Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was tracing of changes in the activity of glutathione peroxidase (GSHPx), glutathione transferase (GSH S-Tr), aspartate aminotransferase (AspAT) and alanine aminotransferase (A1AT) in the brain as a result of diet enrichment with antioxidants: selenium (Se), vitamin E and vitamin B15 (pangamic acid). The experiment was carried out on Wistar rats with initial body weight 150 g. Following prolonged enrichment of diet with Se (0.1 ppm of sodium selenite), vitamin E (6 mg/100 g of diet) and vitamin B15 (2.5 mg/100 g of diet) the following results were obtained. The activity of GSHPx in brain microsomes was not changed after one year of vitamin E administration when it was measured against hydrogen hydroxide and against cumene hydrochloride; vitamin E administration increased the activity of GSH S-Tr in the cytoplasmic fraction of brain cells. Diet enrichment with selenium increased after 12 and 18 months the activity of GSHPx measured against both substrates, and GSH S-Tr activity increased considerably. Presence of vitamin B15 in diet reduced GSHPx activity after one-year or longer administration, after 18 months the activity of GSH S-Tr was reduced also. No changes were noted in the activity of AspAT and A1AT.
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PMID:The effect of long-term enrichment of diet with selenium, vitamin E and B15 on the activity of certain enzymes in rat brain. 345 69

Concentrations of sodium, potassium, chloride, inorganic phosphorus, total magnesium, total calcium, iron, urea, creatinine, total protein, albumin, total bilirubin, alkaline phosphatase (ALP), alanine transaminase (ALT), lactate dehydrogenase (LD), creatine kinase (CK), gamma-glutamyltransferase (GGT) and aspartate transaminase (AST) were determined in serum specimens collected from 53 free-ranging mountain reedbuck (Redunca fulvorufula) during live capture using nets. Considerable variations in the concentrations of the enzymes ALP, LDH, CK, GGT and AST were found as well as in the concentrations of creatinine, bilirubin and iron. This wide variation in results seriously questions the usefulness of similar blood investigations on heterogenous groups of mechanically restrained animals.
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PMID:Blood chemical and electrolyte concentrations in the mountain reedbuck Redunca fulvorufula. 350 6

Concentrations of sodium, potassium, chloride, inorganic phosphorus, total calcium, total magnesium, albumin, total protein, cholesterol, urea, creatinine, cortisol as well as the activities of alkaline phosphatase, alanine transaminase, aspartate transaminase, gamma-glutamyltransferase, creatine kinase and lactate dehydrogenase were determined in serum specimens collected from 100 free-ranging warthogs Phacochoerus aethiopicus within five minutes after they were killed with a shotgun. Average concentrations for the following chemical constituents were found: sodium (145 mmol l-1), potassium (8.6 mmol l-1), chloride (102.5 mmol l-1), phosphorus (2.31 mmol l-1), calcium (2.93 mmol l-1), magnesium (1.23 mmol l-1), albumin (26.4 g l-1), serum proteins (62.2 g l-1), cholesterol (1.82 mmol l-1) and urea (8.74 mmol l-1). The cortisol concentrations ranged from 55-340 nmol l-1 (n = 30). Wide variations were recorded in the concentration of creatinine as well as in the activities of the various enzymes.
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PMID:Blood chemical parameters in the warthog Phacochoerus aethiopicus. 350 7

Four experiments were carried out with 10 to 12 day old leghorn chicks weighing approximately 93 to 101 g. The chicks were injected intraperitoneally with sterigmatocystin (STG) dissolved in olive oil. The LD50 values as established in the first two experiments were 10.0 and 14.0 mg/kg body weight with most of the deaths occurring between 9 and 21 h following injection. Histopathological studies demonstrated that there was hemorrhage, foci of degeneration and necrosis with fibroblastic proliferation in sinusoids of the liver while the kidneys showed tubular degeneration and necrosis. Biochemical analysis of blood sera demonstrated that STG caused a marked elevation in the activities of lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase, and a depression of creatine kinase, but no effects on gamma-glutamyl transferase, amylase and lipase. Free and conjugated bilirubin were elevated in the sera while total protein, albumin, glucose, potassium, chloride and phosphorous concentrations were depressed. In addition, total white blood cells and circulating agranulocytes were depressed while circulating granulocytes were elevated. STG did not significantly affect the concentration of uric acid, cholesterol, triglycerides, calcium, magnesium and sodium in blood.
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PMID:Acute toxicity of sterigmatocystin to chicks. 356 71

