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)

The hydroxyl groups of poly(ethyleneglycol) have been esterified (partly) with a number of carboxylic acids. When these esters are included in dextranpoly(ethyleneglycol)-water biphasic systems the partitions of proteins and membranes between the two phases (and the interface) are in some cases strongly affected. The affinity of serum albumin for the poly(ethyleneglycol)-rich phase is strongly increased when the fatty acid group consists of more than 10 carbon atoms. The partition also depends on the number of double bonds in the fatty acid. A corresponding relationship is found for membranes from spinach chloroplasts. The partitions of ovalbumin, lysozyme (EC 3.2.1.17) and ribonuclease (EC 3.1.4.22) are not influenced by the fatty acid esters. Esters of dibasic carboxylic acids show a minute but marked effect on the partition of proteins in general while malate and tartrate esters affect strongly the partition of chloroplast membranes. The partitions of both proteins and membranes are influenced by poly(ethyleneglycol) deoxycholate. Experiments with malate dehydrogenase (EC 1.1.1.37), lactate dehydrogenase (EC 1.1.1.27), fumarase (EC 4.2.1.2), enolase (EC 4.2.1.11) and glutamate-ocaloacetate transaminase (EC 2.6.1.1) show that their partitions, measured on enzymic activity basis, is changed when esters of benzoic, linolenic, tartaric or deoxycholic acid are included in the biphasic system. The mechanism behind the effect of the esterified poly (ethyleneglycol) on the partition of biomaterial, in this type of aqueous biphasic systems, is discussed in terms of a direct binding of the esters to the partitioned material.
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PMID:The effect of poly(ethyleneglycol) esters on the partition of proteins and fragmented membranes in aqueous biphasic systems. 99 68

Because of the difficulties in drawing blood for clinical chemistry in small laboratory animals there exist many methods for sampling blood and the preparation of serum, none of which is generally accepted or well standardised. It was the aim of this study to investigate the effects of sampling techniques on normal values of enzyme activities in the serum of rat and mouse. The activities of the following enzymes were determined: sorbitol dehydrogenase, lactate dehydrogenase, malate dehydrogenase, glutamate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, pyruvate kinase, creatine kinase, myokinase, alkaline phosphatase and leucine aminopeptidase. In addition plasmaproteins, urea and inorganic phosphorus were measured. In rats blood was obtained from the following sites: retroorbital venous plexus, jugular vein, heart and ventral aorta. In mice blood was sampled from the jugular vein and the ventral aorta. Shifts of water from the interstitial to the intravascular space due to hypovolemia occurring during the experimental procedure were followed up by measuring the hematocrit and the distribution of radioiodide labelled albumin. In rats the activities of lactate dehydrogenase, malate dehydrogenase, aspartate aminotransferase, pyruvate kinase, creatine kinase and myokinase found in blood serum obtained from the retroorbital venous plexus and the ventral aorta were too high compared to the other sampling sites. Activities of alkaline phosphatase and alanine aminotransferase were slightly elevated when blood was sampled from the punctured retroorbital venous plexus. Small differences in plasmaproteins and hematocrit values were found to be due to acute shifts of water within the extracellular space. In mice the activities of lactate dehydrogenase, malate dehydrogenase, aspartate aminotransferase and myokinase were found to be too high in blood serum obtained from the ventral aorta. Efflux of enzymes from damaged cells and the interstitial space ive caused erroneous results too, but only to a minor extent. The most reliable method for blood sampling in rat and mouse is the cannulation of the jugular vein. The heart puncture can be recommended too. Attention should be paid, however, to the possibility of aspirating disrupted muscle cells through the inserted needle.
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PMID:[Effects of blood sampling on enzyme activities in the serum of small laboratory animals (author's transl)]. 108 84

