Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

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

Adult GH deficiency (AGHD) has been established as a syndrome associated with various metabolic disturbances such as hyperlipidemia, impaired glucose tolerance and protein catabolism, in addition to changes in body composition such as increased visceral fat, decreased muscle mass and bone density. We investigated the clinical findings, complications and prognosis of AGHD in Japan. The questionnaire was sent to various expert facilities of endocrinology and metabolism to gather cross-sectional information as well as longitudinal follow-up data on adult patients with hypopituitarism. We received answers on 422 subjects, of which number the GH stimulation test was performed in only 63% of them. An age- and sex-matched group of 259 adults with hypopituitarism (125 male and 134 female subjects) was finally selected for this investigation. Of them 185 subjects (81 male and 104 females) were diagnosed as AGHD with plasma peak GH levels less than 3 ng/ml after GH stimulation test. Male adult patients with GHD had significantly lower ratio of smoking and drinking in their life style compared with those without GHD. Male adult patients with GHD revealed significantly higher BMI on physical examination, and significantly higher plasma ALT, AST, total cholesterol, and LDL cholesterol in blood chemistry compared with those without GHD (P < 0.05). Though patients with ischemic heart disease were more frequent in female patients than male patients, the rate of frequency was not different between female adult patients with and without GHD. Clinical characteristics found in especially male adult patients with GHD in Japan were consistent with findings reported so far in foreign countries. However, consequent complications such as atherosclerosis seemed less severe than expected. Moreover, GH stimulation test for the diagnosis of AGHD as well as clinical test to perform when AGHD was suspected is still less frequently carried out. Therefore, the clinical outcome of AGHD in our country requires further investigation.
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PMID:Adult growth hormone deficiency in Japan: results of investigation by questionnaire. 1262 8

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

The dysfunction of muscles, especially that of the cardiac muscle, is one of the most dangerous for the life pathological states. The determination of biochemical indexes such as AST, ALT, CK, LDH, mioglobin, etc., which has been used so far in animals is not a sufficient diagnostic method. Therefore, new markers, levels of which could reflect the state of a patient more precisely, have been sought. Troponin, a protein found in skeletal and cardiac muscles only, has been considered a reliable index of myocardial ischemia in animals, especially in dogs. Its diagnostic properties have appeared to be a valuable complementation of the other diagnostic methods and thus could have gained a lot of veterinary practitioners interest.
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PMID:Troponin--a new marker in the diagnostics of muscle diseases in animals. 1470 75

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

The pathological role of the non-enzymatic modification of proteins by reducing sugars has become increasingly evident in various disorders. It is now well established that early glycation products undergo progressive modification over time in vivo to the formation of irreversible cross-links, after which these molecules are termed "AGEs (advanced glycation end products)". AGEs have been implicated in the development of many of the pathological sequelae of diabetes and aging, such as diabetic microangiopathy, ischemic heart disease and neurodegenerative diseases. Recently, digested food-derived AGEs are also found to play an important role in the pathogenesis of AGE-related disorders. Diet is a major environmental source of pro-inflammatory AGEs. Indeed, restriction of dietary glycotoxins decreases excessive AGE levels and subsequently reduces the inflammatory responses in patients with diabetes. These observations suggest that inhibition of absorption of dietary AGEs may be a novel target for therapeutic intervention in the above-mentioned AGE-related disorders. AST-120 (Kremezin) is an oral adsorbent that attenuates the progression of chronic renal failure (CRF) by removing uremic toxins. We have recently found that AST-120 binds to carboxymethyllysine (CML), one of the well-characterized, digested food-derived AGEs in vitro and that administration of AST-120 decreases serum levels of AGEs in non-diabetic CRF patients. These findings suggest that digested food-derived AGEs such as CML may be a novel molecular target for oral adsorbent AST-120 and that AST-120 could exert beneficial effects on CRF patients by adsorbing diet-derived AGEs and subsequently decreasing serum AGE levels. If our speculation is correct, AST-120 may have therapeutic potentials for the treatment of patients with various AGE-related disorders as well. In this paper, we would like to propose the possible ways of testing our hypotheses. Does the long-term treatment of AST-120 decrease serum and tissue levels of AGEs in diabetic patients? Does this treatment also reduce the risk for the development and progression of diabetic vascular complications such as diabetic retinopathy or ischemic heart disease? If the answers are yes, do the serum and/or tissue levels of AGEs after AST-120 treatment predict its beneficial effects on diabetic vascular complications? How about the effects of AST-120 on Alzheimer's disease, another AGE-related neurodegenerative disorder? Does the treatment of AST-120 reduce the risk for Alzheimer's disease and/or improve the cognitive impairment of patients with this disorder? These prospective studies will provide further valuable information whether the inhibition of absorption of dietary AGEs by AST-120 could be clinically relevant.
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PMID:Oral administration of AST-120 (Kremezin) is a promising therapeutic strategy for advanced glycation end product (AGE)-related disorders. 1733 65

