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)

Serum activity of angiotensin converting enzyme (ACE) was serially measured in 47 hospitalized chronic alcoholics with liver disease. Compared to healthy controls, ACE activity, on admission, in the serum of alcoholics was significantly elevated (42.5 +/- 16.6 U/ml vs. 32.4 +/- 9.6 U/ml; p less than 0.005). About 36% of the patients had an elevated ACE level exceeding an upper normal value of 42 U/ml (mean +/- SD). In contrast to the rapid normalization of such enzymes as aspartate transaminase (AST), alanine transaminase (ALT) and lactic dehydrogenase (LDH) which represent parenchymal liver cell injury, the activity of ACE remained elevated over a period of 4 weeks even with abstinence. The serum level of ACE was significantly correlated with levels of alkaline phosphatase, gamma-glutamyltranspeptidase and monoamine oxidase, but not with those of AST, ALT and LDH. These data suggest increased ACE activity in alcoholics may be related to the influence of chronic consumption of alcohol on hepatic nonparenchymal systems.
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PMID:Mild but prolonged elevation of serum angiotensin converting enzyme (ACE) activity in alcoholics. 302 46

Phenobarbitone pretreatment potentiated hepatocyte lesions in male rats 24 hr after treatment with 1-fluoropentane (3.5 mg/kg body weight) and 1-fluorohexane (0.17 mg/kg body weight). Serum levels of the enzymes ornithine carbamyltransferase, glutamic-pyruvic transaminase and gamma-glutamyltranspeptidase were significantly elevated by the test compounds with the peak effect occurring 24-72 hr after a single ip administration. Significant elevation of hepatocyte triglyceride content and mitochondrial calcium and citrate levels were demonstrated 24 and 48 hr after a single ip injection of 1-fluoropentane or 1-fluorohexane, respectively.
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PMID:A comparative study of the hepatotoxicity of 1-fluoropentane and 1-fluorohexane. 319 37

Serum concentrations of sodium, potassium, chloride, total protein, albumin, aspartate transaminase, creatine kinase, lactate dehydrogenase, gamma-glutamyltranspeptidase, alkaline phosphatase and alanine transaminase were determined in free-living white rhinoceroses Ceratotherium simum (n = 20). Single serum cortisol (n = 20), oestradiol-17 Beta (n = 14) and progesterone (n = 14) concentrations are also presented. Low serum sodium (129.6 +/- 4.2 mmol/l) chloride (94.2 +/- 3.05 mmol/l) and albumin (26.1 +/- 3.71 mmol/l) as well as high globulin (alpha 1, alpha 2, beta and gamma) concentrations were outstanding features.
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PMID:Blood chemical parameters in free-living white rhinoceros Ceratotherium simum. 383 4

Serum levels of cortisol, sodium, potassium, chloride, urea, creatinine, total protein, albumin, phosphorus, aspartate transaminase, creatine kinase, lactate dehydrogenase, iron, total magnesium, total calcium, alkaline phosphatase, alanine transaminase and gamma-glutamyltranspeptidase were determined in 11 short Cape Mountain Zebra Equus zebra zebra.
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PMID:Blood chemical parameters in shot Cape Mountain Zebra Equus zebra zebra. 407 40

Biliary glycoprotein I (BGP I), a constituent of normal bile and serum, is a glycoprotein (mol. wt. approximately 90,000) containing about 40% carbohydrate. Serum BGP I (S-BGP I) was determined by means of a double-antibody radioimmunoassay in patients with liver and gastrointestinal disease and in healthy individuals. The serum levels of five liver enzymes (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase (S-ALP), gamma-glutamyltranspeptidase (S-GT), and lactic dehydrogenase), bilirubin (total and conjugated), and bile acids (cholic and chenodeoxycholic acid) were determined in parallel. Healthy individuals had 0.5 +/- 0.3 mg/l of S-BGP I (mean +/- 2 S.D.; range, 0.2-0.9 mg/l). Most patients with liver disease (chronic hepatitis, alcoholic cirrhosis, primary biliary cirrhosis) had elevated levels, up to 5-10 times the upper reference limit, whereas most patients with gastrointestinal disease (ulcerative colitis, Crohn's disease, other GI diseases) had normal values. In patients with liver disease S-BGP I was positively correlated (p less than 0.0005) to S-GT. In primary biliary cirrhosis a positive correlation (p less than 0.005) between S-BGP I and S-ALP was also obtained. All other comparisons between S-BGP I and the other liver function tests showed non-significant correlations. It is concluded that S-BGP I is a determinant of cholestasis of similar use as S-GT.
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PMID:Serum level of biliary glycoprotein I, a determinant of cholestasis, of similar use as gamma-glutamyltranspeptidase. 611 67

