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)

1. The effects of implanting turkeys with trienbolone acetate (TA) upon fluid balance and blood chemistry were studied. 2. The Na and water contents of skeletal muscles were increased by TA treatment while K was unaltered. 3. The extracellular space expressed as a proportion of starved body weight was unaffected by TA implantation. 4. Plasma or serum concentrations of P, Ca, Mg, Na and K and activities of the enzymes aspartate aminotransferase [EG 2.61.1], creatine kinase [EC 2.7.3.2] and gamma-glutamyl transferase [EC 2.3.2.2] were not changed by TA treatment. 5. Packed cell volume was significantly increased by TA implantation after a delay of some 2 to 3 weeks while plasma protein concentrations were immediately decreased for a period of two weeks before nearly normal concentrations were obtained again. 6. Erythrocyte sedimentation rate was decreased by TA treatment, but serum protein electrophoretic pattern was unchanged.
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PMID:The effects of trienbolone acetate implantation of turkeys upon fluid balance and blood chemistry. 726 Jul 1

In this study, isozyme patterns for 14 different enzymes were compared for culture strains of Leishmania braziliensis, L. hertigi, L. mexicana, L. donovani, L. tropica, and L. adleri. The isozyme separation was made by means of cellulose acetate electrophoresis. Each of the species had distinct isozyme patterns for aspartate aminotransferase, glucose 6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and fructokinase. For other enzymes, two or more species had identically migrating bands; however, by using combinations of the other 10 enzymes it was possible to separate any one of the six species. In addition to these interspecific differences the Panama strains of L. braziliensis had two different malic dehydrogenase isozyme patterns; therefore, they fell into two distinct groups. These strains otherwise had identical isozyme patterns.
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PMID:Characterization of Leishmania spp. by isozyme electrophoresis. 736 38

Cardiac metabolism following hypothermic potassium cardioplegia was studied in 23 patients undergoing isolated aortic valve replacement. All had normal coronary arteries. Cardioplegia was induced by infusing 700-1 000 ml of cold Ringer's acetate containing 20 mekv K+ selectively into the left coronary artery. Simultaneous blood samples were taken from the radial artery, a central vein and from the coronary sinus before and after cardioplegia. The PO2, O2-saturation and content, PCO2, pH, lactate, glucose, potassium, myoglobin, total creatine kinase (CK), its isoenzyme CK-MB, aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) were assessed. Before bypass lactate was extracted by the heart. During the initial 10 to 20 min after cardioplegia there was a marked release of lactate in the coronary sinus. Myoglobin concentration and CK-MB serum activity peaked during the first 4 hours after the release of the aortic cross-clamping. In order to determine the best indicator of myocardial damage after cardioplegia, duration of extracorporeal circulation (ECC-time), aortic occlusion time (AOT), mean myocardial temperature (MMT) and the product of AOT and MMT, referred to as time-temperature area (TTA), were related to possible indicators of myocardial injury, such as enzyme and myoglobin release. The TTA was the best way of expressing the degree of exposure of the heart to ischaemia. The CK-MB to peak area (CK-MB max area) was the best indicator of the degree of ischaemic injury sustained by the heart during operation.
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PMID:Myocardial protection during aortic valve replacement. Cardiac metabolism and enzyme release following hypothermic cardioplegia. 737 90

Holstein bull calves were used to determine the influence of degradable nitrogen and ration physical form on rumen epithelial transport and enzymic activity. Rations contained 30, 45 and 60% ruminal degradable nitrogen (RDN), each with three forms (ground hay, GR; chopped hay, CH; and all concentrate, CONC). Rumen tissue samples were obtained by biopsy (8 weeks) and at slaughter (20 weeks). Acetate transport across rumen epithelium increased between 8 and 20 weeks in calves fed GR and CH, but not in calves fed CONC. Propionate transport was highest in calves fed GR and lowest in calves fed CONC at both 8 and 20 weeks. Transport of acetate and propionate was incresed with increasing RDN at 20 weeks. There were no differences in ruminal tissue lactate production. Rumen papillae of calves fed CONC were abnormal in morphology and at 20 weeks dry mucosal weights (mg/cm2) were highest. Lactate dehydrogenase and NADP-malic dehydrogenase activities were not different. Propionyl CoA synthetase activity was higher in 20-week calves fed CONC, compared to GR to CH. Glutamate dehydrogenase and aspartate aminotransferase activities were highest in 20-week calves fed 60% RDN rations, regardless of physical form.
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PMID:Influence of ration physical form, ruminal degradable nitrogen and age on rumen epithelial propionate and acetate transport and some enzymatic activities. 744 67

