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)

We measured the activities of two mitochondrial enzymes, the mitochondrial form of aspartate aminotransferase (EC 2.6.1.1) and glutamate dehydrogenase (EC 1.4.1.2), in the serum of apparently healthy persons (n = 84) and patients suffering from chronic liver diseases (n = 43). The distribution of activities for glutamate dehydrogenase, but not mitochondrial aspartate aminotransferase, was sex-dependent. The upper limits of the reference intervals (99th percentile) at 37 degrees C were 3.2 U/L for mitochondrial aspartate aminotransferase, 6.4 U/L for glutamate dehydrogenase (women), and 11.0 U/L for glutamate dehydrogenase (men); there was a weak correlation between the activities of both mitochondrial enzymes (r = 0.439). In patients with chronic liver diseases we found a greater increase in the activity of glutamate dehydrogenase than of mitochondrial aspartate aminotransferase and the correlation between the two mitochondrial enzymes was stronger. The diagnostic sensitivity and specificity of either mitochondrial enzyme was less than that of total aspartate aminotransferase, alanine aminotransferase (EC 2.6.1.2), or gamma-glutamyltransferase (EC 2.3.2.2).
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PMID:Mitochondrial enzymes in human serum: comparative determinations of glutamate dehydrogenase and mitochondrial aspartate aminotransferase in healthy persons and patients with chronic liver diseases. 396 54

Haematological and hepatic effects of testosterone/anabolic steroid self-administration were investigated in five power athletes during 26 weeks of training. During steroid administration blood haematocrit had increased 9.6% (p less than .05) in the study group (n = 5), but not in the control group (n = 6). This erythropoietic phenomenon was supported by increased (p less than .05) RBC and unchanged MCV. Blood haemoglobin concentration did not change markedly and consequently MCHC level in the study group decreased significantly (p less than .001). Also the erythrocyte sedimentation rate decreased (p less than .05) in the study group. The mean values of serum alanine aminotransferase, alkaline phosphatase and gamma-glutamyltransferase were and remained within normal range in both groups, although those of the study group were higher. The mean values of serum aspartate aminotransferase exceeded the normal range (56 U/l, at highest) but this may be of muscular rather than hepatic origin because of the severe training. It can be concluded that erythropoiesis was stimulated and liver function mildly impaired due to sustained high-dose testosterone/anabolic steroid administration.
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PMID:Androgenic steroid effects on liver and red cells. 399 22

Serum levels of sodium, potassium, chloride, phosphorus, iron, total magnesium, total calcium, alkaline phosphatase, alanine transaminase, lactate dehydrogenase, creatine kinase, gamma-glutamyltransferase, aspartate transaminase, urea, creatinine, total protein, albumin and plasma glucose were determined in 49 ostriches (Struthio camelus) kept under semi-extensive conditions.
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PMID:Blood chemical and electrolyte concentrations in the ostrich Struthio camelus. 402 Aug 17

The glutathione and cysteine conjugates of the nephrotoxin chlorotrifluoroethene, S-(2-chloro-1,1,2-trifluoroethyl)glutathione (CTFG) and S-(2-chloro-1,1,2-trifluoroethyl)cysteine (CTFC), are potent nephrotoxins in male rats. Morphological changes in the kidneys were observed 1.5 hr after giving 100 mumol/kg of CTFG (i.v.), and severe damage to the proximal tubules was evident 24 hr after treatment; this dose of CTFG caused a 100-fold increase in urine glucose excretion, a 10-fold increase in urine protein excretion and a 4-fold increase in blood urea nitrogen concentrations 24 hr after administration. Administration of 50 mumol/kg of CTFG or 100 mumol/kg of CTFC produced similar lesions and increases in urine glucose excretion rates and blood urea nitrogen concentrations. Administration of 10 mumol/kg of CTFG produced no discernable effect on the kidneys. CTFG and CTFC did not alter plasma glucose concentrations or plasma glutamate-pyruvate transaminase activities. CTFG and CTFC produced time- and dose-dependent loses of cell viability in isolated rat renal tubular cells. The toxicity of CTFG to isolated renal tubular cells was prevented by the gamma-glutamyltransferase inhibitor AT-125, and the toxicity of CTFC and CTFG to isolated cells was prevented by aminooxyacetic acid, an inhibitor of pyridoxal phosphate-dependent enzymes. Moreover, S-(2-chloro-1,1,2-trifluoroethyl)-DL-alpha-methylcysteine, which cannot be metabolized by pyridoxal phosphate-dependent enzymes, was not toxic to isolated renal tubular cells. The data presented support the hypothesis that the nephrotoxicity of chlorotrifluoroethene is due to the enzymatic formation of a glutathione conjugate, which is metabolized to the ultimate nephrotoxin by the sequential action of renal gamma-glutamyltransferase, cysteinylglycine dipeptidase and cysteine conjugate beta-lyase.
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PMID:Nephrotoxicity of S-(2-chloro-1,1,2-trifluoroethyl)glutathione and S-(2-chloro-1,1,2-trifluoroethyl)-L-cysteine, the glutathione and cysteine conjugates of chlorotrifluoroethene. 407 35

