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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cerebral metabolic effects of 2.5, 5, 7.5, 10, 20, 30 and 60 min exposure to 1% CO were studied in lightly anesthetized rats by measurement of cerebral cortical contents of selected glycolytic and citric acid cylce intermediates, as well as tissue energy phosphates. The initial change in the glycolytic sequence occurred at 2.5 min with decreases in tissue glucose and glucose-6-phosphate and increases in fructose-1-6-diphosphate which indicated an activation of phosphofructokinase and hexokinase. The "crossover" pattern between glucose-6-phosphate and fructose-1,6-diphosphate was present at 5, 7.5 and 10 min, but not at 20, 30 and 60 min and thus confirmed previous observations that detection of phosphofructokinase activation in acute unifactorial cerebral hypoxia requires tissue study during the early phases of the experimental exposure. The initial activation of phosphofructokinase occurred in the absence of detectable changes in the tissue content of ATP, ADP, AMP or phosphocreatine and therefore suggested that an imbalance of tissue energy homeostasis is not a prerequisite for the activation of glycolysis in CO intoxication. One percent CO resulted in an increasing malate/oxaloacetate ratio at 5 min, followed by a decrease in alpha-ketoglutarate and aspartate at 7.5 min which suggested a shift in the aspartate aminotransferase reaction towards the replenishment of oxaloacetate removed via the malate dehydrogenase reaction. Subsequent increases in alpha-ketoglutarate at 10, 20, 30 and 60 min were associated with increases in alanine, indicating a contributing role for a secondary shift of the alanine aminotransferase reaction in the replenishment of alpha-ketoglutarate. A comparison of the CO induced changes in the glycolytic and citric acid cycle pathways with those seen in acute hypoxemia indicates no basic qualitative differences in the metabolic responses of brain tissue to the two conditions.
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PMID:Cerebral carbohydrate metabolism during acute carbon monoxide intoxication. 1 62

One hundred and seven Wistar rats, 8 weeks old and weighing 180-200 g, were housed under conditions of controlled temperature (22 plus or minus 2 degrees) and lighting (light on from 07:00 to 19:00). They were divided into 2 groups and fed diets containing either 15 per cent cas-protein for 23 days. Food consumption was recorded every 2 hours for each animal during 48 hours. Four or five rats from each group were killed every 2 hours for 24 hours and the hepatic activities of PK (EC.2.7.1.40),G6P-DH (EC1.1.1.49), ME (EC1.1.1.40), Acetyl-CoA-carbox (EC.6.4.1.2.),PC(EC.6.4.1.1.), PEP-CK(EC.4.1.1.32), G6Pase (EC.3.1.3.9) and GPT (EC.2.6.1.2.) were measured...
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PMID:[Dietary protein level and circadian variation of enzyme activities for glucose metabolism and lipogenesis in male rats (author's transl)]. 1 10

The serum concentration of bilirubin and the activities of aspartate aminotransferase (ASAT, GOT), alanine aminotransferase (ALAT, GPT), gamma-glutamyltransferase (GT), total amylase and pancreatic isoamylase have been determined in serum of 182 male chronic alcoholics. Twelve per cent had abnormally high levels of bilirubin, 73% increased activity of S-ASAT, 50% increased S-ALAT, and 69% increased S-GT. The highest values were often found after 5-20 years of well documented alcoholism. Some patients with alcoholism of more than 20 years' duration displayed a slight tendency towards normalization of the activities. For all parameters the scatter around the mean was greater in the patients than in the controls. Patients who had had attacks of delirium showed slightly higher S-ASAT and S-ALAT than other alcoholics. Determination of S-ALAT and S-bilirubin did not add to the cases with abnormal laboratory tests demonstrated by the combination of S-ASAT and S-GT. In 14 patients the above mentioned parameters were within normal limits, even though severe alcoholism had lasted for many years. Isoamylase determination disclosed 20% to have decreased activity of pancreatic isoamylases in serum, whereas only 6% had low total serum amylase activity.
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PMID:Amylase, hepatic enzymes and bilirubin in serum of chronic alcoholics. 1 9