1. Rats were given moderate-selenium (4-5 mg/kg) or low-Se (0-5 mg/kg) diets during gestation and lactation. Their young were given diets with high (10 mg/kg), moderate or low Se contents from weaning, and groups of rats were killed at intervals during the 14-week experimental peroid. 2. Compared with young rats which received the low-Se diet, those which received the moderate- or high-Se diets had a high incidence of liver lesions and there were changes in liver Se content, haemoglobin concentration, packed cell volume, prothrombin activity, fibrinogen content, spleen weight, body water and serum glutamic-oxaloacetic and glutamic-pyruvic transaminas (L-aspartate : 2-oxoglutarate aminotransferase; EC 2.6.1.1 and L-alanine : 2-oxoglutarate aminotransferase; EC 2.6.1.2 respectively) and alkaline phosphatase (EC 3.1.3.1) activities. In those rats which received the high-Se diet the changes were more pronounced than in those which received the moderate-Se diet. 3. In young rats from dams given moderate-Se diets, which were themselves given the moderate-Se diet, the liver Se content decreased continuously, whereas rats given the same diet but from dams which had received the low-Se diet, the liver Se content increased continuously. There was a slight improvement of symptoms of Se toxicity in all groups by the 5th week of the experimental peroid. 4. The results suggest that there was an adaptation to chronic Se intake.
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PMID:Effects of ingestion of organic selenium in adapted and non-adapted rats. 112 69

Biochemical variables have been measured in a group of volunteers during and after a long-distance run. Plasma glucose levels remained relatively constant and a significant decrease in plasma bicarbonate was noted. Plasma sodium, chloride, total protein, albumin and calcium showed significant increased of an order compatible with water losses occurring during the run. Plasma potassium, urea, creatinine, uric acid, phosphate and bilirubin all show much more marked and variable increases. The plasma enzymes alkaline phosphatase, lactate dehydrogenase, aspartate aminotransferase and creatine kinase likewise increased significantly throughout the run. Whilst most constituents showed a tendency to return to normal at 20-30 hours after the run, gross increases were observed for aspartate aminotransferase and creatine kinase.
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PMID:The effect of long-distance running on some biochemical variables. 119 11

The hydrogen exchange at the Beta-carbon of L-alanine, L-glutamate and L-asparate with water has been examined during transamination catalyzed by glutamic-oxaloacetic transaminase and by glutamic-pyruvic transaminase. A significant hydrogen exchange at the Beta-carbon has been demonstrated during incubation of L-[3-3H]alanine + glutamic-pyruvic transaminase, L-[3-3H]alanine + alpha-oxo-glutarate + glutamic-pyruvic transaminase, L-[3-3H]glutamate + glutamic-oxaloacetic transaminase, L-[3-3H]glutamate + oxaloacetate +glutamic-oxaloacetic transaminase, and L-[3-3H]glutamate + pyruvate + glutamic-pyruvic transaminase as shown by the appearance of 3H2O. No hydrogen exchange at the Beta-carbon of L-glutamate occurred during incubation of L-[3-3H]-glutamate with glutamic-pyruvic transaminase alone. The hydrogen exchaned at the Beta-carbon of L-glutamate coincides with transamination as demonstrated by nuclear magnetic resonance studies of 2H2O-L-glutamate exchange during transamination by glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase. No hydrogen exchange at the Beta-carbon occurred during transamination of L-aspartate by glutamic-oxaloacetic transaminase as shown by nuclear magnetic resonance spectroscopy and confirmed by nuclear magnetic resonance simulation studies. The results are discussed with special reference to the different equilibria between the pyridoxal form and the pyridoxamine form of glutamic-oxaloacetic transaminase and of glutamic-pyruvic transaminase.
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PMID:Hydrogen exchane at the beta-carbon of amino acids during transamination. 120 22

Release and binding of aspartate aminotransferase, malate dehydrogenase and protein from and to water-shocked vesicles obtained from rat liver mitochondria was shown to occur. The characteristics of this phenomenon were shown to depend on the effectors used. They were in some way different from those observed with whole mitochondria under similar conditions.
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PMID:Release and binding of protein and enzymes from and to water-shocked vesicles obtained from rat liver mitochondria. 122 17