In the present experiments, we studied the effect of poly(ADP-ribose) polymerase inhibitors on the early stage of liver carcinogenesis by diethylnitrosamine (DEN) in rat liver in order to clarify the biological role of this enzyme in cancer induction. We used 3-aminobenzamide(ABA), 5-methylnicotinamide(MNam), and thymidine as the inhibitors and measured the numbers and sizes of gamma-glutamyltranspeptidase (gamma-GTP) positive foci as a marker of initiated cell populations. When ABA was given within 4 hr after DEN treatment, it had almost the same effect as a partial hepatectomy and caused dose-dependent enhancement of the induction of gamma-GTP positive foci. The administration of ABA at a dose of 600 mg/kg was effective to enhance the induction of the foci 1 day before to 1 day after 20 mg/kg DEN initiation. The enhancing effect of MNam and thymidine at a dose of 600 mg/kg was observed to the same extent as that of ABA. Based on these results the experiments were extended to the mechanisms of the enhancing effect of ABA. Liver cell necrosis was not detected by measuring serum GOT and GPT levels and histology after DEN and ABA administration. Further, the initiating and promoting activities of ABA in liver carcinogenesis were studied and ABA per se was not found to take part in either activity. These results indicate that poly(ADP-ribose) polymerase plays an important role in the early stage of liver carcinogenesis by DEN and provides a new avenue for studying the mechanisms of the initiation process in chemical carcinogenesis.
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PMID:Possible role of poly(ADP-ribose) polymerase on the early stage of liver carcinogenesis by diethylnitrosamine in rats. 614 Feb 58

Six benzodiazepine tranquilizers were tested in limited in vivo bioassays for their ability to initiate or promote the development of preneoplastic and neoplastic rat liver lesions. The benzodiazepine produced no liver altered hepatocellular foci during a 14-week period of administration whereas a large number were produced by the liver carcinogen, N-2-fluorenylacetamide. To assay for promoting activity and confirm the lack of initiating activity, N-2-fluorenylacetamide was used to produce altered foci and early neoplastic nodules in rat liver by 8 weeks of dietary administration and the benzodiazepines were then administered for 12 weeks. The liver neoplasm promoter phenobarbital had a substantial enhancing effect upon the persistence of early lesions but none of the benzodiazepines showed a similar effect. Thus in these limited bioassays monitored by histopathology, the benzodiazepine tranquilizers failed to exhibit either an initiating or a promoting action. In these studies, the liver and plasma enzymes, glutamate-pyruvate transaminase, glutamate-oxalacetic transaminase, lactic dehydrogenase, alkaline phosphatases, and gamma-glutamyltranspeptidase were monitored to determine if any alterations correlated with liver pathological changes. gamma-Glutamyltranspeptidase activity in both liver and plasma was markedly increased during initiation by N-2-fluorenylacetamide. Following cessation of carcinogen exposure, gamma-glutamyltranspeptidase remained elevated, providing an indication of past initiation. Administration of phenobarbital after N-2-fluorenylacetamide resulted in an elevation of liver and plasma gamma-glutamyltranspeptidase, but none of the benzodiazepines produced this effect and thus no biochemical evidence of a promoting effect on the liver was observed. Correlations between liver and plasma gamma-glutamyltranspeptidase and the occurrence of foci were excellent, indicating that determination of plasma activity can be used as an index of the process of hepatocarcinogenesis.
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PMID:Lack of initiating or promoting activity of six benzodiazepine tranquilizers in rat liver limited bioassays monitored by histopathology and assay of liver and plasma enzymes. 614 10