Whereas glucocorticoids induce TAT, TRP, GPT in liver and only TAT in HTC cells, no hormonal effect on the synthesis of these enzymes was found in Zajdela hepatoma cells grown in vivo as an ascitic tumor, or in vitro as layer cultures. Although these cells remain uninducible, the hormone penetrates normally, but a strong decrease of the specific binding of cytosol and nuclear proteins with the hormone was observed. The impairment at the level of the hormone receptors could account for the non-inducibility of enzyme synthesis in ZHC cells.
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PMID:Impairment of enzyme induction by glucocorticoids in Zajdela hepatoma cells. 1 35

In previous studies it was found that: (a) aspartate aminotransferase increases the aspartate dehydrogenase activity of glutamate dehydrogenase; (b) the pyridoxamine-P form of this aminotransferase can form an enzyme-enzyme complex with glutamate dehydrogenase; and (c) the pyridoxamine-P form can be dehydrogenated to the pyridoxal-P form by glutamate dehydrogenase. It was therefore concluded (Fahien, L.A., and Smith, S.E. (1974) J. Biol. Chem 249, 2696-2703) that in the aspartate dehydrogenase reaction, aspartate converts the aminotransferase into the pyridoxamine-P form which is then dehydrogenated by glutamate dehydrogenase. The present results support this mechanism and essentially exclude the possibility that aspartate actually reacts with glutamate dehydrogenase and the aminotransferase is an allosteric activator. Indeed, it was found that aspartate is actually an activator of the reaction between glutamate dehydrogenase and the pyridoxamine-P form of the aminotransferase. Aspartate also markedly activated the alanine dehydrogenase reaction catalyzed by glutamate dehydrogenase plus alanine aminotransferase and the ornithine dehydrogenase reaction catalyzed by ornithine aminotransferase plus glutamate dehydrogenase. In these latter two reactions, there is no significant conversion of aspartate to oxalecetate and other compounds tested (including oxalacetate) would not substitute for aspartate. Thus aspartate is apparently bound to glutamate dehydrogenase and this increases the reactivity of this enzyme with the pyridoxamine-P form of aminotransferases. This could be of physiological importance because aspartate enables the aspartate and ornithine dehydrogenase reactions to be catalyzed almost as rapidly by complexes between glutamate dehydrogenase and the appropriate mitochondrial aminotransferase in the absence of alpha-ketoglutarate as they are in the presence of this substrate. Furthermore, in the presence of aspartate, alpha-ketoglutarate can have little or no affect on these reactions. Consequently, in the mitochondria of some organs these reactions could be catalyzed exclusively by enzyme-enzyme complexes even in the presence of alpha-ketoglutarate. Rat liver glutamate dehydrogenase is essentially as active as thebovine liver enzyme with aminotransferases. Since the rat liver enzyme does not polymerize, this unambiguously demonstrates that monomeric forms of glutamate dehydrogenase can react with aminotransferases.
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PMID:Effect of aspartate on complexes between glutamate dehydrogenase and various aminotransferases. 1 47

