h later. There were no adverse reactions, and the equipment did not interfere with the surgical procedures. The peak in troponin T serum levels that occurred 4 h after cardiac arrest was preceded by a peak in troponin T levels in the microdialysates from the interstitium that occurred 1 h earlier. The concentration of troponin T in the microdialysate peak was 300 times higher than in the serum peak. The increase in serum ASAT levels during the first 7 h after cardiac arrest corresponded in time with a decrease in interstitial ASAT levels, which had already reached a maximum during cardiac arrest. The microdialysate/serum concentration ratio was considerably smaller for ASAT than for troponin T. Interstitial peak levels of troponin T correlated positively and significantly with peak levels of ASAT. Of the 22 patients, 15 had no postoperative events according to clinical outcome, ECG and serum tests. Fourteen of these had low to normal levels of interstitial ASAT and troponin T. Conversely, atrial fibrillation and/or premature atrial contractions were recorded in 8/22 patients, 7 of whom had elevated interstitial ASAT and/or troponin T concentrations in one or both of the sampled heart regions. The N-IHD patients had higher levels of troponin T in the interstitium 20-70 h following cardioplegia, while the peak levels did not differ between the groups. In conclusion, microdialysis sampling of troponin T and ASAT is safe and allows a highly sensitive analysis of the ischemic trauma exerted by the cardioplegic arrest.
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PMID:Monitoring of extracellular aspartate aminotransferase and troponin T by microdialysis during and after cardioplegic heart arrest. 1075 46

In albino rats, infarctoid myocardial lesions were produced by intraperitoneal (i.p.) administration of isoproterenol (75 mg/kg, during 3 days). In other groups, the descending anterior left coronary artery was ligated. In both experimental settings, the intracerebroventricular (i.c.v.) administration of (+/-) propranolol (100-200-300 microg/animal/day, during 7 days) or (+/-) verapamil (40-80-160 microg/animal/day, during 7 days) afforded a significant protection (with the exception of the lowest dose) on the investigated parameters: arrhythmias, ischemic zone (in coronary ligated rats), lactate dehydrogenase and aspartate aminotransferase activity of the serum, focal necrosis (in isoproterenol treated rats). This protective activity is lower than that afforded by i.p. administered (+/-) propranolol (5 mg/kg, during seven days) or (+/-) verapamil (5 mg/kg, during seven days). From these data it may be concluded that (+/-) propranolol and (+/-) verapamil have a protective action on the experimental myocardial ischemia and necrosis in rats, not only when the drugs come in direct contact with the heart, but also acting upon the central nervous system.
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PMID:The influence of intracerebroventricular administration of (+/-) propranolol and (+/-) verapamil on experimental myocardial ischemia and necrosis in rats. 1103 53

The pericardial fluid was examined in 26 patients without morphological signs of severe damage to cardiac histiocytes, who died unexpectedly from ischemic heart disease (IHD)--main group. The control group comprised 26 persons, who died from other (not heart diseases-asphyxia, acute blood loss, crania-cerebral trauma). The mean age of the died was 57.4 +/- 1.5 years in the main group and 51.8 +/- 2.7 years in the control group. Cardiac markers were examined in the pericardial fluid of the died in both groups, i.e. the activity of aspartate aminotransferase (AsAT), of creatine kinase (CK), of isoenzyme KK-MB, of lactate dehydrogenase (LDG), and its isoenzyme spectrum, and, finally, the content of the cardiac troponin I (cTnI). The statistically reliable differences were found between the two groups according to the activity of AsAT, LDG, its isoenzyme spectrum and the cTnI content. Isoenzymes LDG1 and LDG2 constituted up to 60% of the LDG activity in the pericardial fluid of those who unexpectedly died from IHD. As for the control group, the LDG activity was virtually evenly distributed between all isoenzymes. No differences were found in the activity of CK and isoenzyme KK-MB between the main and control groups. Thus, the obtained data are indicative of the "cardiac" origin of enzymes in the pericardial fluid. Finally, a number of assumptions were put forward on mechanisms of hyper-fermentation in the ischemic damage of the cardiac muscle.
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PMID:[Cardiac markers in the pericardial fluid in sudden coronary death]. 1282 98

In this report, we describe a simple and fast method for creating a murine myocardial infarction model and providing a useful and convenient tool for the research in ischemic heart disease. We established acute myocardial infarction in the Kunming-strain mouse within 2 minutes by ligating the left anterior descending coronary artery. The model was evaluated by observing the changes in histology and in the serum levels of aspartate aminotransferase and lactate dehydrogenase. Obvious myocardial necrosis was found in the 24-hr experimental (ligation) group. The average size of the infarction was 44.3% +/- 2.9% of the left ventricle. Serum levels of aspartate aminotransferase and lactate dehydrogenase reached their peak in the 24-hr experimental group and were normal in the 72-hr experimental group. We set forth a simple and quick method for producing acute myocardial infarction experimentally in the mouse. The model can be reproduced in a stable manner, under experimental conditions that are easy to duplicate.
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PMID:A simple and fast experimental model of myocardial infarction in the mouse. 1704 83

Hyperlipidemia is a major risk factor for the premature development of coronary heart disease and it has been shown to increase the incidence of myocardial ischemia and cardiac events. Pentacyclic triterpenes possess antiatherosclerotic, antioxidant, anti-inflammatory and cytoprotective effects. To study the effect of plant derived triterpene, lupeol and its ester lupeol linoleate, on lipid status and biochemical changes on heart tissue, male albino Wistar rats were fed high-cholesterol diet (normal rat chow supplemented with 4% cholesterol and 1% cholic acid; HCD) for 30 days. There was a significant (p<0.001) increase in the levels of total cholesterol, triglycerides and phospholipids along with augmented activities of lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase in the heart tissue. Triterpenes treatment reduced the above alterations produced in hypercholesterolemic rats. The transmembrane enzymes, namely Na(+), K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase showed a decrease in their activities. Triterpenes treatment reversed these levels, prevented the hypertrophic cardiac histology and restored the normal ultrastructural architecture. In conclusion, lupeol and lupeol linoleate intervention minimized the lipid abnormalities and abnormal biochemical changes induced by HCD fed rats. This shows that triterpenes possess cardioprotective effects which will be beneficial in hypercholesterolemic condition. Out of these two triterpenes tested, lupeol linoleate appeared to be even more effective than lupeol.
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PMID:Protective effect of lupeol and its ester on cardiac abnormalities in experimental hypercholesterolemia. 1733 64


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