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 field of diagnostic cardiac biomarkers has grown exponentially since the development of an assay for aspartate transaminase activity to diagnose myocardial infarction in 1954. The clinician now has a vast array of clinical tools, which include biomarkers of inflammation, ischaemia and necrosis as well as sensitive imaging technology and coronary anatomy intervention at their disposal when evaluating acute coronary syndromes. Previously the World Health Organisation (1979) defined a myocardial infarction (MI) in the presence of two of the following triad: History of chest pain, electrocardiographic (ECG) changes and a rise in cardiac enzymes to twice the upper limit of normal. At this time, creatine kinase and its MB isoenzyme were the preferred biochemical markers. The clinical requirements of early diagnosis, risk stratification and effective treatment have stimulated the development of numerous new and cardiac specific biomarkers (e.g. cardiac troponins). Cardiac troponins are now integral to the diagnosis of MI and have led to the reclassification of MI into either ST elevated MI (STEMI) or non-ST elevated MI (NSTEMI). Subsequent to the release of each new cardiac specific assay there typically follows an array of studies supporting or refuting its efficacy. Many cardiac biomarkers originally proposed with high sensitivity and specificity for ACS are now of questionable clinical value or require the addition of significant caveats once they have been fully evaluated. Indeed, acute exercise often stimulates perturbations in cardiac biomarkers; such as elevations in creatine kinase, cardiac troponins or reductions in Ischemia Modified Albumin (IMA). Such an influence of exercise upon commercially available cardiac biomarkers may hamper or distort the viability of such assays in the clinical arena. The purpose of this review is to examine the influence of exercise upon a number of established and novel cardiac biomarkers, including markers of necrosis, inflammation, cardiac function and ischemia. We will also address the clinical relevance of such exercise-induced perturbations.
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PMID:The influence of exercise upon cardiac biomarkers: a practical guide for clinicians and scientists. 1758 54

Ischemia -modified albumin was regarded as an early marker of cardiac ischemia. On the other hand, it has been reported that increased ischemia-modified albumin levels are associated with unstable plaque processes like percutaneous coronary intervention, acute coronary syndrome or myocardial infarction. This prospective study aimed to investigate the role of ischemia-modified albumin in patients with peripheral vascular disease undergoing peripheral vascular intervention, a plaque-altering procedure without evidence of tissue ischemia. Peripheral vascular intervention was performed in 21 consecutive patients (68.2+/-13.3 years) with typical leg claudication and documented peripheral vascular disease. Additionally, 96 consecutive patients (66+/-12.0 years) undergoing routine exercise stress test for the exclusion of functionally relevant coronary artery disease were defined as controls. It was assumed that in the latter patients no unstable plaque-altering processes were present. Blood samples were drawn before, and 30 min and 3 h after, revascularization in the peripheral vascular intervention group, as well as before, and 30 min and 3 h after, maximum stress testing in the control group, respectively. Ischemia-modified albumin levels were analyzed using the albumin cobalt-binding test. In patients undergoing peripheral vascular intervention, ischemia-modified albumin increased from 116.6+/-19.1 U/ml at baseline to 132.0+/-19.3 U/ml 30 min after intervention (+14.4+/-15.7%, P<0.001) and decreased to 123.5+/-17.8 U/ml 3 h later (-5.7+/-10.5%, P<0.001 compared with postintervention, P<0.001 compared with baseline). The control group showed a slight but significant decrease in ischemia-modified albumin from 103.0+/-11.0 to 100.2+/-11.6 U/ml poststress (-2.2+/-11.5%, P<0.05) and returned close to baseline 3 h later (101.8+/-10.3 U/ml, +2.4+/-10.9%, P=NS, compared with poststress and with baseline). For both groups, ischemia-modified albumin showed no correlation with albumin (at baseline P=0.62) and total protein (P=0.67), but significant correlation with creatinine (P=0.04) and C-reactive protein (P=0.02). In addition, ischemia-modified albumin was independent of age, sex, alanine aminotransferase, aspartate aminotransferase, creatine kinase, creatine kinase-MB, cholesterol, and triglycerides. This study showed an increased basal ischemia-modified albumin level in patients with peripheral vascular disease undergoing peripheral vascular intervention. Ischemia-modified albumin levels transiently increased shortly after peripheral vascular intervention, indicating a strong correlation between serum concentration of ischemia-modified albumin and processes associated with acute plaque disruption/rupture.
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PMID:Effects of peripheral vascular intervention on ischemia-modified albumin. 1762 87

