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:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our previous studies showed that polybrominated biphenyl (PBB) induced hepatic microsomal cytochrome P-450 in dairy cattle but did not elevate hepatic cytosolic ornithine decarboxylase or serum isocitrate dehydrogenase. These enzymes would be expected to increase during hepatotoxic injury and regeneration. Thus, PBB appeared to be a hepatotoxin in rats but not in cattle. In order to identify and confirm the response capability of bovine liver to hepatotoxins, we administered thioacetamide, a hepatotoxin known to induce hepatonecrosis, to a dairy calf. A progression of clinical signs of toxicosis was evident until the animal was moribund by 23 hr postdosing. Histolopathologic alterations in the liver included centrilobular necrosis with congestion and subcapsular microhemmorrhage. Marked changes in serum protein profiles were not noted. However, distinct increases in serum Fe and bilirubin occurred with progressing toxicosis, as did sharp declines in glucose and triglycerides. Serum lactic dehydrogenase, alkaline phosphatase, glutamic-oxaloacetic transaminase, isocitrate dehydrogenase and glutamic-pyruvate transaminase were elevated. Elevation of ornithine decarboxylase was dramatic when compared to the level in normal fetal bovine liver. From studies of its kinetic properties, bovine liver ornithine decarboxylase appears to have an apparent Km for ornithine decarboxylase of .45 mM. Liver homogenates from PBB-treated animals did not form inhibitors to ornithine decarboxylase. Compared with the thioacetamide-treated calf, the normal adult bovine, pregnant adult and 6-month fetus had relative activities of .2 .4 and 5.8%, respectively. These studies show that ornithine decarboxylase is low in liver of normal cattle, but is elevated markedly by agents that cause hepatonecrosis.
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PMID:Ornithine decarboxylase, serum isocitrate dehydrogenase and clinical chemistry changes during thioacetamide-induced hepatotoxicity in a calf. 734 23

Groups of 10 male Hartley guinea pigs were exposed to 3.0, 2.0, 1.0, or 0.1% (v/v) 1,1-Dichloro-2,2,2-trifluoroethane (HCFC-123) or 1.0% (v/v) halothane by inhalation for 4 hr. A sixth group of 10 guinea pigs received only air. All animals were sacrificed 48 hr postexposure. Gross and histopathologic examination of the liver, heart, and kidney and routine hematology and clinical chemistry analyses [including isocitrate dehydrogenase (ICDH)] were done on all guinea pigs. Lesions related to HCFC-123 and halothane exposure were limited to the liver and included centrolobular vacuolar (fatty) change, multifocal random degeneration and necrosis, and centrolobular degeneration and necrosis. These lesions were observed in 90-100% of the exposed animals and were absent in the air-only controls. There was significant individual animal variation in susceptibility to both HCFC-123 and halothane, resulting in a spectrum of histologic lesions and clinical chemistry values within each exposure group. Alanine aminotransferase, aspartate aminotransferase, and ICDH were the most significant predictors of hepatocellular damage. Similarities in the response between halothane and HCFC-123 in this guinea pig model suggests that humans susceptible to halothane-induced hepatitis may be susceptible to HCFC-123 by a common mechanism of toxicity.
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PMID:Hepatotoxicity in guinea pigs following acute inhalation exposure to 1,1-dichloro-2,2,2-trifluoroethane. 781 29

Rats were injected with gentamicin at doses of 20, 40 and 80 mg/kg per day for 6 consecutive days. The treatment caused nephrotoxicity as evidenced by dose-related increases in serum creatinine concentration and renal tubular necrosis. The nephrotoxicity was accompanied by reduced renal cortical and fasting blood glucose levels, and by increases in serum lactate concentrations. The activities of cortical malate dehydrogenase and alanine transaminase were significantly reduced by the three doses of gentamicin. On the other hand, aspartate transaminase activity was lowered only by the highest dose of antibiotic used. However, the activity of cortical glucose-6-phosphate dehydrogenase was altered by the 20 and 40 mg/kg doses of gentamicin, but not by the 80 mg/kg dose. The two lower doses reduced the lactate content of the cortex but activated lactate dehydrogenase. The activity of isocitrate dehydrogenase was not altered by any of the gentamicin doses used.
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PMID:Effect of gentamicin-induced nephrotoxicity on some carbohydrate metabolic pathways in the rat renal cortex. 785 4

Hepatotoxic effects of inorganic mercury with and without pretreatment of phenobarbitone and promethazine have been described in experiments on domesticated rabbits. The total body weight and the relative liver weight decreased after mercury treatment under all experimental conditions. After phenobarbitone (PB) treatment, the serum glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), isocitrate dehydrogenase (ICDH), and lactate dehydrogenase (LDH) activities decreased to 31%, 77%, 20%, and 27%, respectively, whereas the serum alkaline phosphatase (AP) activity increased 54%. After promethazine (PM) treatment, however, the serum GPT activity was inhibited 73%, whereas the serum LDH activity increased 53%. Both hepatic GPT and AP activities decreased after PB (41% and 46%, respectively) and after PM (50% and 52%, respectively) treatments, while the activities of LDH and ICDH increased (after PB: 924% and 108%, respectively; after PM: 147% and 40%, respectively). After mercuric chloride (HgCl2) treatment, the serum GOT, GPT, LDH, and ICDH activities decreased 69%, 83%, 11%, and 48%, respectively. The hepatic GOT, LDH, and AP activities increased 56%, 129%, and 51%, respectively. The administration of HgCl2 in PB-pretreated animals was associated with a decrease in the activities of serum GOT and AP (57% and 69%, respectively), while the ICDH activity increased 27%. The hepatic GOT, GPT, and AP increased 58%, 135%, and 77%, respectively, after mercury treatment, whereas LDH and ICDH were inhibited 78% and 29%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sublethal effects of inorganic mercury on the body growth rate and liver function enzymes of phenobarbitone-pretreated and promethazine-pretreated rabbits. 788 43