Serum ferritin and hepatic enzyme concentrations were measured in 30 alcoholic subjects. Both the serum ferritin and gamma-glutamyltranspeptidase (GGT) values were raised in 23 subjects and a significant correlation was noted between the two measurements (r = 0,51; P less than 0,01). There was, however, no correlation between the initial serum ferritin concentration and the serum alanine transaminase and serum aspartate transaminase concentrations. The serum ferritin and GGT levels were followed serially during a period of abstinence in 9 subjects; values fell in parallel in all of them. The data indicate that a serum ferritin level above 300 micrograms/l is very unlikely to be the result of alcohol-induced liver damage if the serum GGT value is less than 50 U/l. The combined measurement of serum ferritin and GGT values should therefore prove useful in epidemiological studies concerned with defining the prevalence in different population groups of the HLA-linked iron-loading gene that leads to the clinical disorder of idiopathic haemochromatosis.
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PMID:Effects of heavy alcohol consumption on serum ferritin concentrations. 614 24

To evaluate the potential role of taurine deficiency in the pathogenesis of parenteral nutrition-induced cholestasis, 20 premature (less than 34 weeks AGA) infants were randomized to receive parenteral nutrition with and without taurine (10.8 mg/kg/day) during the first 10 days of life. Birth weight, gestational age, and protein and caloric intake were similar in both groups. Plasma taurine levels and hepatic function were assessed before the study began (3 +/- 1 days of age), at 5 +/- 1 days of age, and at 9 +/- 1 days of age. Although plasma taurine levels were significantly greater at 5 +/- 1 and 9 +/- 1 days of age (p = 0.009) in the group receiving supplementation, no differential effect on hepatocellular function could be detected during this short period of time. A decrease in plasma ammonia (p = 0.001), alanine aminotransferase (ALT) (p = 0.036), gamma-glutamyltranspeptidase (GGTP) (p = 0.05), 5'-nucleotidase (5'N) (p = 0.001), and bile salt concentrations was noted in both groups, indicating the rapid maturation of hepatic function even in the presence of parenteral nutrition during the first 10 days of life.
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PMID:Effect of taurine supplementation on hepatic function during short-term parenteral nutrition in the premature infant. 642 96

The activity of serum enzymes, such as, creatine kinase (CK), pyruvate kinase (PK), aldolase (ALD), lactate dehydrogenase (LDH), sorbitol dehydrogenase (SbDH), malate dehydrogenase (MDH), glutamate-aspartate aminotransferase (AST), glutamate-alanine aminotransferase (ALT), myokinase (MK), glucosephosphate isomerase (GPI), alkaline phosphatase (AlkP), pseudocholinesterase (PsCHE) isocitrate dehydrogenase and gamma-glutamyltranspeptidase (gamma-GTP), was determined in 256 patients with progressing myodystrophy (PMD) (Duchenne's form in 125, Becker's form in 14, pelvicohumeral form in 36, humeroscapulofacial form in 19, ocular form in 10, other rare forms in 34, and nonidentified forms in 13 patients). In the control group (64 men, 56 women and 50 children), the activity of the enzymes was found to depend on the patients' sex and age. With regard to both parameters, i. e. the degree of the enzyme activity rise and the frequency of the pathological values the most informative were CK, then PK and ALD, and then all the other enzymes. Of all the PMD forms the enzymatic activity appeared to be the highest in patients with the pseudohypertrophic malignant form. By determining the activity of five enzymes (CK, ALD, LDH, AST and ALT) and taking into consideration the patient's age, the onset and the duration of the disease one can distinguish between sick and healthy subjects, as well as between various forms of PMD.
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PMID:[Serum enzyme dynamics in progressive muscular dystrophies]. 703 17


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