Currently there has been an increased interest globally to identify antioxidant compounds that are pharmacologically potent and have low or no side effects for use in preventive medicine. This study was designed to evaluate the protective effect of gallic acid on cardiac marker enzymes, troponin-T, LDH-isoenzyme pattern, lipid peroxidation products and antioxidant status in isoproterenol (ISO)-induced myocardial infarction in male Wistar rats. Male albino Wistar rats were pretreated with gallic acid (15 mg/kg) daily for a period of 10 days. After the treatment period, ISO (100 mg/kg) was subcutaneously injected to rats at an interval of 24 h for 2 days. ISO-induced myocardial damage was indicated by increased activities of marker enzymes such as creatine kinase, creatine kinase-MB, aspartate transaminase, alanine transaminase and lactate dehydrogenase in serum and the levels of troponin-T in the serum. Increased LDH-isoenzyme bands (LDH-1 and LDH-2) were also observed in serum of ISO-induced rats. In addition to these diagnostic markers, the levels of lipid peroxidation products in plasma and the heart were significantly (P<0.05) increased and the activities of enzymic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase in the heart and non-enzymic antioxidants such as glutathione, vitamin C and E in plasma and the heart were significantly (P<0.05) decreased in ISO-induced rats. The level of uric acid in plasma was significantly (P<0.05) increased in ISO-treated rats. Gallic acid pretreatment showed significant protective effect on all the biochemical parameters studied. Histopathological findings of gallic acid pretreated myocardial infarcted heart confirmed the biochemical findings of this study. Thus, gallic acid protects the myocardium against isoproterenol-induced oxidative stress.
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PMID:Cardioprotective effect of gallic acid on cardiac troponin-T, cardiac marker enzymes, lipid peroxidation products and antioxidants in experimentally induced myocardial infarction in Wistar rats. 1914 39

During the last 40 year medical laboratory tests per hospital stay have increased 12-fold. This is due to an increase of traditional test as well as by newly introduced analyses. Traditional markers of liver, heart and kidney diseases as well as tumor markers, markers of endocrine and metabolic disorders are critically analysed for regarding their medical needs. Assays which are no longer needed (aspartate aminotransferase, lactate dehydrogenase in heart infarction, acid phosphatase) are assessed differently from those ordered at the wrong time and too often (tumor markers, lipids, HbA (1c), thyroid hormones) and those whose indication has to be continuously renewed because of rapidly changing conditions (autoantibodies, marker of iron status, natriuretic peptides and gene analysis). The rapidly proceeding scientific and technical development allows to conclude, that even under strong and critical control of the medical needs the reduction of tests will contribute little to the further development of total costs of the medical laboratory.
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PMID:[Unnecessary laboratory tests]. 1927 34

We investigated the antioxidant preventive effect of betaine on isoprenaline-induced myocardial infarction in male albino rats. Isoprenaline induced myocardial infarction was manifested by a moderate elevation in the levels of diagnostic marker enzymes (alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase and creatine phosphokinase) and homocysteine in plasma of experimental rats. Significant rise in the level of lipid peroxidation with a concomitant decline in the levels of myocardial non-enzymic (reduced glutathione) and enzymic antioxidants (glutathione peroxidase, glutathione-S-transferase, catalase and superoxide dismutase) was also observed. Oral pretreatment with betaine significantly prevented isoprenaline-induced alterations in the levels of diagnostic marker enzymes and homocysteine in plasma of experimental groups of rats. It counteracted the isoprenaline-induced lipid peroxidation and maintained the myocardial antioxidant defense system at near normal. Histopathological observations also confirmed the protective effect of betaine against isoprenaline-induced myocardial infarction. The results of the present investigation indicate that the protective effect of betaine is probably related to its ability to strengthen the myocardial membrane by its membrane stabilizing action or to a counteraction of free radicals by its antioxidant property.
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PMID:Antioxidant defense of betaine against isoprenaline-induced myocardial infarction in rats. 1928 77

