Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hormonal and biochemical effects of danazol (600 mg a day) and high-dose medroxyprogesterone acetate (MPA; 100 mg a day) were studied in a placebo-controlled, 6-month trial. Serum gonadotrophins and prolactin levels did not change during danazol and MPA treatments, whereas oestradiol and progesterone levels decreased significantly in relation to placebo without any difference between danazol and MPA. Both drugs significantly suppressed the sex hormone-binding globulin level (SHBG), and consequently, the free-androgen index (serum total testosterone nmol/l per SHBG nmol/l x 100) as compared with placebo, the effect of danazol being significantly stronger than that of MPA. Danazol, but not MPA, significantly increased serum aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT) and haemoglobin levels, and also thrombocyte counts, whereas MPA, but not danazol, increased the serum concentration of albumin in relation to placebo. Serum total bilirubin, conjugated bilirubin, gamma-glutamyl transferase, creatinine, alkaline phosphatase, sodium and potassium levels and leucocyte counts remained unchanged during both treatments. Danazol and high-dose MPA did not differ from each other in their ovarian and anterior pituitary effects, while the increase in androgenic activity induced by danazol was greater than that achieved with MPA. Danazol also had more biochemical effects than MPA. It interfered with the functions of the liver and the production of thrombocytes and haemoglobin, whereas MPA affected only albumin synthesis/release.
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PMID:Placebo-controlled comparison of hormonal and biochemical effects of danazol and high-dose medroxyprogesterone acetate. 214 9

Prolactin, in vitro, significantly increased citrate production, mAAT (mitochondrial aspartate aminotransferase) and pmAAT (precursor form of mAAT) activity of prostate epithelial cells derived from rat lateral prostate (LP) and pig prostate cultures. In contrast, prolactin had no effect on the cytosolic isozyme, cAAT. This prolactin effect appeared to be independent of testosterone. The phorbol ester TPA (12-O-tetradecanoyl-phorbol-13-acetate) induced the same effects as prolactin thereby indicating the involvement of protein kinase C. This report demonstrates that prolactin directly regulates citrate production of prostate epithelial cells and the availability of an in vitro model to elucidate the mechanism of action of prolactin.
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PMID:Prolactin directly stimulates citrate production and mitochondrial aspartate aminotransferase of prostate epithelial cells. 238 49

The effect of seven low-dose oral contraceptive preparations on vitamin B6 status was investigated in 55 women. All preparations contained about the same amount of ethinylestradiol but differed in the content and type of progestagen. The following preparations were investigated: monophasic and triphasic levonorgestrel, monophasic and biphasic desogestrel, monophasic norethisterone, monophasic cyproterone acetate and triphasic gestodene. The vitamin B6 status was evaluated by measuring erythrocyte glutamate oxaloacetate transaminase (EGOT) activity and its degree of in vitro stimulation. From these two variables the total EGOT activity was calculated. In addition plasma pyridoxal-5'-phosphate (PLP) levels were estimated. After six months' treatment, EGOT activity and the calculated total EGOT activity were increased, but no changes were observed in the degree of in vitro stimulation (which is a more reliable parameter). Plasma PLP levels initially decreased during the first three months of treatment but after six months a return to normal levels was observed. Differences between the seven preparations were not found. We conclude from these results that the low-dose preparations investigated in this study have no any adverse effects on vitamin B6 status.
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PMID:Effects of seven low-dose combined contraceptives on vitamin B6 status. 252 29

Activity levels of pyruvate dehydrogenase, enzymes of citric acid cycle, aspartate and alanine aminotransferases were estimated in mitochondria, synaptosomes and cytosol isolated from brains of normal rats and those injected with acute and subacute doses of ammonium acetate. In mitochondria isolated from animals treated with acute dose of ammonium acetate, there was an elevation in the activities of pyruvate, isocitrate and succinate dehydrogenases while the activities of malate dehydrogenase (malate----oxaloacetate), aspartate and alanine aminotransferases were suppressed. In subacute conditions a similar profile of change was noticed excepting that there was an elevation in the activity of alpha-ketoglutarate dehydrogenase in mitochondria. In the synaptosomes isolated from animals administered with acute dose of ammonium acetate, there was an increase in the activities of pyruvate, isocitrate, alpha-ketoglutarate and succinate dehydrogenases while the changes in the activities of malate dehydrogenase, aspartate and alanine amino transferases were suppressed. In the subacute toxicity similar changes were observed in this fraction except that the activity of malate dehydrogenase (oxaloacetate----malate) was enhanced. In the cytosol, pyruvate dehydrogenase and other enzymes of citric acid cycle except malate dehydrogenase were enhanced in both acute and subacute ammonia toxicity though their activities are lesser than that of mitochondria. In this fraction malate dehydrogenase (oxaloacetate----malate) was enhanced while activities of malate dehydrogenase (malate----oxaloacetate), aspartate and alanine aminotransferases were suppressed in both the conditions. Based on these results it is concluded that the decreased activities of malate dehydrogenase (malate----oxaloacetate) in mitochondria and of aspartate aminotransferase in mitochondria and cytosol may be responsible for the disruption of malate-aspartate shuttle in hyperammonemic state.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activities of pyruvate dehydrogenase, enzymes of citric acid cycle, and aminotransferases in the subcellular fractions of cerebral cortex in normal and hyperammonemic rats. 272 22

