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)

Assays of serum enzymes, such as aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatine kinase (CK) and isoenzyme MB, are widely performed in the early phase of suspected ischemic myocardial injury. However, these enzymes are not restricted to cardiac muscle tissue and increases in their serum concentrations have been observed in non-cardiac conditions. The levels of CK, and especially those of the myocardial specific isoform (CK-MB), have served as essential components for clinical decision in emergency rooms for over 25 years. This standard diagnostic test is far from perfect in specificity and the time delay necessary for the detection of a rise in levels. The clinician needs specific and sensitive biological parameters that can be rapidly measured in serum immediately after ischemic damage. In the last years, several new serum markers of myocardial damage have been developed. Currently, an important place is reserved for some non-enzyme muscle constituents, such as myoglobin and troponin sub-units, which have better specificity and allow an earlier detection of myocardial damage. The immunoassay of human cardiac troponin is a specific and sensitive diagnostic method for acute and sub-acute myocardial damage. It is ideal for the detection of myocardial necrosis in complex clinical situations when the usual enzymatic markers may be ineffective. An important prognostic value of troponin levels, especially troponin T, is currently under investigation. Myoglobin is a protein with low molecular weight that is abnormally high in serum two hours after myocardial infarction. Despite their high sensitivity, the use of serum measurements in the emergency room is controversial because of their low specificity, requiring the exclusion of skeletal muscle damage. Sensitivity could be lost in patients with renal function damage. The measurement of CK-MB protein weight (CK-MBmass) is another marker that has been confirmed as more accurate than CK-MB activity assays, especially in patients presented within four hours after the onset of chest pain, but could be inaccurate in several circumstances. In this research article, the authors describe the most important parameters of enzymatic and non-enzymatic markers, the kinetics of serum release, the clinical applications and the problems.
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PMID:[Serum markers for ischemic myocardial damage]. 1066 Oct 20

Although serum total sialic acid has been shown to be a cardiovascular risk factor, with elevated levels associated with increased cardiovascular mortality and also with cerebrovascular disease, the reason for the elevation in serum sialic acid content remains obscure. It has been shown that an increased output of serum proteins by the liver due to some type of acute phase reaction may be one of the possible sources of an increased serum sialic acid concentration in patients with myocardial infarction. An increase in the activity of sialidase, which cleaves the terminal sialic acid residues from oligosaccharides, glycoproteins and gangliosides, may also play an important role in the elevation of serum total sialic acid in myocardial infarction. Elevated serum total sialic acid in the blood might result either from the shedding or secreting of sialic acid from the cell membrane surface, or releasing of cellular sialic acid from the cell into the bloodstream due to cell damage after myocardial infarction. The purpose of the present study is to investigate serum total and lipid-bound sialic acid and the enzymes serum lactate dehydrogenase, creatine kinase and aspartate aminotransferase in patients with acute myocardial infarction, at 24 h post-infarction (day 1), 48 h post-infarction (day 2) and 72 h post-infarction (day 3). A possible role of cell damage in the elevation of serum total and lipid-bound sialic acid levels in these patients was also evaluated. In this study, 40 patients with myocardial infarction ranging in age from 42 to 68 years, and 26 healthy volunteers ranging in age from 45 to 71 years were included. Serum total sialic acid determination was carried out by the thiobarbituric acid method of Warren and lipid-bound sialic acfd by the method of Katopodis. Our data shows that a) there is a gradual increase in the levels of serum total sialic acid and lipid-bound sialic acid during the first three days after the acute myocardial infarction and b) the elevation in serum total sialic acid levels correlates with the elevation in lactate dehydrogenase activity only on day 1 following infarction. Therefore, either the shedding or secreting of sialic acid from the cell or cell membrane surface may be partly responsible for an increased serum sialic acid concentration especially on day 1 following myocardial infarction.
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PMID:Serum total and lipid-bound sialic acid levels following acute myocardial infarction. 1120 89