Pancreatic juice gamma-glutamyltransferase (GGT, EC 2.3.2.2) has been proposed as a marker of pancreatic disease. We have collected pancreatic juice endoscopically from 24 control patients and 43 patients with a variety of hepatic, pancreatic, and biliary disorders. Pancreatic juice GGT, alanine transaminase (ALT, EC 2.6.1.2), and alkaline phosphatase (ALP, EC 3.1.3.1) were measured and found to be present in all samples. GGT was significantly higher in patients with pancreatic cancer (range 21-1175 IU/liter, P less than 0.005) compared with controls (range 2-52 IU/liter). Of 17 patients with pancreatic juice GGT concentrations greater than 52 IU/liter, eleven had definite pancreatic disease (seven pancreatic cancer, four chronic pancreatitis) and, in the remaining six, pancreatitis was possible although not proven. Pancreatic juice ALT and ALP provided no useful diagnostic criteria. GGT in pancreatic juice seems to be a nonspecific marker of pancreatic disease and merits further study.
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PMID:Pancreatic juice gamma-glutamyltransferase, alanine transaminase, and alkaline phosphatase in pancreatic disease. 610 99

Results obtained in three successive investigations involving various groups of population are presented. In a first study gamma-glutamyltransferase (gammaGT) activity was found to exceed the upper limit of the normal in 70% of the 36 subjects from a rural community in Northern Transylvania who were known by the local physician as being addicted to alcohol since at least five years. In a subsequent study gammaGT activity was determined in 86 patients seeking psychiatric help for a drinking problem. Only 55% of these patients were presenting increased gammaGT values and this finding could be explained by the fact that some of the psychiatric patients were admitted to the clinic for pathological bouts of dipsomania and not because of longstanding chronic intake of alcohol. When studied in connexion with the behaviour of serum triglyceride and alanineaminotransferase (GPT) levels, gammaGT activity was found to be particularly high in hypertriglyceridemic alcoholics and in those presenting a moderate increase of serum transaminases. Population studies emphasized that gammaGT activity exceeded the upper normal limit in 49.2% of the men and in 21.6% of the women working for more than five years in the industry of alcoholic beverages, while an increased activity of this enzyme was detected only in 19% of the men and in 1.7% of the women in a random population.
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PMID:Behaviour of gamma-glutamyltransferase in chronic consumers of alcohol. 610 56

In a trial of the Netherlands coupled external/internal quality control program a control serum and an enzyme standard were analysed over a period of eight weeks, five times each week. Five enzymes were determined: alkaline phosphatase, creatine kinase, lactate dehydrogenase, alanine aminotransferase, and gamma-glutamyltransferase. The measured values in the serum were converted to the standards. Those laboratories using the recommended methods also submitted their non-transformed serum values. The following standardisation techniques have been compared: (a) no standardisation of methodology but use of enzyme standards; (b) standardisation of methodology; (c) standardisation of methodology combined with use of an enzyme standard. Results were submitted to analysis of variance. Standardisation of methodology did not yield smaller interlaboratory variation than the standardisation with enzyme standards. In this trial a combination of both standardisation techniques yielded generally better results. Results for gamma-glutamyltransferase indicate that standardisation of substrate may be necessary apart from the use of an enzyme standard. The preparation of stable enzyme standards is stressed.
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PMID:Standards versus standardised methods in enzyme assay. 613 88