A 2 x 2 x 2 factorial arrangement of treatments consisting of dietary aflatoxin (3.5 micrograms/g), ochratoxin A (2.0 micrograms/g), and hydrated sodium calcium aluminosilicate (HSCAS, .5%) was used to evaluate the individual and combined effects of these treatments. There were six replicate pens of 10 broilers per pen for each of the eight treatments. The broilers were maintained on these treatments from 1 day to 3 wk of age with feed and water available for ad libitum intake. Aflatoxin and ochratoxin A each significantly decreased body weight, serum protein, albumin, and cholesterol and increased the relative weight of the liver, kidney, and proventriculus. Aflatoxin increased the relative weight of the heart and decreased serum aspartate aminotransferase activity and ochratoxin A increased serum uric acid. The toxicity resulting from the combination of aflatoxin and ochratoxin A was more severe than when either of these mycotoxins were present alone. Addition of HSCAS alone did not alter any of the parameters evaluated. The HSCAS reduced the toxicity of aflatoxin, but had little effect on either the toxicity of ochratoxin A alone or the toxicity resulting from the combination of aflatoxin and ochratoxin A.
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PMID:Efficacy of hydrated sodium calcium aluminosilicate to reduce the individual and combined toxicity of aflatoxin and ochratoxin A. 131 50

Coccinia indica (Family: Cucurbitaceae, locally known as telakucha) leaves were extracted with 95% ethanol. Following evaporation of the solvents, the residue was suspended in distilled water. When this suspension was fed orally to male normal-fed and 48-hr starved rats, the blood glucose was lowered 21% (P less than 0.01) in normal-fed and 24% (P less than 0.001) in 48-hr starved animals respectively. Starvation had induced a 3-fold increase in the activity of glucose-6-phosphatase and this activity was depressed 19% (P less than 0.05) by extract feeding while basal activity of the enzyme in normal-fed rats remained unaffected. Consistent with the depression of glucose-6-phosphatase, urea cycle enzyme arginase was also depressed 21% (P less than 0.001) and 12% (P less than 0.01) in the liver of 48 hr-starved and normal-fed animals respectively. Unlike glucose-6-phosphatase, starvation induced levels of gluconeogenic enzymes alanine aminotransferase and aspartate aminotransferase were not affected by Coccinia extract. These results suggest that the hypoglycemic effect of C. indica is partly due to the repression of the key gluconeogenic enzyme glucose-6-phosphatase.
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PMID:Hypoglycemic effects of Coccinia indica: inhibition of key gluconeogenic enzyme, glucose-6-phosphatase. 133 43

Male and female Sprague-Dawley rats were administered drinking water containing 300, 600, 1200, or 2400 mg/L chloral hydrate for 90 days. A control group received distilled water only. No animals died during the study and no differences were observed in body weight gain or food and water consumption, except for males at the highest-dose level. Minor treatment-related effects were observed for organ weights and hematological parameters and these did not appear to be of toxicological significance. Some indications of toxicity were evident in the 2400 mg/L male group (equivalent to 168 mg/kg-day) including a significant decrease in food and water consumption and in weight gain. In addition, histopathological examination of these animals revealed an apparent increase in the incidence of focal hepatocellular necrosis. Increases in AST, ALT, and LDH, which occurred at several dose levels in males, but particularly at 200 mg/L, are consistent with the hepatocellular necrosis of minimal to mild severity diagnosed by microscopic examination. These liver changes, except for sporadic enzyme changes, were not seen in the female rats which actually consumed higher doses of chloral hydrate (e.g., 288 mg/kg-day at 2400 mg/L). On the basis of the mild liver toxicity (histopathological and clinical) observed in males at the highest doses (168 mg/kg-day), the no observed adverse effect level (NOAEL) for oral exposure of rats to chloral hydrate for 90 days is considered to be 96 mg/kg-day (600 mg/L).
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PMID:Ninety-day toxicity study of chloral hydrate in the Sprague-Dawley rat. 142 61

A moderate malignant hyperthermia developed in a Labrador Retriever anaesthetized with isoflurane for a femoral shaft fracture repair. Signs of malignant hyperthermia included progressive increases in PETCO2 and rectal temperature up to 39.8 degrees C, tachycardia, cyanosis, and elevated serum levels of potassium, inorganic phosphorus, AST, CK and alkaline phosphatase. Treatment initiated in the early recovery period consisted of hyperventilation with 100% oxygen, stomach lavage with iced water, body surface cooling, and intravenous administration of cold isotonic saline solution. Cooling was continued until the rectal temperature had dropped to 37.3 degrees C. After treatment the dog recovered uneventfully. Clinical signs, pathophysiology, therapy, prevention of malignant hyperthermia and its association with other disorders are discussed.
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PMID:[Malignant hyperthermia as a complication of anesthesia in the dog]. 144 May 99


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