We prospectively and blindly assessed the diagnostic and prognostic impact of implementation of the European Society of Cardiology/American College of Cardiology recommendations for redefinition of myocardial infarction (MI) in an unselected cohort of patients with suspected cardiac chest pain, with particular attention to prespecified clinical groups. All patients admitted to our institute with suspected cardiac chest pain were enrolled. Physicians provided usual care using serial electrocardiograms/creatine kinase (CK)/aspartate transaminase according to World Health Organization (WHO) criteria for MI, while blinded to additional measurements of cardiac troponin T (cTnT) and CK-MB mass. After discharge, diagnoses based on WHO and new criteria were compared, and major adverse cardiac events monitored for 6 months. Implementation of the new recommendations classified an additional 26.1% of patients as having MI compared with WHO criteria, and produced an overall diagnostic alteration in 11.5%. Two thirds of the additional patients with MI were previously diagnosed with unstable angina, whereas one third had "other cardiac" or "noncardiac" diagnoses. A similar MI cohort to the cTnT diagnosis was identified using a CK-MB mass discriminator value of 5 microg/L, but not 10 microg/L. The 6-month prognosis was similar in patients diagnosed with MI by new (cTnT) and WHO criteria, with the new criteria thus identifying a further high-risk cohort in the WHO negative group. In our cohort, the new Joint European Society of Cardiology/American College of Cardiology recommendations identify one fourth more patients as having MI. The 6-month prognosis of those patients reclassified as having MI was similar to those diagnosed with MI by both criteria.
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PMID:Impact of the recommendations for the redefinition of myocardial infarction on diagnosis and prognosis in an unselected United Kingdom cohort with suspected cardiac chest pain. 1505 Apr 81

This study was designed to examine the effects of squalene on tissue antioxidant status in isoproterenol-induced myocardial infarction in male albino rats. Levels of diagnostic marker enzymes [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)] in plasma, lipid peroxides, reduced glutathione, and the activities of glutathione-dependent antioxidant enzymes [glutathione peroxidase (GPx) and glutathione-S-transferase (GST)] and antiperoxidative enzymes [catalase (CAT) and superoxide dismutase (SOD)] in the heart tissue of experimental groups of rats were determined. The prior administration of squalene at 2% level along with feed for 45 days significantly prevented the isoproterenol-induced elevation in the levels of diagnostic marker enzymes in plasma of experimental rats. Squalene also exerted an antioxidant effect against isoproterenol-induced myocardial infarction by blocking the induction of lipid peroxidation. A tendency to prevent the isoproterenol-induced alterations in the level of reduced glutathione and in the activities of glutathione-dependent antioxidant enzymes and antiperoxidative enzymes was also observed. The cardioprotective effect of squalene might be ascribable to its antioxidant property and membrane stabilizing action.
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PMID:Effect of squalene on tissue defense system in isoproterenol-induced myocardial infarction in rats. 1522 64

We have examined the protective effect of taurine on the myocardial antioxidant defense system in isoprenaline (isoproterenol)-induced myocardial infarction in rats, an animal model of myocardial infarction in man. Levels of diagnostic marker enzymes in plasma, lipid peroxides and reduced glutathione, and the activity of glutathione-dependent antioxidant enzymes and anti-peroxidative enzymes in the heart tissue were determined. Intraperitoneal administration of taurine significantly prevented the isoprenaline-induced increases in the levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and creatine phosphokinase in the plasma of rats. Taurine exerted an antioxidant effect against isoprenaline-induced myocardial infarction by preventing the accumulation of lipid peroxides and by maintaining the level of reduced glutathione and the activity of glutathione peroxidase, glutathione-S-transferase, catalase and superoxide dismutase at near normality. The results indicated that the cardioprotective potential of taurine was probably due to the increase of the activity of the free radical enzymes, or to a counteraction of free radicals by its antioxidant nature, or to a strengthening of myocardial membrane by its membrane stabilizing property.
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PMID:Protective effect of taurine on myocardial antioxidant status in isoprenaline-induced myocardial infarction in rats. 1625 60

Isoproterenol (ISPH) induced myocardial infarction was confirmed by disturbances in serum and heart tissue marker enzymes such as lactate dehydrogenase (LDH), creatine phospho kinase (CPK), aspartate transaminase (AST) and alanine transaminase (ALT), increased level of lipid peroxidation and histopathological changes in the heart of ISPH administered rats. Pretreatment with mangiferin (10 mg/100 g body weight) for 28 days was found to ameliorate the effect of ISPH-induced pathological changes, reduced the lipid peroxide formation and retained the myocardial marker enzyme activities at near normal level. The above results indicate the cardioprotective effect of mangiferin against ISPH-induced myocardial infarction in rats.
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PMID:Cardioprotective effect of mangiferin on isoproterenol induced myocardial infarction in rats. 1653 59

