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)

Rat liver mitochondria, stored with the energy-linked functions preserved or in aging conditions, were used to assay the activity of various enzymes during five days. The preservation of energy-linked functions was monitored by the respiratory control coefficient. ATPase, cytochrome oxidase and NADH dehydrogenase showed increased activity when the energy-linked functions were preserved. In aging conditions, cytochrome oxidase, NADH dehydrogenase and ATPase showed decreased activity. The ATPase activity increased only when mitochondria were stored in the presence of inhibitors of the electron transport chain. The activity of NADH oxidase did not change, and succinate oxidase and succinate dehydrogenase showed a small decrease in their activity. The enzymes of the matrix, alpha-ketoglutarate dehydrogenase, malate dehydrogenase and aspartate aminotransferase showed little decrease in activity under either of the conditions of storage. The total protein content decreased slightly under both conditions of storage. These results show that the activity of the enzymes analysed was maintained at reasonable levels, when the energy-linked functions of isolated mitochondria were preserved.
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PMID:Studies on rat liver mitochondria: 4. Enzyme activities in mitochondria preserved at 0-4 degrees C. 646 13

To better characterize the role of skeletal muscle in chronic heart failure we studied energetic charge, metabolites and enzyme activity in the energy production pathway. We selected 15 males with severe chronic heart failure (NYHA class III, stable clinical conditions and in normal nutritional status) and seven controls. Controls and patients were submitted to biopsy of the vastus lateralis muscle in resting and fasting conditions. Hormone profiles were also evaluated. Our results showed near normal ATP, ADP and AMP concentrations, but there were substantially more reductions in glycogen (46 +/- 5 vs 77 +/- 6 mumoles glycosidic units.g-1 fresh tissue) and creatine phosphate (5 +/- 1 vs 13 +/- 1 mumoles.g-1 fresh tissue) in patients than in controls. We also found a reduction in glycolytic activity (pyruvate kinase 1009 +/- 79 vs 1625 +/- 26 nmoles. min-1.mg protein-1), despite normal tricarboxylic acid cycle velocity, an increase in alanine amino-transferase (964 +/- 79 vs 425 +/- 34 nmoles. min-1.mg protein-1) and in aspartate aminotransferase (515 +/- 44 vs 291 +/- 56 nmoles.min-1.mg protein-1). An increase was also observed in total NADH cytochrome c reductase (128 +/- 14 vs 68 +/- 5 nmoles.min-1.mg protein-1), while cytochrome oxidase activity was normal. The cortisol/insulin ratio was slightly elevated (77 +/- 4 vs 32 +/- 12). In conclusion, normonutritive patients with severe heart failure show an imbalance in the energy production/utilization ratio. The impairment is probably due both to a decrease in production and an increase in consumption of energy owing to greater cellular workload and/or a hypercatabolic state.
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PMID:Biochemical analysis of muscle biopsy in overnight fasting patients with severe chronic heart failure. 892 17

Morphological and biochemical changes in mitochondrial have been reported early in the course of cocaine-induced hepatotoxicity. This study was designed to examine the effects of repeated cocaine exposure in vivo on mitochondrial respiration, activities of respiratory chain enzymes, and lipid peroxide measures in liver. Male Sprague-Dawley rats were exposed to cocaine (5 i.p. injections of 25 mg/kg; 3-day period). Blood and liver samples were taken, and hepatic mitochondria were isolated by differential centrifugation. The cocaine-treated rats developed oxidative stress in hepatic mitochondria as evidenced by a significant increase in malonaldialdehyde (MDA; 52%; p < 0.0001) and a decreased glutathione (GSH; 22%; p < 0.0003). Blood aspartate aminotransferase (AST) and glutathione s-transferase (GST) levels in cocaine groups were significantly elevated (2.6 and 3.2 fold, respectively; p < 0.0001 for both). Cocaine caused a decrease in state-3 respiration and respiratory control ratio (RCR) ratio when exposed to site I and II substrates; these changes were parallelled by a decrease in complex I (22%; p < 0.003), succinate cytochrome c reductase (27%; p < 0.004), and complex IV (24%; p < 0.003). In conclusion, functional abnormalities of hepatic mitochondria accompany lipid peroxidation caused by cocaine, supporting the hypothesis that the mitochondria is one of the major intracellular targets of cocaine hepatotoxicity.
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PMID:Impairment of mitochondrial respiration and electron transport chain enzymes during cocaine-induced hepatic injury. 907 24

