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)

Female BALB/c and B6C3F1 mice were examined after a 3-wk exposure to dietary estradiol (0, 400, 800, 1600, and 3200 ppb) in a purified (AIN-76A) or a natural-ingredient (NIH-07) diet. The use of AIN-76A was associated with a 9-13% greater (p less than 0.001) body weight and a 36-43% higher (p less than 0.001) serum cholesterol in both mouse genotypes when compared to mice fed NIH-07. Conversely, when fed NIH-07, both mouse genotypes had a 20-22% higher (p less than 0.003) serum urea nitogren and 2-3.5% higher erythrocyte count (p less than 0.001) and hemoglobin concentration (p less than 0.04) than when fed AIN-76A. Reduced erythrocyte parameters suggest that chronic feeding of the purified diet might result in anemia. No significant compound or diet-related differences were noted for serum creatinine, alanine aminotransferase, aspartate aminotransferase, or gamma-glutamyl transferase. Although there was no diet effect on absolute or differential white blood cell count, estradiol caused a decrease in the total white blood cell count (p less than 0.014) and an increase in the percentage of polymorphonuclear leukocytes (p less than 0.014) in BALB/c and decreased the percentage of lymphocytes (p less than 0.005) in B6C3F1 females. In addition, estradiol increased uterine weight and inhibited thymic and splenic weights in one or both genotypes. Spleen and thymus weight responses to estradiol were not significantly influenced by diet. However, the uterine weight responses to estradiol were apparently influenced by diet in both genotypes. In B6C3F1 mice, the uterus weighed more at each level of estradiol when mice were fed AIN-76A compared to NIH-07 diet. In BALB/c mice, this was true only at the two lower dietary concentrations of estradiol. In conclusion, mice fed the purified diet, AIN-76A, differed from those fed the cereal-based diet, NIH-07, in hematology, clinical chemistry, and uterine weight response to estradiol.
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PMID:Effects of purified (AIN-76A) and natural-ingredient (NIH-07) diets on responses of BALB/c and B6C3F1 female mice to estradiol. 368 22

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

Two elderly people were given intravenous infusion of dimethylsulphoxide (DMSO) as treatment for arthritis. One became seriously ill, the other remained well. Both had similar changes in aspartate transaminase, hydroxybutyrate dehydrogenase, and creatine kinase and evidence of haemolysis. This is the first report of serum enzyme changes and anaemia after intravenous DMSO in man.
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PMID:Dimethylsulphoxide-induced toxicity. 610 30

Haematology and serum aspartate aminotransferase and alanine aminotransferase activities were studied during the migration phase of Stephanurus dentatus in the livers of experimentally infected pigs. There was no evidence of anaemia but total leucocyte counts were raised and peripheral eosinophilia began 2 to 3 weeks after infection. Peak eosinophilia occurred 6 to 7 weeks after infection and levels were still elevated at 20 weeks. Lymphocyte and neutrophil numbers remained constant. Reinfection did not stimulate a secondary eosinophil response. Only aspartate aminotransferase was temporarily elevated. The gross pathology resulting from the infections is described. Several clinicopathological differences in the response of pigs to invasion of the liver by S. dentatus were noted compared to those produced by Ascaris suum but none are pathognomonic.
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PMID:Clinical pathology of experimental stephanuriasis in pigs. 622 77

Eleven adult Basenji dogs with immunoproliferative small intestinal disease (IPSID) were studied. Two items of history related to the digestive tract were characteristic: (i) chronic intractable diarrhea in most dogs, and (ii) progressive emaciation. Anorexia was intermittent in only a few dogs. In addition, skin lesions of various degrees of severity were observed, including alopecia of pinnae and ventrum, hyperpigmentation and hyperkeratosis of pinnae, and necrosis and ulcerations of margins of pinnae. The cause of the skin lesions was not determined; however, hypothyroidism did not appear to contribute to the skin changes. Standard hematologic and serum chemical values were not consistently abnormal. However, a poorly regenerative anemia, mild neutrophilia, and increased aspartate aminotransferase and alanine aminotransferase activities were generally observed in severely affected dogs. The Pelger-Huet anomaly was identified in dog 3. Maldigestion and malabsorption as determined by the N-benzoyl-L-tyrosyl-p-aminobenzoic acid and d-xylose test was documented to varying degrees in dogs with IPSID. Maldigestion was correlated with functional pancreatic exocrine insufficiency. Severe malabsorption was documented in only 3 dogs. Serum gastrin values were evaluated in these dogs because of a prior observation of parietal cell hyperplasia and gastric ulceration. Hypergastrinemia was documented in 3 dogs. Additional studies will be necessary to determine whether an acid hypersecretory state contributes to the pathogenesis of IPSID in Basenjis.
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PMID:Clinical and laboratory characterization of Basenjis with immunoproliferative small intestinal disease. 660 87