The study aimed to evaluate the protective role of myricetin obtained from Vitis vinifera (Vitaceae) on heart rate, electrocardiographic (ECG) patterns, vascular reactivity to catecholamines, cardiac marker enzymes, antioxidant enzymes together with morphological and histopathological changes in isoproterenol (ISO) induced myocardial infarction (MI) in male Wistar rats. Rats treated with isoproterenol (85 mg/kg, administered subcutaneously twice at an interval of 24 h) showed a significant increase in heart rate and ST elevation in ECG, and a significant increase in the levels of cardiac marker enzymes - lactate dehydrogenase (LDH), creatine kinase (CK) and aspartate aminotransferase (AST) in serum. Isoproterenol significantly reduced superoxide dismutase (SOD) and catalase (CAT) activity and increased vascular reactivity to various catecholamines. Pretreatment with myricetin (100 mg/kg, p.o. and 300 mg/kg, p.o.) for a period of 21 days significantly inhibited the effects of ISO on heart rate, levels of LDH, CK, AST, SOD, CAT, vascular reactivity changes and ECG patterns. Treatment with myricetin (100 mg/kg and 300 mg/kg) alone did not alter any of the parameters compared with vehicle treated Wistar rats. Myricetin treated animals showed a lesser degree of cellular infiltration in histopathological studies. Thus, myricetin (100 mg/kg and 300 mg/kg) ameliorates the cardiotoxic effects of isoproterenol and may be of value in the treatment of MI.
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PMID:Cardioprotective potential of myricetin in isoproterenol-induced myocardial infarction in Wistar rats. 1930 80

The present study was designed to evaluate the cardioprotective potential of salvianolic acid A on isoproterenol-induced myocardial infarction in rats. Hemodynamic parameters and lead II electrocardiograph were monitored and recorded continuously. Cardiac marker enzymes and antioxidative parameters in serum and heart tissues were measured. Assay for mitochondrial respiratory function and histopathological examination of heart tissues were performed. Isoproterenol-treated rats showed significant increases in the levels of lactate dehydrogenase, aspartate transaminase, creatine kinase and malondialdehyde and significant decreases in the activities of superoxide dismutase, catalase and glutathione peroxidase in serum and heart. These rats also showed declines in left ventricular systolic pressure, maximum and minimum rate of developed left ventricular pressure, and elevation of left ventricular end-diastolic pressure and ST-segment. In addition, mitochondrial respiratory dysfunction characterized by decreased respiratory control ratio and ADP/O was observed in isoproterenol-treated rats. Administration of salvianolic acid A for a period of 8 days significantly attenuated isoproterenol-induced cardiac dysfunction and myocardial injury and improved mitochondrial respiratory function. The protective role of salvianolic acid A against isoproterenol-induced myocardial damage was further confirmed by histopathological examination. The results of our study suggest that salvianolic acid A possessing antioxidant activity has a significant protective effect against isoproterenol-induced myocardial infarction.
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PMID:Cardioprotective effect of salvianolic acid A on isoproterenol-induced myocardial infarction in rats. 1944 21