Gamma-GT, alcaline phosphatase and other parameters of abnormal liver functions were estimated in 54 consecutive in-patients having active RA but without a previous history or clinical signs of liver disease, and compared with a matched control group, suffering from degenerative rheumatic disease. There was a slight to moderate elevation of gamma-GT in 40.4% of the RA-patients (mean value 27.2 IU/l) and in 32.1% (mean value 22.3 IU/l) of the control group, respectively. The difference was not significant. Abnormal values in the control group occurred mainly in patients with peri-arthropathia of the shoulder, before mobilisation under anaethetic (3 of 5) and - coxarthrosis before total hip replacement (4 of 12). Alkaline phosphatase was elevated in 25.9% of the RA-patients (mean value 41.3 +/- 21.9 IU/l) and in 14.8% of the control group (mean value 34.3 +/- 15.9 IU/l). The difference was significant. There was a correlation between gamma-GT and alcaline phosphatase in the RA-group (r = 0.549, p less than 0.001) but not in the control group (r = 0.102). Abnormal values found in the control group were mainly found among patients with osteoporosis, following fractures, and coxarthrosis. The frequency of abnormal results and the value of the means increased with raising disease activity. Two groups of 30 and 32 patients, respectively, were examined at intervals of 2 or 4 weeks over a period of 6-10 and 18 months, respectively, and showed temporary elevations os gamma-GT in 3/4 of all patients, of GOT in 2/3 of alcaline phosphatase in 1/2 and of GPT in 1/3. Compared with other parameters of liver disease gamma-GT did not react in a different but in a more sensitive way. In our opinion it is the most sensitive indicator of reactive changes of the liver in RA.
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PMID:[Gamma-glutamyltranspeptidase in chronic polyarthritis. I. Comparison with a control group and relationship with alkaline phosphatase]. 1 55

Liver tests were performed postoperatively on 25 women with "healthy" livers. Patients were divided into 3 groups according to the type of anesthesia used: 1. halothane; 2. neuroleptic; 3. peridural. In all 3 groups the variations in serum proteins and liver enzymes were similar up to the 15th postoperative day. Variations of LDH, AP, LAP, and CHE were within normal range; slight to moderate increases above normal were observed for GPT, GOT, GLDH, and gamma-GT. All 3 groups barely differ with respect to enzyme levels during the postoperative course. We therefore interpret these changes to indicate a reaction of the liver to the stress of operation rather than to the mode of anesthesia.
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PMID:[The effect of anesthesia on the postoperative behavior of liver enzymes and protein fractions]. 1 75

In 34 cases of skull traumas and in 14 cases of acute cerebral accidents, CK, GOT, GPT, LDH and its isoenzymes were assessed in the patient's serum and CSF. Results show that the increase of the enzymatic level in the CSF seems due to cerebral tissue damage for the main part, when in the serum the increase is influenced by combined traumas. The CSF dosages allow to define a threshold of severeness, unlike serum dosages without any pronostic value.
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PMID:[Do enzyme determinations have any prognostic value in neurotraumatology?]. 1 85

We report the intermediate-term effects of three consecutive evenings of moderate ethanol ingestion (0.75 g/kg body weight each evening) on activity values for alkaline phosphatase, gamma-glutamyltransferase, creatine kinase, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase in sera of nine apparently healthy young adults. We define "intermediate-term" effects as those occurring between 10 h and 100 h after completion of the ethanol consumption schedule. The most pronounced changes in enzyme activity for the group of volunteers were: gamma-glutamyltransferase, +25% at 60 h after ethanol ingestion; alanine aminotransferase, +12% at 60 h after ethanol; and aspartate aminotransferase,--12% at 60 h after ethanol. All three enzymes exhibited similar time courses, i.e., mean peak activity changes were observed at 60 h, and all three mean enzyme activity values returned to near baseline by 100 h. The possible explanations for the observed changes and the clinical significance are discussed.
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PMID:The effects of ethanol (0.75 g/kg body weight) on the activities of selected enzymes in sera of healthy young adults: 1. Intermediate-term effects. 1 40

Gamma-GT, which appears as a sensitive indicator in the enzyme pattern during postoperative examination, is especially recommended (besides the GOT and GPT enzymes) in detecting and watching the course of hepatocellular lesions. Distinction between parenchymatous and obstructive icterus can in some cases be made at an early stage by comparison with AP. Distinction between increases in biliary and ossal AP activity is possible with the help of Gamma-GT. Where liver metastases are suspected clinically, increased Gamma-GT activity makes metastization into the liver appear likely.
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PMID:[The influence of surgery on serum enzyme changes]. 1 33


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