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)

Viable toadfish hepatocytes were separated into distinct subpopulations by gradient centrifugation. Although 3-5 density subpopulations were obtained for each fish, only two metabolically and enzymatically different subpopulations could be discerned. In all cases, hepatocytes with the lowest density (less than 1.040 g ml-1) were more oxidative in scope, as judged by the activities of mitochondrial enzymes (citrate synthase, aspartate aminotransferase, glutamate dehydrogenase); activities of these enzymes (normalised to cell protein) were on average two- to threefold higher than in subpopulations with higher densities. Lower-density hepatocytes also contained higher levels of the urea cycle enzymes arginase and ornithine carbamoyltransferase. The higher-density subpopulations showed no significant differences from each other in enzymatic activities. Compared with lower-density cells, these hepatocytes had higher activities of two cytosolic enzymes, malate dehydrogenase and glutathione-S-transferase. There was no distinct distribution pattern for alanine aminotransferase and glutamine synthetase. Despite generally lower oxidative enzyme content, higher-density hepatocytes were metabolically more active, with 2.5- to fourfold higher rates of urea synthesis, gluconeogenesis and oxidation of lactate. We conclude that, although the toadfish liver shows distinct enzymatic and metabolic heterogeneity, this heterogeneity is dissimilar to the zonation pattern in the livers of mammals, in that separated toadfish hepatocyte types did not appear to possess exclusive metabolic functions. Notably, all cells were capable of metabolic functions that are strictly localised in mammalian liver. In nitrogen metabolism, glutamine synthetase displays a distribution pattern commensurate with its unique metabolic function in the liver of the ureogenic toadfish. Further, all subpopulations possessed detoxification capabilities as indicated by high levels of glutathione-S-transferase, a 'phase II' conjugation enzyme.
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PMID:Metabolic and enzymatic heterogeneity in the liver of the ureogenic teleost Opsanus beta. 205 Nov 31

Safety data have been gathered in US clinical trials of nabumetone on 1912 patients from August 1981 to May 1988. Dosing in the double-blind trials was 100 mg at bedtime, but in open-label trials patients could increase the dosage of nabumetone to 1500 or 2000 mg if required. Adverse experiences reported in the double-blind and open-label studies that were considered related to nabumetone treatment, or of unknown origin, occurred most commonly in two body systems: the body as a whole, and the digestive system. Incidence rates greater than 10% for adverse experiences categorised by preferred term occurred in the 'body as a whole' category for abdominal pain, and in the digestive system for diarrhoea and dyspepsia. Dosage increases to 2000 mg appeared to cause a dose-related increase in diarrhoea. In the long term studies, gastrointestinal ulcers have been confirmed in 13 (0.7%) patients. Hepatic and renal function was well preserved in patients treated with nabumetone. Overall, only 7 nabumetone-treated patients (0.4%) showed a marked elevation in both ALT (SGPT) and AST (SGOT). Two nabumetone-treated patients showed marked elevations in renal parameters, serum creatinine and blood urea nitrogen. Overall, nabumetone was well tolerated, and the adverse experience profile was clinically acceptable and presented no unusual or unexpected patterns.
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PMID:An overview of the long-term safety experience of nabumetone. 208 90

Through the present delta value check used in quality control programs is a powerful tool for detecting random errors in clinical chemistry analysis, it has some problems, such as missed true errors and delays in reporting time, because it also has the potential of showing erroneous positive results. Recently, new calculation methods for delta check with delta difference, delta percent change, rate difference, and rate percent change have been suggested by Lacher and Connelly (Clin Chem 34:1966-1970, 1988). Based on this new delta check method, we made the new criteria of which calculation method is applied to the clinical chemistry tests, i.e., the differential application of rate and delta check, and selectively applied the new method to 17 chemistry tests in order to solve the above problems. The applied criteria were the time dependence of the test item and the coefficient of variation of the absolute delta difference. Calcium, inorganic phosphorus, total protein, albumin, sodium, potassium, and chloride were classified as delta difference calculation method group; glucose and cholesterol as delta percent change group; creatinine, total and direct bilirubin as rate difference group; and urea nitrogen, uric acid, ALP, ALT, and AST as rate percent change group. With the previous criteria by Whitehurst et al. (Clin Chem 221:87-92) for 5045 specimens, the check-out rate was 47.8% (2,411 out of 5,045), and the positive predictive value was 0.41% (10 out of 2,411). For the new criteria, the check-out rate was 12.7% (621 out of 5,045), and the positive predictive value was 1.8% (nine out of 621).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential application of rate and delta check on selected clinical chemistry tests. 210 Jan 25