Lycopene, a carotenoid rich in tomato fruit (ripe), is an effective antioxidant and free radical scavenger. In this study n-hexane extract of tomato was evaluated for its protective action against oxidative stress in experimental myocardial infarction induced by administration of adrenaline in rats. Adrenaline produced significant elevation of malondialdehyde content of heart, an indicator of lipid peroxidation, with a significant rise in serum aspartate aminotransferase (AST) level and different grades of necrotic changes in myocardium. Rats were treated with two doses of n-hexane extract of tomato, intragastrically daily for one month prior to administration of adrenaline on the 31st and 32nd day. Pretreatment of tomato extract (1 mg/kg, 2 mg/kg) and vitamin E (50 mg/kg) significantly reduced the malondialdehyde concentration in heart and significantly lowered the serum AST level in adrenaline treated rats. Myocardial necrosis was significantly prevented by pretreatment. These results suggest that n-hexane extract of tomato possesses antioxidative property that may protect heart against catecholamine induced myocardial infarction.
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PMID:Protective effect of tomato against adrenaline-induced myocardial infarction in rats. 1947 57

Acute coronary syndrome is a set of symptoms interpreted as being the result of cardiac ischemia. The subtypes of acute coronary syndrome, depending on the degree of cardiac ischemia, include unstable angina and two forms of myocardial infarction. Determination of serum cardiac markers plays a key role in the diagnosis of acute myocardial infarction. Serum markers such as aspartate transaminase, lactate dehydrogenase, and creatine kinase are no longer used because they lack cardiac specificity and sensitivity. According to the NACB (National Academy of Clinical Biochemistry) recommendations, two serum cardiac markers need to be determined for routine diagnosis of acute myocardial infarction, i.e. one showing early elevation in serum (up to six hours after chest pain), and the other, late marker that is elevated six to nine hours after chest pain, has high sensitivity and specificity for detection of myocardial injury, and remains elevated for several days of the symptom onset. In current clinical practice, myoglobin, CKMB mass (improved diagnostic sensitivity in relation to CKMB activity) and cardiac troponins are commonly determined. CKMB mass is a cardiospecific marker, but can also be elevated in skeletal muscle damage. Myoglobin is not cardiospecific, but has high early sensitivity (fast and reliable exclusion of acute myocardial infarction) and the possibility of rapid assessment of the success of thrombolytic therapy. Cardiac troponins are late markers for the diagnosis of myocardial injury. They are markers with highest specificity and sensitivity for acute myocardial infarction. New markers such as ischemia modified albumin, heart fatty acid binding protein, glycogen phosphorylase isoenzyme BB, carboanhydrase 3, and new tehnologies are under investigation to advance our knowledge about heart disease.
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PMID:[Biochemical markers in the diagnosis of acute coronary syndrome]. 1968 56

The protective effect of aspartate and glutamate in isoproterenol induced myocardial infarction (MI) was investigated in experimental animals. Male albino wistar rats were pretreated with aspartate [100mg (kg body weight)-1 day-1] or glutamate [100mg (kg body weight)-1 day-1] intraperitoneally for a period of 7 days. Following amino acid treatment, MI was induced in rats by subcutaneous injection of isoproterenol [200mg (kg body weight)-1 day-1] for 2 days. After 24h following the last injection, the animals were sacrificed and the biochemical analysis was carried out. The activities of cardiac marker enzymes (alanine transaminase, aspartate transaminase, lactate dehydrogenase and creatine phosphokinase) were increased significantly (P<0.05) in the serum of MI induced rats as compared to control rats. The levels of glutathione and mitochondrial ATP and the activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase and glutathione reductase) were decreased whereas lipid peroxides increased significantly (P<0.05) in the heart of MI induced rats as compared to control rats. However, pretreatment with aspartate or glutamate to MI induced rats significantly (P<0.05) reduced the activities of cardiac marker enzymes and increased the activities of antioxidant enzymes as compared to MI induced rats. Aspartate or glutamate pretreatment also increased the levels of glutathione and mitochondrial ATP while decreased the level of lipid peroxides in the cardiac tissue. The overall effects of aspartate and glutamate in reducing the oxidative stress in MI induced rats are similar. There was no significant difference between the control rats and aspartate or glutamate treated control rats. The present study shows that aspartate and glutamate could reduce oxidative stress in MI induced rats.
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PMID:Aspartate and glutamate prevents isoproterenol-induced cardiac toxicity by alleviating oxidative stress in rats. 1996 69


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