Skeletal muscle biopsies were performed on 12 healthy sedentary subjects and on 22 non-dyalized chronic renal failure patients (CRF) on a free diet and after overnight fasting. Parathormone, glucagon and insulin were determined at the same time of biopsies. CRF patients showed significantly low ATP and creatine phosphate levels. Regarding enzyme activities, a high hexokinase Vmax was found, while the pyruvate kinase activity was lower than in the control group. For the tricarboxylic acid cycle, citrate synthase, succinate dehydrogenase and malate dehydrogenase activities were higher; total NADH cytochrome c reductase activity was also high, while cytochrome oxidase activity was slightly lower. Both alanine aminotransferase and aspartate aminotransferase activities were considerably high in comparison with the control group. In conclusion, our study revealed a hypermetabolic TCA cycle, but impaired oxidative phosphorylation, which partly explained the reduced ATP concentration. Excessive protein intake and hormonal derangements may play a role in these metabolic changes.
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PMID:Altered muscle energy metabolism in post-absorptive patients with chronic renal failure. 924 94

Experiments were performed on eight subjects affected by peripheral arterial occlusive disease (PAOD) of the lower limbs. Each patient was submitted to Ecodoppler, angiography and the "Treadmill test". Two bioptic muscle of these patients. A sample was used for the spectrophotometric and spectrophotofluorimetric determinations of: glycogen, pyruvate, lactate, citrate, alpha-ketoglutarate, malate, aspartate, glutamate, AMP, ADP, ATP and creatine phosphate (CP). The other bioptic sample was used to determine the following enzyme activities: hexokinase, phosphofructokinase, pyruvate kinase, lactate dehydrogenase, citrate synthase, succinate dehydrogenase, malate dehydrogenase, total NADH cytochrome c reductase, cytochrome oxidase, aspartate aminotransferase and alanine aminotransferase. Patients showed an increase in lactate dehydrogenase, total NADH cytochrome c reductase and succinate dehydrogenase activities, a decrease in glycogen, ATP and CP concentrations. Telethermographic data showed patient muscle thermic emission quantitatively different from control group. The telethermographic test can be used as an additional diagnostic tool to determine and monitor the efficiency of a muscle undergoing metabolic failure.
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PMID:Instrumental and metabolic evaluation of patients affected by peripheral arterial occlusive disease (PAOD) following surgical revascularization surgery. 928 78

Continuous warm blood cardioplegia was widely used, as an effective means of myocardial preservation, in open heart surgery. The comparisons of myocardial protective effects between traditional cold crystalloid and warm blood cardioplegia, however, have been based mainly on hemodynamics, cardiac function and myocardial metabolism, other than clinical outcome. The present study was designed to examine myocardial protective effects by assessing clinical outcome, enzyme levels and myocardial cytochemistry. Twenty patients undergoing heart valve replacement were divided randomly into two groups: Group I was given intermittent perfusion of cold crystalloid (St. Thomas Hospital solution) with hypothermic cardiopulmonary bypass (CPB) and Group II was given continuous administration of warm blood cardioplegia with normothermic CPB. The groups were similar with respect to sex, age, body surface area and preoperative ventricular function. Blood samples were obtained from an indwelling radial arterial catheter or from the arterial end of the oxygenator. Biopsy specimens from the right atrium were obtained immediately before aortic declamping (ischemic period) and 30 minutes after crossclamp removal (reperfusion period). Serum enzymes, including alanine transaminase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and its isoenzymes and creatine phosphokinase (CK) and its isoenzyme, were determined. Myocardial cytochemistry were chiefly assessed by grey-scale image processing of adenosine triphosphatase (ATPase), succinate dehydrogenase (SDH) and cytochrome oxidase (CCO) examinations. Relations among the results were discussed. Reperfusion time was reduced and ventilation support time decreased in Group II (33.50 +/- 3.78 min vs. 25.00 +/- 4.46 min, p < 0.05; 38.98 +/- 16.55 h vs. 19.84 +/- 1.11 h, p < 0.05). Rates of atrial beating during aortic crossclamp and spontaneous recovery to normal sinus rhythm were much higher in Group II than in Group I (80% vs. 20%, p < 0.05; 70% vs. 10%, p < 0.05). Differences in hospital morbidity and mortality between groups were nonsignificant. Serum AST, ALT, LDH and LDH1 + LDH2 all showed no significant intergroup differences. There was a higher serum CK-MB level with a delayed peak in Group II. The cytochemistry activities of ATPase was not different between groups and periods and SDH was the highest during reperfusion period in Group I and of CCO significantly much promoted in Group II in both periods. Continuous warm blood cardioplegia resulted in higher spontaneous recovery to sinus rhythm, shorter reperfusion and ventilation support time. Damage to the myocardium, skeletal muscle and liver always occur in warm blood cardioplegic patients. However, warm blood cardioplegia is still a practical method for myocardial preservation in open heart surgery.
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PMID:A generalized consideration of myocardial preservation with cold crystalloid versus warm blood cardioplegia in heart valve replacement. 961 11