The consumption of diets rich in plant foods is associated with a reduced risk of cardiovascular diseases. This study aimed to evaluate the preventive role of rutin on lipid peroxides and antioxidants in normal and isoproterenol-induced myocardial infarction in rats. Subcutaneous injection of isoproterenol (150 mg kg(-1)) to male Wistar rats at an interval of 24 h for two days showed a significant increase in the activity of serum cardiac marker enzymes (creatine kinase, lactate dehydrogenase, aspartate transaminase and alanine transaminase) and a significant decrease in the activity of these enzymes in the heart. Lipid peroxidative products (thiobarbituricacid reactive substances and lipid hydroperoxides) were significantly increased and enzymic (superoxide dismutase, catalase and glutathione peroxidase) and non-enzymic (reduced glutathione and vitamin C) antioxidants showed a significant decrease in isoproterenol-treated rats. Pretreatment with rutin (40 or 80 mg kg(-1)) to isoproterenol-treated rats orally for a period of 42 days daily caused a significant effect. Administration of rutin to normal rats did not have any significant effect on any of the parameters studied. The results of our study show that rutin possesses antioxidant activity in isoproterenol-induced experimental myocardial infarction.
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PMID:Preventive effect of rutin, a bioflavonoid, on lipid peroxides and antioxidants in isoproterenol-induced myocardial infarction in rats. 1664 Aug 40

Recently, erythropoietin was shown to have both hematopoietic as well as tissue-protective properties. Erythropoietin (EPO) had a protective effect in animal models of cerebral ischemia, mechanical trauma of the nervous system, myocardial infarction, and ischemia-reperfusion (I/R) injury of the kidney. It is not known whether EPO protects the liver against I/R injury. Using a rat model of liver I/R injury, we aimed to determine the effect of the administration of human recombinant erythropoietin (rhEPO) on liver injury. Rats were subjected to 30 min of liver ischemia followed by 2 h of reperfusion. When compared with the sham-operated rats, I/R resulted in significant rises in the serum levels of aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, gamma-glutamyl transferase, tissue lipid peroxidation, caspase-3 activity and altered histology. Administration of rhEPO 5 min before ischemia was able to reduce the biochemical evidence of liver injury; however, this protection was not evident when rhEPO was administered 5 min before reperfusion. Mechanistically, early administration of rhEPO was able to reduce the oxidative stress and caspase-3 activation, suggesting the subsequent reduction of apoptosis. This study provides the first evidence that rhEPO causes a substantial reduction of the liver injury induced by I/R in the rat.
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PMID:Recombinant human erythropoietin protects the liver from hepatic ischemia-reperfusion injury in the rat. 1701 28

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

Diets rich in natural antioxidants are associated with reduced risk of heart diseases. This study was aimed to evaluate the preventive role of naringin on cardiac troponin T (cTnT), lactate dehydrogenase (LDH)-isoenzyme, cardiac marker enzymes, electrocardiographic (ECG)-patterns and lysosomal enzymes in isoproterenol (ISO)-induced myocardial infarction (MI) in male Wistar rats. Rats subcutaneously injected with ISO (85mg/kg) at an interval of 24h for 2 days showed a significant increase in the levels of cTnT, intensity of the bands of LDH-isoenzyme (LDH1 and LDH2) and the activities of cardiac marker enzymes such as creatine kinase-MB (CK-MB), creatine kinase (CK), LDH, aspartate transaminase (AST) and alanine transaminase (ALT) in serum with subsequent decrease in the activities of CK, LDH, AST and ALT in the heart and alterations in ECG-patterns. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetyl glucosaminidase, beta-galactosidase, cathepsin-B and cathepsin-D) were increased significantly in serum and the heart of ISO-induced rats, but the activities of beta-glucuronidase and cathepsin-D were decreased significantly in the lysosomal fraction of the heart. Pretreatment with naringin (10, 20 or 40mg/kg) daily for a period of 56 days positively altered the levels of cTnT, intensity of the bands of the LDH1 and LDH2-isoenzyme and the activities of cardiac marker enzymes, ECG-patterns and lysosomal hydrolases in ISO-induced rats. Thus, naringin possess cardioprotective effect in ISO-induced MI in rats.
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PMID:Preventive effect of naringin on cardiac markers, electrocardiographic patterns and lysosomal hydrolases in normal and isoproterenol-induced myocardial infarction in Wistar rats. 1718 15


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