The effects of soman poisoning on hematological (counts of red blood cells (RBC), white blood cells (WBC), and platelets and measurement of hematocrit) and coagulation parameters (prothrombin time, activated partial thromboplastin time, thrombin time and concentrations of fibrinogen, factor V, factor VII, and factor XI) and serum biochemistry (concentration of albumin, protein, calcium, cholesterol, triglycerides, blood urea nitrogen (BUN), magnesium, and creatinine and activities of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, cholinesterase, creatinine phosphokinase (CPK), hydroxybutyrate dehydrogenase, and amylase) were determined at 1, 2, 4, 24, and 48 hours after poisoning of rabbits. There were significant (p less than 0.05) decreases in the RBC counts in all treatment groups that were measured initially at 4 hours and were reflected by parallel decreases in the hematocrit values. These changes were probably due to an increase in the hemolysis of the RBC rather than a decrease in the production of RBC. There were minor changes in the coagulation parameters. Generally, the fibrinogen content increased. The activated partial thromboplastin time decreased significantly (p less than 0.05) 24 and 48 hours after soman (50 micrograms/kg) poisoning. Blood cholinesterase values were significantly reduced in all treatment groups at all time periods. The CPK activity was increased after 4 and 24 hours in the 20 and 50 micrograms/kg soman groups. There were minor changes in the other biochemistry values, but none that showed a dose-response relationship; thus, they were considered to be of limited significance with regard to the toxic manifestations of soman exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of soman poisoning on hematology and coagulation parameters and serum biochemistry in rabbits. 212 98

2-Phenyl-1,2-benzisoselenazol-3(2H)-one (ebselen) is classified as a relatively nontoxic selenium compound, probably because of its bound selenium moiety. In thiol-rich tissues, such as the kidneys, ebselen is converted into selenol intermediates. Selenols are nucleophilic agents which might be able to react with platinum compounds. The influence of ebselen on cis-diamminedichloroplatinum(II) (cisplatin)-induced nephrotoxicity in mice was assessed, using single doses of both compounds. Ebselen prevented cisplatin-induced elevations of blood urea nitrogen and serum creatinine levels and morphological kidney damage in BALB/c mice. This protective effect of ebselen was dose dependent: at a cisplatin dose of 14.5 mg/kg, maximal protection was achieved when a single dose of 10 mg of ebselen/kg was administered 1 h before cisplatin. Administration of ebselen, 10 mg/kg, 1 h after cisplatin also protected against severe nephrotoxicity. Treatment with ebselen did not reduce the antitumor activity of cisplatin against MPC 11 plasmacytoma or Prima breast tumor in BALB/c mice. However, this reduction of cisplatin-induced nephrotoxicity would be of little clinical value if it was achieved at toxic doses of ebselen. Ebselen, 10 mg/kg, did not induce blood urea nitrogen, serum creatinine, serum glutamic pyruvate transaminase, or serum glutamic oxalate elevations in the mice. These results are in agreement with the reported low toxicity of ebselen, which is now in Phase I clinical trials as an antiinflammatory drug. The present results indicate that ebselen may provide protection against cisplatin-induced nephrotoxicity, when it is given before or after cisplatin. This might open new perspectives in cancer chemotherapy.
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PMID:Selective reduction of cis-diamminedichloroplatinum(II) nephrotoxicity by ebselen. 220 70