Enhancing the portal venous blood flow (PVBF) has been shown to reduce portal pressure and intrahepatic vascular resistance and to improve liver function in isolated cirrhotic rodent livers in vitro. The aim of this study was to assess the short-term effect of mechanically pumping the portal inflow on hepatic microcirculation (HM), oxygenation, and function in an animal model of extensive hepatic fibrosis. New Zealand white rabbits underwent laparotomy and exposure of the liver: group 1 (n = 7) were normal controls; group 2 (n = 7) had hepatic fibrosis. Total hepatic blood flow (THBF) and HM was measured along with continuous monitoring of intrahepatic tissue oxygenation using near infrared spectroscopy (NIRS). Baseline hepatic hemodynamics and liver function were measured in both groups. PVBF was then increased by 50% over a 3-hour period in the hepatic fibrosis group using a miniature portal pump designed for human implantation, and the hemodynamics were monitored continuously. Liver function tests were repeated after portal pumping. In comparison with normal controls, animals with hepatic fibrosis had a higher portal pressure (13.0 +/- 3.6 vs. 3.7 +/- 1.4 mm Hg, P <.001, mean +/- SD vs. controls), reduced PVBF (52.4 +/- 24.6 vs. 96.9 +/- 21.1 mL/min, P =.003), and increased portal vascular resistance (P =. 001). THBF and flow in the HM was lower than in controls, and liver function tests were abnormal. After a 3-hour period of enhanced portal flow in animals with hepatic fibrosis, the portal pressure greatly reduced (13.0 +/- 3.6 to 2.5 +/- 1.1 mm Hg, P <.001) as did the intrahepatic portal resistance (0.32 +/- 0.18 to 0.04 +/- 0.03 mm Hg/mL/min, P =.006). Flow in the HM improved (143 +/- 16 to 173 +/- 14 flux units, P =.006) and was associated with improved hepatic tissue oxygenation, tissue oxy-hemoglobin (HbO2) and cytochrome oxidase being increased by 24.4 +/- 7.5 and 5.65 +/- 2.30 micromol/L above the baseline value (P <.001), respectively. A 3-hour period of mechanical portal pumping produced a dramatic improvement in liver function, bilirubin (41.1 +/- 25.9 to 10.0 +/- 5.9 micromol/L, P =. 040), aspartate transaminase (AST) (135.5 +/- 52.3 to 56.3 +/- 19.8 U/L, P =.006) and lactate dehydrogenase (LDH) (2,030.1 +/- 796.3 to 1,309.8 +/- 431.6 IU/L, P =.006; prepumping vs. postpumping, all P <. 050). In conclusion, portal pumping in this rabbit model with extensive hepatic fibrosis improved liver parenchymal perfusion, oxygenation, and function.
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PMID:The effect of mechanically enhancing portal venous inflow on hepatic oxygenation, microcirculation, and function in a rabbit model with extensive hepatic fibrosis. 1038 37