The kidney is probably the major site of production of the plasma enzyme glutathione peroxidase (GSHPx-P). For this study, GSHPx-P activity was determined in 40 healthy people, in 34 patients with differing degrees of renal impairment, and in hemodialysis patients from whom blood samples were withdrawn either before or after each session (18 patients) or throughout the dialysis session (27 patients). Hemodialysis patients were treated by means of different techniques (bicarbonate hemodialysis, hemodiafiltration, and acetate free biofiltration), and different membranes (cuprophane, polyacrylonitrite, and polymethylmethacrylate). The following results were obtained: 1) GSHPx-P activity was significantly decreased in renal impairment patients; 2) GSHPx-P activity negatively correlated with serum creatinine values in renal impairment patients (r = -0.55; p < 0.001); and 3) the enzyme activity slightly increased after the session in hemodialysis patients. The following conclusions can be drawn: GSHPx-P activity could be new index of renal function, because it was decreased in patients with renal failure; the decrease in GSHPx-P activity paralleled the severity of renal impairment, and was maximal in hemodialysis patients; GSHPx-P activity was slightly raised at the end of the hemodialysis session, concomitant with other enzyme activities (aspartate transaminase, alanine transaminase, and alkaline phosphatase) and total protein concentration. This seems to be attributable to the process of water loss rather than other hypothetical mechanisms, such as A) enzyme activation by either peroxide generation during blood-membrane contact, or by the removal of a hypothetical inhibitor; and B) de novo synthesis in the residual renal mass or in other sites of production.
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PMID:The plasma glutathione peroxidase enzyme in hemodialyzed subjects. 785 33

Weiss et al. (Circ. Res. 70: 392-408, 1992) proposed a model of the citric acid cycle (CAC) in myocytes and a system of 17 differential equations that can be used to describe the changes over time in enrichment of carbons C-2 and C-4 of glutamate under conditions of metabolic steady state. They also proposed an empirical measure (KT) of flux through the CAC, which has been shown to be correlated to O2 consumption in rat hearts perfused with acetate or a mixture of glucose and acetate. We report a new method for estimation of the absolute rate of the flux through the CAC in heart (vTCA), without the numerical solution of differential equations. Unlike KT, our estimate is equal to the rate of flux catalyzed by the alpha-ketoglutarate dehydrogenase complex (vTCA), not merely correlated with it. We also estimate the rate of flux catalyzed by aspartate aminotransferase (vTA) and by NADP(+)-dependent malic enzyme (an anaplerotic reaction). The formula for vTCA during administration of [2-13C]acetate is as follows: vTCA = M[(C-2ssLC-4)/[C-4ss(LC-4-LC-2)]], where C-2ss and C-4ss represent steady-state fractional enrichment, LC-2 and LC-4 represent dominant rate constants of C-2 and C-4 of glutamate, respectively, and M is the sum of concentrations of aspartate, glutamate, and intermediates of the CAC. The assumptions underlying our formula are as follows: 1) metabolic steady state is maintained, 2) exchange of molecules between cytosolic and mitochondrial compartments is rapid, 3) 13C enters pools of the CAC only from acetyl CoA via citrate synthase, 4) [citrate]/[glutamate] < 1 + (vTCA/vTA), and 5) (m-[glutamate])/M < C-2ss/C-4ss.
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PMID:Estimation of TCA cycle flux, aminotransferase flux, and anaplerosis in heart: validation with syntactic model. 790 Jul 86

Hepatic and renal subacute toxicity induced by the antineoplastic drugs chlorambucil, cisplatin, epirubicin and methotrexate and the steroid alkylating agent 3 beta-hydroxy-13 alpha-amino-13,17-seco-5 alpha-androstan-17-oic-13, 17-lactam (p-[bis(2-chloroethyl) amino] phenyl) acetate was investigated in rats using serum biochemical parameters. Toxicological evaluation was performed in serum samples following the administration of dose regimens of the agents that were previously shown to be effective in suppressing malignant tumor growth or to prolong survival in tumor bearing animals. Hepatic and renal subacute toxicity was evaluated by measuring enzyme activity or concentrations of: alanine aminotransferase, alkaline phosphatase, aspartate aminotransferase, total cholesterol, gamma-glutamyltransferase, glucose, potassium, sodium, blood urea nitrogen and uric acid. The use of the above serum biochemical parameters indicated that the overall toxicity impact of the antitumor drugs was methotrexate < cisplatin < epirubicin < chlorambucil. The homo-azasteroid ester only transiently affected the biochemical parameters associated with renal toxicity, while it affected some of the biochemical parameters associated with hepatic toxicity, though to a significantly lower extent than the antitumor drugs.
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PMID:Evaluation of kidney and liver subacute toxicity of antitumor agents using serum biochemical parameters in rats. 790 82