In an attempt to elucidate the role of hepatic macrophages in liver injury, we investigated galactosamine-treated rats (500 mg per kg body weight). The rats received an i.v. injection of latex particles (2 x 10(9) particles per animal) prior to (latex-galactosamine) or 12 to 16 hr subsequent to the galactosamine treatment (galactosamine-latex). Effect of superoxide dismutase on hepatic injury induced by galactosamine or galactosamine-latex treatment was also examined. Oxygen-derived free radical-generating capacity of isolated hepatic macrophages was measured as chemiluminescence with the stimulation of phorbol myristate acetate or latex particles. As compared with normal rats, chemiluminescence of hepatic macrophages from galactosamine-treated rats was 5- to 10-fold enhanced 12 hr following galactosamine treatment and remained elevated for 48 hr. Chemiluminescence of the latex particle-pretreated macrophages in the liver was markedly suppressed even following the galactosamine treatment (p less than 0.01). Compared to galactosamine-treated rats, both lipid peroxide level in the liver tissue and AST and ALT concentration in serum were significantly decreased in the latex-galactosamine-treated rats (p less than 0.01) and increased in the galactosamine-latex-treated rats (p less than 0.01). Furthermore, superoxide dismutase supplementation protected against liver injury induced by the galactosamine-latex treatment. From these results, pretreatment with latex particles suppressed the free radical-generating capacity of hepatic macrophages and protected against hepatic injury induced by galactosamine. In contrast, injection of latex particles after galactosamine treatment aggravated hepatic injury, which was prevented by superoxide dismutase. These data suggest that liver injury induced by galactosamine is modulated by oxygen-derived free radicals from hepatic macrophages.
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PMID:Modulation of hepatotoxicity by macrophages in the liver. 283 5

The relationship between nitrogen assimilation, metabolism and aflatoxin formation has been investigated in a toxigenic and a non-toxigenic strain of Aspergillus parasiticus. Ammonia from the medium is mainly assimilated via NADP-requiring glutamate dehydrogenase. During growth NAD-requiring glutamate dehydrogenase followed an inverse pattern of activity with respect to NADP glutamate dehydrogenase. Alpha-ketoglutarate, the product of NAD glutamate dehydrogenase, stimulated acetate incorporation into aflatoxins. Glutamine synthetase, ornithine transcarbamylase, both utilizing glutamate as substrate were assayed under different growth conditions. An important regulatory role for glutamine synthetase is suggested. The metabolic route of asparagine utilization was also investigated. Both the known pathways, glutamate oxaloacetate transaminase and glutamate pyruvate transaminase are operative simultaneously.
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PMID:Nitrogen metabolism in Aspergillus parasiticus NRRL 3240 and A. flavus NRRL 3537 in relation to aflatoxin production. 287 96

Activity of enzymes participating in metabolism of glutamate and content of nicotinamide nucleotides was studied in rat liver tissue within 24 hrs after intramuscular administration of alpha-tocopheryl acetate at doses of 30 mg and 300 mg per kg of body mass. Excess of the vitamin was responsible for a decrease in the ratio NAD+/NADH in cytosol, for stimulation of glutamate dehydrogenase reaction, for a decrease of aspartate aminotransferase activity in mitochondria and of alanine aminotransferase activity in cytosol as well as for an increase of NADPH content.
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PMID:[Effect of alpha-tocopherol on glutamic acid metabolism and nicotinamide coenzyme levels in hepatocytes]. 287 84