A 9-month-old male German Shepherd dog was referred for evaluation of progressive exercise intolerance. Clinical examination revealed a stiff, stilted gait and marked atrophy and hypotonia of skeletal muscle. The dog had raised creatine kinase (181 U/liter), lactate dehydrogenase (510 U/liter), and aspartate aminotransferase (123.6 U/liter) levels, suggesting a muscle disease. Histochemical evaluation of muscle biopsies revealed the presence of subsarcolemmal oxidative activity, reduced nicotinamide adenine dinucleotide, and succinate dehydrogenase, and the absence of cytochrome oxidase activity. Ragged red fibers were demonstrated with Gomori trichrome stain. Ultrastructural examination of the muscle confirmed the presence of subsarcolemmal accumulations of mitochondria and morphologically atypical mitochondria.
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PMID:Mitochondrial myopathy in a german shepherd dog. 1294 7

IPC (ischaemic preconditioning) may protect the steatotic liver, which is particularly susceptible to I/R (ischaemia/reperfusion) injury. Hepatic steatosis was induced in Sprague-Dawley rats with a high-cholesterol (2%) diet for 12 weeks after which rats were subjected to I/R (ischaemia/reperfusion; 45 min of lobar ischaemia followed by 2 h of reperfusion). Rats were divided into three study groups (n=6 each) receiving: (i) sham laparotomy alone, (ii) I/R, and (iii) IPC (5 min of ischaemia, followed by 10 min of reperfusion) before I/R. Hepatic extra- and intra-cellular oxygenation and HM (hepatic microcirculation) were measured with near-infrared spectroscopy and laser Doppler flowmetry respectively. Plasma liver enzymes and hepatic tissue ATP were measured as markers of liver injury. Histology showed moderate-grade steatosis in the livers. At the end of 2 h of reperfusion, I/R significantly decreased extra- and intra-cellular oxygenation concomitant with a failure of recovery of HM (21.1+/-14.4% of baseline; P<0.001 compared with sham animals). IPC increased intracellular oxygenation (redox state of the copper centre of cytochrome oxidase; P<0.05 compared with rats receiving I/R alone) and flow in HM (70.9+/-17.1% of baseline; P<0.001 compared with rats receiving I/R alone). Hepatocellular injury was significantly reduced with IPC compared with I/R injury alone (alanine aminotransferase, 474.8+/-122.3 compared with 5436.3+/-984.7 units/l respectively; P<0.01; aspartate aminotransferase, 630.8+/-76.9 compared with 3166.3+/-379.6 units/l respectively; P<0.01]. In conclusion, IPC has a hepatoprotective effect against I/R injury in livers with moderate steatosis. These data may have important clinical implications in liver surgery and transplantation.
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PMID:Effect of ischaemic preconditioning on hepatic oxygenation, microcirculation and function in a rat model of moderate hepatic steatosis. 1534 10

Piscicidal activities of aqueous extracts of Euphorbia tirucalli were very well established, but their ultimate mode of action on fish metabolism was not yet known. Exposure of fishes over 24h or 96h to sub-lethal doses (40% and 80% of LC(50)) of aqueous extract of E. tirucalli stem-bark and latex, significantly (P<0.05) altered the level of total protein, total free amino acids, nucleic acids, glycogen, pyruvate, lactate and activity of protease, alanine aminotransferase, aspartate aminotransferase, acetylcholinesterase and cytochrome oxidase enzyme in liver and muscle tissues of freshwater fish Channa punctatus. The alterations in all these biochemical parameters were significantly (P<0.05) time- and dose-dependent. After 7d of withdrawal of treatment of 80% of LC(50) of E. tirucalli extracts shows that there was a partial recovery in the levels of glycogen but nearly complete recovery in total protein, total free amino acids, pyruvate, lactate, nucleic acids level and activity of protease, aspartate aminotransferase, alanine aminotransferase, acetylcholinesterase and cytochrome oxidase enzyme in both the tissues of fish. Thus aqueous extracts of E. tirucalli adversely affect respiratory pathway of fish and cause energy crisis during stress by suppressing ATP production. The reversibility of the action of the aqueous extracts would be an additional advantage in their use.
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PMID:Biochemical stress response in freshwater fish Channa punctatus induced by aqueous extracts of Euphorbia tirucalli plant. 1642 80


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