Aflatoxins B1, B2, G1 & G2 were administered in a low concentration (100 ppb of each aflatoxin (AN] in a mash offered to Baladi rabbits. An other group of rabbits were fed on the same contaminated mash in addition to 0.25% charcoal (CC). The two groups were compared to control animals fed on AN-free mash. Inclusion of AN in the diet decreased feed and water consumption, body weight and survival rate. Charcoal improved somewhat feed and water consumption and growth rate than AN-group. However, CC-group affected digestibility of organic matter more than AN-group. Relative weights of liver, kidneys, heart and adrenal glands were significantly higher in AN and CC groups than the control group. Blood haemoglobin content, packed cell volume percentage and sedimentation rate were lower in AN group. Although there were an increase in each of serum, calcium, inorganic phosphorus, cholesterol, phospholipids and glutamic-pyruvic transaminase in AN group, yet the serum nitrogen and glutamic-oxalacetic transaminase were reduced. Charcoal had alleviated AN-effects concerning N, GPT and phospholipids. Chemical analysis revealed elevation of water, ash and silica contents of liver and water content of muscles from AN-animals. On the other hand, fat content, GOT and vitamin A in the liver as well as muscles ash were reduced. Addition of CC to the diet reduced AN-effects on liver fat, ash and silica but resulted in a rise of the water content of liver and muscles and liver GPT activity. Charcoal also resulted in a sharp decrease in vitamin A content of the liver. Aflatoxin treatments (in AN and CC groups) reduced bone ash, silica and magnesium as well as bone volume. Charcoal administration increased Ca-content of bones. Aflatoxin feeding (in AN group) resulted in a high residual percentage of AN in muscles, serum, liver, heart and kidneys with relationships of 51 :24 : 3 :2 : 1, respectively. Only 1.42% of the fed AN was excreted in the faeces. Charcoal usage had a good effect as it prevented AN to accumulate in the organs. Aflatoxin contaminated diets (in AN and CC groups) resulted in paralysis, disorder of fat deposition, discolouration and haemorrhages of some organs. Scanning electron microscopic examination revealed no ill effect on the surface structure of the small intestine due to either AN or AN + CC. Pathological examination showed that the main affected organs were liver, heart and spleen, respectively. The changes include hepatic round cell infiltration, irregularities of lobular plats, focal necrosis and periportal fibrosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of low level of dietary aflatoxins on baladi rabbits. 224 71

Diets containing 0.8, 2.53 and 8.0% field variety morning glory seed were fed to male and female rats (20 per group) in a 90-day subchronic feeding study. Gross clinical observations, body weight, and feed and water intake were recorded weekly. At 90 days, all surviving rats were autopsied, organs were weighed, and blood chemistry analyses, haematology, and bone-marrow evaluation for evidence of clastogenic effects were performed. Tissues from control (0% seed) and high-dose (8.0% seed) rats were examined histologically. Effects of morning glory seed were noted mainly in the high-dose group of both sexes. These included increases in mortality, feed consumption (on a body-weight basis), water consumption, serum alkaline phosphatase and potassium, white blood cell count, and brain and liver weights (as a percentage of body weight); body-weight gain and serum glucose were decreased. Significant changes seen in high-dose females alone were: increased haemoglobin, serum constituents (urea nitrogen, glutamic-pyruvic transaminase, glutamic-oxaloacetic transaminase, and ornithine carbamyl transferase), and organ weights (heart, kidney, spleen and pancreas as a percentage of body weight), and decreases in serum albumin, total protein, albumin:globulin ratio, and calcium. Significant changes occurring in high-dose males alone were: increased testicular weight (as a percentage of body weight), increased serum phosphorus, and decreased serum cholesterol. Liver degeneration in the high-dose females was greater than that in the controls. Mortality at 8.0% seed in the diet was 40% in males and 10% in females. At 0.8% seed, the only parameter that differed significantly from that of the controls was a final body-weight reduction in females without a corresponding reduction in feed consumption.
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PMID:Toxicological evaluation of morning glory seed: subchronic 90-day feeding study. 224 29