Previous studies have demonstrated that alpha-tocopheryl hemisuccinate (TS) protects hepatocyte suspensions from chemical-induced toxicity. It has been suggested that TS cytoprotection is related to unique properties of the TS molecule or is dependent on the cellular release and activity of unesterified alpha-tocopherol (T). To test the unique cytoprotective nature of TS in vivo, the protective ability of T and tocopherol esters against carbon tetrachloride (CCl4)-induced hepatotoxicity in rats was examined. Hepatoprotection [determined by serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and histopathology] was not observed after T (or tocopheryl acetate and tocopheryl nicotinate) administration, even though this treatment resulted in a fivefold elevation in hepatic T content. Only pretreatment with TS (100 mg/kg, intraperitoneally) resulted in partial hepatoprotection against CCl4 (2.9 g/kg, orally) toxicity. These findings suggest that hepatoprotection results not from the cellular accumulation of T but rather from the intact TS molecule. To test this hypothesis, the hepatoprotective capacity of cholesteryl hemisuccinate (CS), unesterified cholesterol, and cholesteryl acetate (CA) was examined against CCl4 toxicity. As observed with the tocopherol derivatives, pretreatment with unesterified cholesterol or CA demonstrated no protective ability. However, when rats were pretreated with CS (100 mg/kg), the hepatotoxic effects of CCl4 (elevated serum AST and ALT levels and centrilobular necrosis) were completely prevented. The prevention of CCl4-induced hepatotoxicity by CS and TS do not appear to result from an alteration in hepatic drug metabolism. These data clearly demonstrate that CS and TS are unique and powerful cytoprotective agents against CCl4 hepatotoxicity in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protection against carbon tetrachloride-induced hepatotoxicity by pretreating rats with the hemisuccinate esters of tocopherol and cholesterol. 813 82

Subclinical nutritional myopathy was induced in 5-month-old sheep by feeding them a diet low in vitamin E and selenium. Subsequently clinical myopathy was induced by dosing with protected polyunsaturated fatty acids. Plasma activities of creatine kinase (CK), pyruvate kinase, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase and aldolase, enzymes of muscle origin, all remained above their reference ranges in clinically affected sheep, but fluctuated widely. Similar fluctuations occurred in subclinically affected animals, resulting in some activities being within the reference ranges and some above, at different times. Plasma malondialdehyde, an indicator of lipid peroxidation, proved of no diagnostic value. Terminal plasma CK activities were significantly correlated with microscopic damage in the vastus lateralis (VL), but not the vastus intermedius (VI) or the tensor fascia lata (TFL) muscles. AST was the most highly correlated with damage in VI and VL. In two clinically affected sheep successfully treated with an oral dose of alpha-tocopherol acetate all enzymes decreased steadily to within their reference ranges, at rates probably related to their plasma half-lives. These results suggest that measurement of plasma CK activity would be useful in monitoring recovery of treated sheep.
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PMID:Plasma indicators of muscle damage in a model of nutritional myopathy in weaner sheep. 817 46

The effects of calcitonin (CT) on oxyradical generation and cellular damage induced by carbon tetrachloride (CCl4) were investigated in rat hepatocytes. Addition of CCl4 to the cells concentration dependently increased intracellular production of hydroperoxides and release of aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The hepatocytes expressed mRNA for a CT receptor, C1b. Coaddition of CT to the cells concentration dependently suppressed the CCl4-induced increase in hydroperoxide production and also decreased the release of AST and ALT. The suppressive effect of CT on hydroperoxide production was reversed by further addition of H7 or by pretreatment with phorbol 12-myristate 13-acetate for 24 h. These results suggest that CT prevents CCl4-induced oxyradical production and cellular damage through activation of protein kinase C in hepatocytes.
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PMID:Calcitonin prevents CCl4-induced hydroperoxide generation and cytotoxicity possibly through C1b receptor in rat hepatocytes. 857 6


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