Male Fischer 344 rats were used to investigate the hepatic effects of exposure to halothane under normoxic conditions (FIO2 = 0.21) in isoniazid-treated rats. Animals were treated with saline or isoniazid (50 mg/kg) for 7 days and then were exposed to either 1% halothane or air for 2 hr. One-half of the rats from each treatment and exposure group were killed 24 hr postexposure; the remaining were killed 4 days postexposure. Twenty-four hours following halothane exposure, serum transaminase levels were significantly elevated in isoniazid- compared with saline-treated rats (i.e., aspartate aminotransferase = twofold; alanine aminotransferase = seven-fold). Cholesterol levels were significantly depressed by halothane exposure in both saline- and isoniazid-treated rats. Other serum parameters indicative of hepatic and renal function were not different: alkaline phosphatase, total protein, total bilirubin, hematocrit, uric acid, creatinine, urea nitrogen, Na+, K+, Ca2+, and inorganic phosphate. Neither saline-treated nor isoniazid-treated rats exposed to air exhibited histologic evidence of hepatic damage. Halothane-exposed rats, however, showed a circumscribed disruption of cellular morphology. The most severe lesions were observed with isoniazid-treated animals with extensive pericentral hepatocellular necrosis and infiltration by leucocytes and Kupffer cells. Serum concentrations of two products of the oxidative metabolism of halothane, trifluoroacetic acid and bromide, were significantly elevated in isoniazid- compared with saline-treated rats. Serum levels of fluoride, a product of reductive metabolism, were not different. These results strongly suggest that hepatic injury following halothane administration can be produced by intermediates of oxidative metabolism.
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PMID:Halothane hepatotoxicity in Fischer 344 rats pretreated with isoniazid. 356 16

Cysteinesulfinate decarboxylase, purified from male rat livers and homogeneous by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, is resolved into five distinct enzyme species (isoforms) by gel isoelectric focusing. Since the isoforms are present in fresh liver homogenates and do not arise by proteolysis, the enzyme is apparently heterogeneous in vivo. Although female rat livers contain only 5% of the cysteinesulfinate decarboxylase activity of male livers, immunological and enzymatic studies indicate that the distribution of isoforms is similar in both sexes. Rat brain and kidney also contain multiple isoforms which are cross-reactive with polyclonal antibodies prepared to the liver enzyme. The enzyme exhibits a protomer Mr of 53,000, and the native enzyme is shown by cross-linking studies to be dimeric. Purified enzyme contains no carbohydrate or phosphate and does not bind excess pyridoxal 5'-phosphate. Two pools of enzyme activity are resolved preparatively by chromatofocusing chromatography and have been examined with respect to substrate and inhibitor specificity. Both pools are most active toward L-cysteinesulfinate and L-cysteinesulfonate. Aspartate, homocysteinesulfinate, homocysteinesulfonate, 2-amino-3-phosphonopropionate, and glutamate are decarboxylated at rates less than 1% of that observed with L-cysteinesulfinate; D-cysteinesulfinate is not decarboxylated but is an effective inhibitor. The enzyme isoforms cannot be distinguished on the basis of substrate affinity or specificity. The enzyme is irreversibly inactivated by the mechanism-based inhibitors beta-methylene-DL-aspartate and beta-ethylidene-DL-aspartate. beta-Ethylideneaspartate, in contrast to the beta-methylene derivative, does not inhibit aspartate aminotransferase, an enzyme also important in cysteinesulfinate metabolism. beta-Ethylidene aspartate or related beta-ethylidene compounds may be useful in selectively altering cysteinesulfinate metabolism in vivo.
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PMID:Multiple forms of rat liver cysteinesulfinate decarboxylase. 358 15

Seasonal (in January, April, July, October) changes of aspartate aminotransferase (AST), alanine aminotransferase (ALT), protein, bilirubin, glucose, cholesterol, creatinine, blood urea nitrogen, Cl-, K+, Na+ content were studied in the blood plasma of mice at different time of day (6 p. m., midnight, 6 a. m., midday). The analysis of the average daily indices has shown that the most expressed variations were the following: AST (spring maximum is 3.7 times higher than autumn minimum), ALT (winter maximum is 2.9 times higher than autumn minimum), creatinine (summer maximum is 2.5 times higher than winter minimum), blood urea nitrogen (summer maximum is 2.5 times higher than autumn minimum). Bilirubin and protein content in spring is insignificant, but it is significantly higher than in other seasons. Cholesterol content is lower in winter. No differences in glucose, Cl-, K+, Na+ content in different months have been revealed. The largest circadian synchronization was observed in winter in AST, glucose, cholesterol, protein, Cl-, K+, Na+ (the level observed at 6 p. m. and at midday is higher than that observed at midnight and 6 a. m.) and in autumn in AST, ALT, glucose, cholesterol, blood urea nitrogen, with the circadian curves inverse as compared to the winter period. In spring practically no circadian synchronization was observed.
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PMID:[Seasonal and circadian fluctuations of the biochemical indices of the blood in mice]. 368 50

