Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Crocodilians such as caimans and alligators are uricotelic and ammoniotelic animals. They are carnivorous but they excrete ammonium ions in an alkaline urine. The metabolic organization of the kidney of the Mississippi alligator was studied by measuring the renal metabolite profile, the activities of enzymes, and the behavior of kidney tubules in vitro. The liver and tail muscle were also studied. Both awake and anesthetized animals were in a state of low plasma bicarbonate and low blood pH with high plasma lactate concentration. This did not prevent the excretion of an alkaline urine (pH 7.76). alpha-Ketoglutarate was low in all three tissues and lactate was high. Glutamate concentration and glutamate dehydrogenase activity were highest in the kidney with a low equilibrium constant for alanine aminotransferase (KGPT). Glutaminase I was found only in the kidney. It could not be detected in liver or muscle. Glutamine synthetase was found only in the liver. Phosphoenolpyruvate carboxykinase (PEPCK) was present in both liver and kidney. Alanine aminotransferase and malic enzyme showed high activity in the kidney but were inconspicuous in liver and muscle. Malate dehydrogenase and lactate dehydrogenase were present in all three tissues. Renal tubules incubated with glutamine and alanine were ammoniagenic and gluconeogenic. Lactate was gluconeogenic. Enzyme activities were measured at both 30 and 37 degrees C. The studies on renal tubules were also performed at these two temperatures. Temperature had little effect on the data including acid-base values in the blood. Our findings demonstrate that the kidney of the alligator is perfectly equipped for various metabolic functions and especially for ammoniagenesis and gluconeogenesis.
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PMID:Metabolic machinery of the alligator kidney. 649 95

The present study was designed to test if both the intensity and duration of the 45-min Square-Wave Endurance Exercise Test (SWEET) would produce changes in serum enzyme activities. Nine men, four sedentary (S) and five athletes (A), performed VO2 max and SWEET, at their Maximal Intensity of Endurance (MIE45) as defined by maximal heart rate and the impossibility of maintaining MIE 45 + 5% for 45 min. Arterial blood was sampled at rest (R), exercise (Ex) (45th min) and during recovery (15th min) for measurements of levels of Haemoglobin (Hb), Haematocrit (Hct), pH and seven serum enzymes: Creatine kinase (CPK), Hexose-phosphate isomerase (PHI), Aldolase (ALD), Lactate dehydrogenase (LDH), Malate dehydrogenase (MDH), Aspartate amino-transferase (ASAT or GOT), and Alanine aminotransferase (ALAT or GPT). Five enzymes increased significantly during exercise (MIE45), the delta % (Ex - R/R) increases were as follows: PHI (72%), MDH (28%), LDH (21%), CPK (17%), and GOT (13.5%), whilst only a 10% increase was observed for Hct and Hb and there was no significant change in the arterial pH. There was no correlation between the delta % of Hb, Hct, pH, and the results for the enzymes. Thus, it does not seem that haemoconcentration and arterial blood acidosis which occur during exercise are only at the origin of the observed increases in enzymes. A difference between "sedentary" and "athletes" subjects was found at rest and exercise (delta % = A - S/S) for CPK (R = 222%; Ex = 235%), GOT (R = 90%; Ex = 75%) and ALD (R = 99%; Ex = 54%). These results suggest that the MIE45, by measured increases in enzymatic activity, seems to require great muscular effort.
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PMID:Serum enzyme variations in men during an exhaustive "square-wave" endurance exercise test. 653 38

Serum biochemical analyses were done on F344 rats in the early and late stages of mononuclear cell leukemia. There were marked increases in serum bilirubin, alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase and alkaline phosphatase. Increases in these parameters generally were more severe in the late stages of leukemia. Both direct and indirect-reacting bilirubin were increased with the unconjugated form predominating early and the conjugated form predominating late in the course of the disease. Lactate dehydrogenase isoenzyme determination correlated with histological examination indicated that liver damage was responsible for the observed changes. Urinalysis revealed marked hemoglobinuria, bilirubinuria and increased urine urobilinogen. Serum protein electrophoresis revealed marked reductions in the alpha globulin fractions.
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PMID:Pathology of the mononuclear cell leukemia of Fischer rats. III. Clinical chemistry. 664 40