It was shown that splenectomized mice could develop a certain resistance to Plasmodium berghei but usually no real immunity, since the infection became chronic, often with high parasitemias. A patent infection lasting at least 2 weeks was necessary for the development of this degree of protection. Prolonged suppression to subpatent levels (sulfonamide treatment), rather than radical cure (chloroquine), after 2 weeks of patency yielded a higher proportion of mice resistant to superinfection. An increasing proportion of B10LP, but not C57BL/Rij or BALB/c, mice cleared their chronic infection spontaneously in time. Chronic patent infections were accompanied by anemia, elevated serum glutamate oxaloacetate transaminase levels, indicating liver pathology, and decreased immune reactivity, but the magnitude to these pathological changes was limited compared with changes in primary, lethal infections in intact controls. Parasitemia and pathology did not always develop synchronously.
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PMID:Chronic, patent Plasmodium berghei malaria in splenectomized mice. 704 Feb 49

The clinical chemical changes induced by Anaplasma marginale infection were determined in 16 adult, intact cows infected with either of 2 virulent isolates and in 8 others treated with a live sheep-attenuated A marginale vaccine and were compared with the clinical chemical analyses in 7 noninfected controls. Blood samples from the cows were analyzed for various serum components and during clinical disease. Cows infected with the 2 virulent isolates had maximum erythrocyte parasitemias (0.5% to 66%) between 1 and 11 days of patency (DP); 7 of the 16 infected animals died within 5 to 12 DP. Cows given the sheep-attenuated anaplasma vaccine had maximum parasitemias (0.1% to 4.2%) between 1 and 16 DP and none died. Infection with the virulent isolates produced severe anemia (mean RBC count = about 2 million/mm3) and caused increases in serum total bilirubin (TBILI), direct bilirubin (DBILI), serum urea nitrogen (SUN), alkaline phosphatase (ALP), and serum aspartate aminotransferase (AST) that were significantly higher than comparable changes in control values. These increases were highest after peak parasitemias in surviving animals. Vaccination with the attenuated isolate produced a mild anemia (mean RBC count = about 5 million/mm3) and a significant increase only in ALP. Marked increase in TBILI, DBILI, SUN, ALP, and AST were detected 0 to 1 day before death in 3 cows. However, such increases were not observed 2 to 4 days before death in the other cows that died.
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PMID:Clinical chemistry of anaplasmosis: blood chemical changes in infected mature cows. 725 83

Hemolytic or blood loss anemia was induce in six ponies and red blood cell concentrations of creatine, glucose-6-phosphate dehydrogenase (G-6-PD), lactate dehydrogenase (LDH), and aspartate transaminase (AST) were measured during the ensuing regenerative period. Creatine and G-6-PD levels correlated well and increased concentration of either was good indication of increased erythrogenesis. Erythrocyte LDH levels were of value in assessing the response to hemolytic anemia but not to blood loss anemia. The difference may be, at least in part, the result of differing degrees of regenerative effort seen in the two experimental groups. Red cell AST concentrations fluctuated markedly and were of no value in assessing the anemia in either group.
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PMID:Biochemical changes in equine erythrocytes during experimental regenerative anemia. 726 89

A rare isozyme of serum creatine kinase (CK) migrating cathodic to CK-MM on electrophoresis was found in a 30-year-old male with stomach cancer complicated by disseminated intravascular coagulation leading to massive upper gastrointestinal bleeding and marked anemia. Serum CK activity rose to a maximum of 374 U/l without detectable CK-MB isoenzyme. The patient was also characterized by a marked increase in serum lactate dehydrogenase (all isozymes elevated) and by preferential leakage of mitochondrial aspartate aminotransferase and glutamate dehydrogenase, indicating the presence of extensive tissue damage involving mitochondria. Skeletal muscle mitochondria were considered the most likely source of the additional CK isozyme.
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PMID:Cathodic isozyme of serum creatine kinase in a case of stomach cancer complicated by disseminated intravascular coagulation. 744 49

As compared to intoxication with lead or selenium alone, the concurrent administration of lead and selenium to broiler chickens produced more deleterious effects characterized by adverse changes in haematological parameters and severe alterations in serum total protein, aspartate aminotransferase (AST), cholesterol and alkaline phosphatase levels. Deleterious effects were more pronounced when lead was administered as second toxic chemical in the presence of selenium in the diet of the birds. Significant haematological depressions leading to anaemia were recorded during subacute lead toxicosis when selenium was concurrently administered in the feed, indicating an enhancement of lead toxicity in the presence of selenium.
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PMID:Effects of concurrent administration of lead and selenium on some haematological and biochemical parameters of broiler chickens. 811 92


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