Compared with controls, patients with alcoholic fatty liver showed a significant increase of gamma-glutamyltransferase activity both in the liver and serum, whereas alkaline phosphatase activity was raised only in the liver but not in the serum. The activities of other enzymes such as aspartate aminotransferase, alanine aminotransferase and glutamate dehydrogenase remained virtually unchanged in the liver of patients with alcoholic fatty liver but were strikingly enhanced in the serum. The hepatic and serum alterations of enzymic activities observed in patients with alcoholic fatty liver could be reproduced in the rat model of alcoholic fatty liver only for gamma-glutamyltransferase but not for the other enzymes tested, substantiating evidence that the animal model may serve as an appropriate tool for studying interactions between alcohol and gamma-glutamyltransferase. The present experiments also indicate that the primary cause for increased serum gamma-glutamyltransferase activities associated with prolonged alcohol consumption is hepatic enzyme induction rather than liver cell injury.
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PMID:Hepatic gamma-glutamyltransferase activity in alcoholic fatty liver: comparison with other liver enzymes in man and rats. 613 56

Hepatic infarction was observed post mortem in a 27-year-old man who died of aortic dissection. Blood had been sampled at admission and 12 and 19 hours later. Values for aspartate aminotransferase and alanine aminotransferase in serum were markedly above normal, whereas those for alkaline phosphatase and gamma-glutamyltransferase were only marginally increased. A threefold-increased creatine kinase was ascribable solely to isoenzyme CK-3, suggesting muscle breakdown. Moreover, total lactate dehydrogenase activity was increased threefold, accounted for by a ninefold increase in LD-5 isoenzyme. Those enzyme activities in serum that evidently are associated with acute hepatocellular necrosis increase quickly in hepatic infarction, and CK isoenzyme assay is a useful adjunct if LD-5 increases are significant.
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PMID:Hepatic infarction: biochemical study of a case. 613 94

Alcoholism is a common disease; it is found in 10% to 15% of all patients admitted to general hospitals. There is no single characteristic finding, but on the other hand, changes as compared with normal values have been reported in the literature for more than 30 frequently assayed clinical chemical and haematological parameters. In the project reported here all 24 clinical chemical parameters and all 8 haematological parameters frequently assayed were studied in each of 82 hospitalized men with a confirmed diagnosis of alcoholism. The diagnosis of alcoholism was made on the basis of the Munich Alcoholism Test (MALT) together with the following standardized assessments and examinations: past history, an alcohol questionnaire, general physical examination and neurological examination. All forms were filled in completely. All steps in the clinical laboratory investigations were standardized, and all were subject to ongoing reliability control. The clinical problem is usually not to differentiate alcohol abusers or alcoholics from healthy persons but rather to identify the alcoholics among a population of patients with a variety of illnesses. For this reason 70 patients from two hospitals who were clearly neither alcohol abusers nor alcoholics were studied in exactly the same manner as the alcoholics. In this combined group of 152 hospitalized patients significant differences were found in the distribution of the values for the alcoholics and the non-alcoholics for the following clinical chemical and haematological parameters: at the 0.1% level gamma-glutamyltransferase, aspartate aminotransferase, urea, creatinine and mean corpuscular volume (MCV), and at the 1% level glutamate dehydrogenase, alanine aminotransferase and alkaline phosphatase. From these eight parameters those combinations of between two and six parameters were selected that discriminated best between the alcoholics and the non-alcoholics. Using conventional decision limits the following was found: For the alcoholics two or more of the results for the following five parameters were outside the decision limits given in parentheses: gamma-glutamyltransferase (greater than or equal to 28 U/l), aspartate aminotransferase (greater than or equal to 18 U/l), alanine aminotransferase (greater than or equal to 22 U/l), MCV (greater than or equal to 96 fl), creatinine (less than or equal to 66.3 mumol/l). The diagnostic sensitivity (alcoholics) is 85%, the diagnostic specificity (non-alcoholics) is 64%.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Detection and exclusion of alcoholism in men on the basis of clinical laboratory findings. 614 78


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