The present study was designed to examine the effects of methanolic extract (PE-ME), isoflavonoid fraction (PF-IF), triterpenoid saponin fraction (PF-SP) and N-acyl-N1-glucosyl-tryptophan (PF-P) isolated from puerariae flos on alcohol-induced unusual metabolism (as for glucose (BG), triglyceride (TG), and urea nitrogen (BUN) level in blood) and experimental liver injury (model: CCl4- and high fatty food induced) in mice. These alcohol-induced increasing responses were inhibited by the extracted and refined substances from puerariae flos. In short, PF-ME (4500 mg/kg) and PF-P (400 mg/kg) inhibited an increase in BG level induced by alcohol, whereas PF-IF (1000 mg/kg) and PF-SP (1000 mg/kg) did not. Similary, PF-ME and PF-SP inhibited an increase in TG induced by alcohol, whereas PF-IF did not. In addition, PF-IF and PF-SP inhibited increasing BUN level. Still more, PF-IF and PF-SP significantly inhibited an increase in gulutamate oxalacetate transaminase or gulutamate pyruvate transaminase level induced by high-fatty food and CCl4 in control animals. Especially PF-IF (250 mg/kg) administration showed a remarkable effect (inhibition: 76.3%) in control animals. These results suggested that puerariae flos or its combination drugs may be a useful drug as a traditional medicinal system for counteraction to drinking.
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PMID:[Pharmacological studies on puerariae flos. II. The effects of puerariae flos on alcohol-induced unusual metabolism and experimental liver injury in mice]. 227 52

Growth, feed conversion, serum chemistry and gross slaughter characteristics were determined in 20 steers (initially 9 mo of age, 231 +/- 18 kg) receiving daily injections of either saline (S) or recombinantly derived bovine somatotropin (rBST, 20.6 mg/d) for 112 d. Live weight gains were 15% greater for steers treated with rBST than for those treated with S. Feed intake was not different between S- and rBST-treated steers; thus, feed conversion was 12% more efficient in rBST steers. Scanogram backfat measurements were not affected by treatments. Serum electrolytes, protein, glucose and most enzyme activities were similar in S and rBST steers. Serum urea, creatinine and cholesterol (toward the end of treatment) concentrations, however, were lower (P less than .05) in rBST steers, suggesting that nitrogen retention was increased and lipid turnover was decreased by rBST. Total (P less than .1) and conjugated (P less than .05) bilirubin concentrations and glutamate-pyruvate transaminase activity (P less than .05) were lower in rBST steers. Carcass weights were not altered, but dressing percentages were lower (P less than .05) in rBST steers. This indicated that weight gain response to rBST was primarily in noncarcass components; further examination showed that this gain was predominantly in gut fill (approximately 2/3 of the greater live weight gain in rBST steers). Alternative protocols, such as administering the hormone to younger animals and (or) for a longer duration, may be necessary in order to achieve desirable responses in carcass growth.
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PMID:Growth and metabolism in somatotropin-treated steers: I. Growth, serum chemistry and carcass weights. 228 55

The importance of accurate quantitative blood biochemical analysis for the diagnosis and management of disease is recognized by most veterinarians. In recent years, several biochemical analyzers have become available for the veterinary market. One of these analyzers was evaluated for its suitability in measuring several biochemical variables--alkaline phosphatase, urea nitrogen, creatinine, glucose, alanine transaminase (dog and cat only), and aspartate transaminase (horse only)--in dogs, cats, and horses. Instrument within-day precision ranged from 1.0 to 7.1%, and between-day precision ranged from 1.6 to 7.4%. During the 6-month period of the study, the analyzer required recalibration for only 1 analyte (creatinine). Concentrations of individual analytes were similar when blood (collected in anticoagulant), plasma, and serum were assayed in parallel. The accuracy of the analyzer, as measured by correlation to a reference method, ranged from 0.861 for creatinine in horses to greater than 0.950 for each of the other analytes in the 3 species. Mean values for each analyte were similar, except for alkaline phosphatase, which had consistently lower values by use of the analyzer method. A data base was established for reference values in each species.
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PMID:Evaluation of an automated tabletop blood biochemical analyzer for the veterinary clinical pathology laboratory. 229 56


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