Eighty-six patients who required heparin therapy were randomly assigned to receive bovine or porcine heparin. Abnormal concentrations of alanine transaminase and aspartate transaminase developed during treatment in 59.3% and 26.7% of patients, respectively. Patient characteristics that significantly influenced the development of abnormal alanine transaminase concentrations were male sex and higher baseline enzyme values. Transaminase concentrations returned to normal in 80% of patients after heparin therapy was discontinued and in 20% during therapy. Analysis of transaminase concentrations in all 86 patients showed that 95% had some increase in enzymes during treatment. Mean maximal increase over baseline for all patients was 3.6 for alanine transaminase and 3.1 for aspartate transaminase (range, 1.0 to 15). Lactate dehydrogenase concentrations became abnormal in 35.7% of patients. Lactate dehydrogenase isoenzyme determinations in 6 patients showed elevated hepatic fractions. No clinical symptoms of hepatic dysfunction were seen.
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PMID:Transaminase elevations in patients receiving bovine or porcine heparin. 671 30

The biochemical and morphological effects of 2, 10 and 100 mM of D-galactosamine (GalN) were studied in isolated rat hepatocytes during 2 h of incubation. Lactate dehydrogenase (LDH), alanine aminotransferase (ALAT) and cell viability did not change, whatever the concentration used. The variations observed, which were dose dependent, included a large drop in ATP levels and inhibition of RNA and protein synthesis. A very high concentration of GalN was necessary, however, to induce a significant decline in methionine adenosyltransferase activity compared to control cells. The use of L-[methyl-14C]methionine during cell incubation with GalN demonstrated a decrease of S-adenosyl-L-methionine (SAMe) and an accumulation of L-methionine content related to the GalN concentration. These results suggested that an hepatotoxic agent such as GalN was able to induce disturbances of methionine metabolism. Some of the ultrastructural changes observed were different from those previously found in vivo, in rats given GalN intraperitoneally, underlining the marked difference between in vivo and in vitro intoxication.
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PMID:Methionine metabolism and ultrastructural changes with D-galactosamine in isolated rat hepatocytes. 674 76

Renal adaptation to chronic metabolic acidosis was studies in Arbor Acre hens receiving ammonium chloride by stomach tube 0.75 g/kg/day during 6 days. During a 14-day study, it was shown that the animals could excrete as much as 60% of the acid load during ammonium chloride administration. At the same time urate excretion fell markedly but the renal contribution to urate excretion (14%) did not change. During acidosis, blood glutamine increased twofold and the tissue concentration of glutamine rose in both liver and kidney. Infusion of L-glutamine led to increased ammonia excretion and more so in acidotic animals. Glutaminase I, glutamate dehydrogenase, alanine aminotransferase (GPT), and malic enzyme activities increased in the kidney during acidosis but phosphoenolpyruvate carboxykinase (PEPCK) activity did not change. Glutaminase I was not found in the liver, but hepatic glutamine synthetase rose markedly during acidosis. Glutamine synthetase was not found in the kidney. Renal tubules incubated with glutamine and alanine were ammoniagenic and gluconeogenic to the same degree as rat tubules with the same increments in acidosis. Lactate was gluconeogenic without increment during acidosis. The present study indicates that the avian kidney adapts to chronic metabolic acidosis with similarities and differences when compared to dog and rat. Glutamine originating from the liver appears to be the major ammoniagenic substrate. Our data also support the hypothesis that hepatic urate synthesis is decreased during acidosis.
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PMID:The kidney of chicken adapts to chronic metabolic acidosis: in vivo and in vitro studies. 681 56