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

This study was designed to investigate the protective effect of oleanolic acid (OA) against isoproterenol-induced myocardial ischemia in rat myocardium. Wistar strain rats were pretreated with OA (20, 40, and 60 mg/kg, s.c) for 7 days and then intoxicated with isoproterenol (ISO, 85 mg/kg, sc for 2 consecutive days). Heart were excised from the experimental animals and assessed for the activities of marker enzymes [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)], the levels of lipid peroxide products [thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (HP) and conjugated dienes (CD)], myeloperoxidase (MPO), lipid profiles [total cholesterol (TC), free cholesterol, ester cholesterol, triglycerides (TG), free fatty acids (FFA) and phospholipids (PL)], and membrane-bound ATPase enzymes (total ATPase, Na(+)K(+) ATPase, Ca(2 +) ATPase, and Mg(2 +) ATPase). Troponin T and I were estimated in plasma. Leakage of cardiac markers, elevated lipid peroxidation with increased lipid profiles and decreased activities of membrane-bound ATPase enzymes were confirmed the severe myocardial damage occurring as a consequence of isoproterenol-induced ischemia, and they also showed the significant improvement effected by oleanolic acid pretreatment. These findings provided evidence that oleanolic acid was found to be protecting rat myocardium against ischemic insult and the protective effect could attribute to its anti-oxidative, anti-hyperlipedemic, and anti-arrhythmic properties as well as its membrane-stabilizing action.
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PMID:Cardioprotective effect of oleanolic acid on isoproterenol-induced myocardial ischemia in rats. 1745 91

L-arginine a semi essential amino acid and a precursor of nitric oxide (NO) was orally supplemented in diet (standard rabbit feed) of hypercholesterolemic (n=6) and normal rabbits (n=6) for 16 weeks. Myocardial ischemia was produced in both groups of rabbits by subcutaneous single bolus injection of isoproteronol. Severity of myocardial ischemia was assessed by estimating the serum CPK and AST levels after 6 hour of ischemia-reperfusion. The result suggests that severity of ischemia was lesser in the L-arginine primed hypercholesterolemic group.
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PMID:Effect of long term oral administration of L-arginine on experimentally produced myocardial ischemia in rabbits. 1817 58

D-ribose, a naturally occurring pentose carbohydrate, has been shown to replenish high- energy phosphates following myocardial ischemia and high intensity, repetitive exercise. Human studies have mainly involved short-term assessment, including potential toxicity. Reports describing adverse effects of D-ribose with prolonged ingestion have been lacking. Therefore, this study assessed the toxicity of extended consumption of D-ribose in healthy adults. Nineteen subjects ingested 20 grams/Day (10 grams, twice a Day) of ribose with serial measurements of biochemical and hematological parameters at Days 0, 7, and 14. No significant toxic changes over the 14-day assessment period occurred in complete blood count, albumin, alkaline phosphatase, gamma glutamyltransferase, alanine amiotransferase, and aspartate aminotransferase. However, D-ribose did produce an asymptomatic, mild hypoglycemia of short duration. Uric acid levels increased at Day 7, but decreased to baseline values by Day 14. D-ribose consumption for 14 days appears not to produce significant toxic changes in both hematological and biochemical parameters in healthy human volunteers.
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PMID:Assessment of Hematological and Biochemical parameters with extended D-Ribose ingestion. 1879 39


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