A patient who developed chronic salicylism associated with salicylate therapy for treatment of juvenile rheumatoid arthritis is described, and the clinical presentation and treatment of chronic salicylism are reviewed. A 5 1/2-year-old boy was receiving aspirin 150/mg/kg/day for treatment of juvenile rheumatoid arthritis. While on salicylate therapy, the patient developed tachypnea and became increasingly hyperthermic, lethargic, and disoriented. The patient developed a maculopapular rash, weakness, and a decreased level of consciousness during the 11 days before admission to the hospital. Physical examination and laboratory determinations revealed that the patient had hypoprothrombinemia, hypoglycemia, and severe hepatic encephalopathy secondary to long-term salicylate toxicity. The patient was treated for hypoglycemia, electrolyte imbalances, thrombocytopenia, and anemia and was discharged after 24 days. Diagnosing chronic salicylism with hepatic dysfunction was difficult because the symptoms are similar to those of stage I to stage II Reye's syndrome. Liver enzymes, including aspartate aminotransferase (also called SGOT), alanine aminotransferase (also called SGPT), alkaline phosphatase, and lactate dehydrogenase, may be elevated in juvenile arthritis patients with hepatic dysfunction. Liver dysfunction usually improves when salicylate therapy is discontinued. Supportive therapy should always be used in symptomatic patients. Children on long-term, high-dose salicylate therapy should be monitored closely, and baseline liver function tests should be performed. The clinical effectiveness of administering sodium bicarbonate in attempts to alkalinize urine and increase salicylate elimination is controversial. In patients with juvenile rheumatoid arthritis who develop chronic salicylism, careful analysis of the patient's medication history, laboratory values, and clinical presentation are necessary to rule out Reye's syndrome.
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PMID:Chronic salicylism in a patient with juvenile rheumatoid arthritis. 370 82

Using fully mechanized analytical equipment, interference by haemolysis in the determination of 26 clinical chemical parameters was determined quantitatively by adding haemolysate to serum. Haemoglobin concentrations up to 6.6 g/l caused essentially no interference in the following determinations: albumin (immuno-nephelometric), alpha-amylase, calcium, chloride, cholesterol, cholinesterase, creatinine, iron, glucose, glutamate dehydrogenase, uric acid, urea, sodium, inorganic phosphate, total protein, transferrin and triglycerides. In the presence of haemoglobin, erroneously high values were found for: lactate dehydrogenase (haemoglobin higher than 0.2 g/l), aspartate aminotransferase, potassium and acid phosphate (haemoglobin higher than 1.5 g/l), creatine kinase (haemoglobin higher than 2.5 g/l) and alanine aminotransferase (haemoglobin higher than 3.4 g/l). Erroneously low values were found for bilirubin (haemoglobin higher than 0.8 g/l), alkaline phosphatase and albumin (by electrophoresis) (haemoglobin higher than 1.5 g/l) and gamma-glutamyltransferase (haemoglobin higher than 3.0 g/l).
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PMID:Haemolysis as an interference factor in clinical chemistry. 371 97

A reference range data base containing serum chemistry and hematology values on over 3000 animals is described. Data listed include the mean, standard deviation, and 10th and 90th percentiles for each of the following parameters. Serum chemistry: sodium, potassium, chloride, calcium, inorganic phosphorus, urea nitrogen, creatinine, total bilirubin, total protein, glucose, cholesterol, triglycerides, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase (monkey only), lactate dehydrogenase (dog only), and creatine kinase (dog only). Hematology: hematocrit, hemoglobin, red blood cells, reticulocytes, mean cell volume, mean cell hemoglobin, mean cell hemoglobin percent, platelets, white blood cells, neutrophils, eosinophils, basophils, lymphocytes, monocytes, and stabs. The species included are mouse, rat, hamster, rabbit, beagle dog, and cynomolgus monkey. The use of the reference ranges in routine computerized data collection is discussed.
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PMID:Reference range data base for serum chemistry and hematology values in laboratory animals. 371 84


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