Serial estimations of activities of creatine kinase and its MB isoenzyme, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase and of concentrations of alpha(1)-acid glycoprotein were performed in 15 healthy well-trained male marathon runners. Estimations were made initially within three days before a race and then one, 24, and 96 hours after the race. Technetium-99m pyrophosphate myocardial scintigraphy was carried out at the initial prerace assessment and repeated 48 to 96 hours after the race. None of the subjects developed cardiac symptoms during or after the race.Activities of creatine kinase and creatine kinase MB became maximal 24 hours after the race. One and 96 hours after the race two and five subjects, respectively, showed amounts of creatine kinase MB totalling 5% or more of total creatine kinase. Lactate dehydrogenase activity peaked at one hour after the race, and activities of aspartate and alanine aminotransferases peaked at 24 and 96 hours after the race, respectively. Activities of all these enzymes showed a significant increase from prerace values during the rest of the study. Electrocardiographic features noted were similar to those reported elsewhere in athletes under similar conditions. They included first-degree heart block, incomplete right bundle-branch block, left ventricular hypertrophy, pseudoischaemic T-wave changes, and early repolarisation of variant ST-segment elevations in precordial leads. Technetium-99m pyrophosphate myocardial scintigraphy did not show evidence of myocardial damage before or after the race. Alpha(1)-acid glycoprotein concentrations were normal throughout.These data suggest that reliance on standard enzyme estimations and electrocardiographic criteria may yield false-positive indicators of myocardial injury during prolonged strenuous exercise. Technetium-99m pyrophosphate scintigraphy and alpha(1)-acid glycoprotein measurements offer additional information and may usefully be employed in evaluating circulatory collapse associated with such exercise.
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PMID:Abnormal cardiac enzyme responses after strenuous exercise: alternative diagnostic aids. 681 29

Calcium stimulated efflux of four enzymes from human rectus abdominis muscle was studied in vitro. The ratio of efflux of creatine kinase (EC2.7.3.2) increased with increasing calcium concentrations reaching a maximum level with 5mM calcium of 1.9 times that in the absence of calcium. Lactate dehydrogenase (EC 1.1.1.27) efflux at this calcium concentration increased to 2.6 times that in the absence of calcium. However, alanine aminotransferase (EC 2.6.1.2) and aspartate aminotransferase (EC 2.6.1.1) showed a slower increase in the rate of efflux in the presence of 5OmM calcium reaching levels of only 1.3 and 1.5 times respectively that in the absence of calcium. These observations suggest that calcium may be involved in augmenting enzyme efflux from human muscle and may therefore be of relevance in the pathogenesis of Duchenne muscular dystrophy.
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PMID:Calcium stimulated enzyme efflux from human skeletal muscle. 740 66

Intravenous administration of a single dose (100 micrograms/kg bw) of recombinant tumour necrosis factor-alpha (TNF, cachectin) to rats increased the rate of in vitro fatty acid synthesis in interscapular brown adipose tissue (IBAT) from both glucose and alanine, without changes in the oxidation of these substrates to 14CO2. Lactate production and glycerol release were also unaffected by treatment with the cytokine. Additionally, the presence of TNF in the incubation media did not affect fatty acid synthesis, suggesting an indirect effect of the cytokine. The activities of different enzymes of glucose and alanine metabolism such as hexokinase, phosphofructokinase, pyruvate kinase, glucose-6-phosphate dehydrogenase and alanine transaminase, did not suffer changes as a consequence of TNF administration. The same applied to the enzymatic activities involved in fatty acid synthesis such as fatty acid synthase, acetyl-CoA carboxylase and ATP-citrate lyase. Conversely, citrate levels in IBAT were increased in animals treated with TNF, suggesting that it could be the cause for the increased fatty acid synthesis in this tissue.
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PMID:Metabolic effects of tumour necrosis factor-alpha on rat brown adipose tissue. 759 46

Lactate dehydrogenase (LDH), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) concentrations and platelet counts were measured in 26 normal pregnant women and 51 preeclamptic women. In the normal-pregnancy group, no significant changes were found in the results of these tests. In the preeclampsia group, ALT and AST concentrations were not significantly higher than those in normal pregnancy, but the LDH concentrations increased and the platelet counts decreased significantly through the pregnancy. The increases in LDH did not correlate with changes in ALT or AST. Preeclamptic women with small-for-gestational-age (SGA) infants had significantly higher LDH concentrations than those in the appropriate-for-gestational-age (AGA) group, but ALT and AST concentrations did not increase significantly. As reasons for the LDH increase in our subjects, liver damage was excluded and more active glycolysis in addition to severe cell damage due to chronic anoxemia were inferred. It is suggested that an increase in LDH is predictive of SGA infants in preeclamptic pregnancy, especially in those with normal liver function.
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PMID:Increased concentrations of lactate dehydrogenase in pregnancy with preeclampsia: a predictor for the birth of small-for-gestational-age infants. 763 66


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