We studied intestinal absorption of vitamin E in 26 adults with primary biliary cirrhosis (PBC) and 6 control subjects. Seven (27%) PBC patients were vitamin E-deficient based on the ratio of serum vitamin E to serum total lipid concentrations. An oral vitamin E tolerance test was performed in all patients and control subjects using a loading dose of 2000 IU alpha-tocopheryl acetate with measurement of serial serum vitamin E concentrations over 24 h. Vitamin E absorption was expressed as the maximal rise in serum vitamin E above baseline, the area under the oral tolerance test curve, and these two values divided by the fasting total serum lipid concentration. Absorption of vitamin E was significantly impaired in all PBC patients vs. control subjects (p less than 0.01), in vitamin E-deficient vs. vitamin E-sufficient PBC patients (p less than 0.05 to p less than 0.01), and in PBC patients with serum vitamin E levels below 10 micrograms/ml vs. those with serum vitamin E levels above 10 micrograms/ml (p less than 0.01). Vitamin E absorption was inversely related to stage of PBC, serum cholylglycine, total bilirubin, cholesterol, alkaline phosphatase, aspartate aminotransferase, and prothrombin time. Patients with serum vitamin E below 10 micrograms/ml, serum total bilirubin above 3 mg/dl, serum cholylglycine above 600 micrograms/dl, or serum alkaline phosphatase above 1000 IU/L had severe malabsorption of vitamin E and would be at high risk for the development of vitamin E deficiency. Therefore, vitamin E supplementation should be considered not only in patients in whom overt vitamin E deficiency is present, but also in PBC patients meeting these criteria.
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PMID:Intestinal malabsorption of vitamin E in primary biliary cirrhosis. 291 Jul 63

As part of a series of epidemiological and ecological studies of leishmaniasis in Jordan, we have made functional studies of four isolates from human lesions and from ear lesions of three field-collected Psammomys obesus. Primary isolates were subcultured, frozen stabilates prepared and BALB/c mouse infectivity experiments initiated. Each mouse was inoculated with 4-8 x 10(4) promastigotes into a hind footpad. Quantitative evaluation of the footpads showed enlargement three to four weeks postinoculation. Amastigotes were readily identified in smears from footpad lesions and promastigotes in culture. At 47 days, liver and spleen samples grew out promastigotes. Biochemical characterization of these seven isolates was made by isozyme analysis using cellulose acetate membrane electrophoresis of fructokinase, phosphoglucose isomerase, phosphoglucomutase, aspartate aminotransferase, malate dehydrogenase, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase. Reference isolates used for comparison were Leishmania major, L. tropica minor, L. donovani, L. aethiopica and L. m. mexicana. All seven Jordan isolates showed enzyme electromorphs identical to L. major, confirming our ecological/epidemiological studies that P. obesus is a major reservoir for human cutaneous leishmaniasis in Jordan.
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PMID:Cutaneous leishmaniasis in Jordan: biochemical identification of human and Psammomys obesus isolates as Leishmania major. 304 29

Six Leishmania isolates from 3 indigenous Kenyans (2 isolates from one patient) and 2 Canadian visitors in Kenya were characterized by cellulose acetate electrophoresis. The isolates were compared among themselves and with reference strains of Leishmania donovani, L. aethiopica, L. major, L. tropica, and L. arabica using 9 enzymes: malate dehydrogenase (MDH), malic enzyme (ME), phosphogluconate dehydrogenase (6PGD), glucose-6-phosphate dehydrogenase (G6PD), aspartate aminotransferase (ASAT), adenylate kinase (AK), mannose phosphate isomerase (MPI), glucose phosphate isomerase (GPI), and phosphoglucomutase (PGM). Enzyme migration patterns of isolates from the 3 indigenous Kenyans were indistinguishable from those of 2 L. tropica reference strains. The isolates from the 2 Canadians yielded migration patterns of 7 enzymes that were indistinguishable from those of 2 L. tropica reference strains. However, migration patterns of 2 enzymes, PGM and ME, differed from all migration patterns of the 10 reference strains. Balb/c mice were inoculated with stationary phase promastigotes cultured from 3 stabilates from the lesions of 2 of the Kenyan patients. The mice developed no gross pathological lesions in 6 months time. All of the study patients developed cutaneous leishmaniasis while living in or visiting districts in Central and Rift Valley Provinces, Kenya. This is the first report of human cutaneous leishmaniasis caused by L. tropica indigenous to Africa south of the Sahara.
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PMID:Indigenous human cutaneous leishmaniasis caused by Leishmania tropica in Kenya. 317 40


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