The influence of enhancing the supply of hydrogen donors on respiratory rates, NAD(P)H fluorescence, and membrane potential was investigated. Addition of 5 mM malate to mitochondria during oxidation of 10 mM isocitrate, oxoglutarate, succinate, proline, or glycerol-3-phosphate under steady-state conditions resulted in an inhibition of respiration, coincident with a decrease in both transmembrane electrical potential and percentage reduction of NAD(P). Half-maximum inhibition of NAD(P) reduction in the resting state of 10 mM isocitrate respiration was reached at 10 mM malate. This inhibition was concluded to be due to oxaloacetate formed immediately from malate by succinate dehydrogenase. Addition of 5 mM isocitrate caused higher respiratory rates, accompanied by an increase in both delta psi and percentage of NAD(P) reduction, in mitochondria oxidizing 10 mM oxoglutarate, glutamate, proline, hydroxybutyrate, glycerol-3-phosphate, or 0.025 mM palmitoyl carnitine. The half-maximum increase in percentage NAD(P) reduction with 10 mM 2-oxoglutarate as primary substrate was found at 0.24 mM isocitrate. Within the citric acid cycle, succinate dehydrogenase and NAD-isocitrate dehydrogenase play an important role in changes in the rate of NADH formation. Therefore, they participate in flux control. Furthermore, mitochondrial aspartate aminotransferase and oxidoreductases of the beta-oxidation pathway of fatty acids are additionally involved in adjusting the rate of NADH formation.
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PMID:Contribution to control of mitochondrial oxidative phosphorylation by supplement of reducing equivalents. 791 69

The flux through different segments of the tricarboxylic acid cycle was measured in rat brain synaptosomes with gas chromatography-mass spectrometry using either deuterated glutamine or [13C]aspartate. The flux between 2-oxoglutarate and oxaloacetate was estimated to be 3.14 and 4.97 nmol/min/mg protein with and without glucose, respectively. These values were 3-5-fold faster than the flux between oxaloacetate and 2-oxoglutarate (0.92 nmol/min per mg protein) measured in the presence of glucose. The pattern of intermediates labeling suggests that the overall rate-controlling reaction involves either citrate synthase or pyruvate dehydrogenase but not 2-oxoglutarate or isocitrate dehydrogenase. The enrichment in [3,3,4,4-2H4]glutamate from [2,3,3,4,4-2H5]glutamine was as rapid as in [2,3,3,4,4-2H5]glutamate, which indicates that the aspartate aminotransferase reaction is severalfold faster than the flux through the tricarboxylic acid cycle. [13C]Aspartate was rapidly converted to [13C]malate, suggesting that in intact synaptosomes aspartate entry into the mitochondrion is very slow. The finding that aspartate is taken up by mitochondria as malate, along with the observed high enrichment in [3-2H]malate (from [2,3,3,4,4-2H5]glutamine), is consistent with the substantial synaptosomal activity of the malate/aspartate shuttle.
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PMID:Tricarboxylic acid cycle in rat brain synaptosomes. Fluxes and interactions with aspartate aminotransferase and malate/aspartate shuttle. 796 53

Indian River male broiler chickens growing from 7 to 28 d of age were fed on diets containing 120, 210 and 300 g crude protein/kg diet and 0, 1.67 or 16.7 g added tryptophan (TRP)/kg diet. The hypothesis tested was that crude protein levels and TRP would affect both growth and neurotransmitter metabolism. Heart, brain and pancreatic neurotransmitter (noradrenaline (NA), dopamine (DA), serotonin (5-HT) and 5-hydroxy-indole-3-acetic acid (5-HIAA)) concentrations were determined by HPLC separation and electrochemical detection. Malate dehydrogenase (2-oxoglutarate decarboxylating) (NADP+) (MDH(NADP+); EC 1.1.1.40), isocitrate dehydrogenase (NADP+) (ICD(NADP+); EC 1.1.1.42) and aspartate aminotransferase (AAT; EC 2.6.1.1) activities were also measured. Supplemental TRP decreased growth and feed intake. Increasing dietary crude protein decreased MDH(NADP+), but increased (ICD(NADP+) and AAT activities. Additional dietary TRP decreased MDH(NADP+) activity, but had no effect on other enzyme activities. Cardiac NA concentrations were directly related to dietary crude protein levels while pancreatic levels were inversely related. An increase in dietary crude protein decreased both brain NA and DA. Supplemental dietary TRP increased both 5-HIAA and 5-HT. Changes in feed intake caused by different levels of both dietary crude protein and TRP are accompanied by altered levels of neurotransmitters. The present study indicates that much larger amounts of TRP are required to make simultaneous changes in feed intake and neurotransmitters.
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PMID:Crude protein and supplemental dietary tryptophan effects on growth and tissue neurotransmitter levels in the broiler chicken. 877 19

Electrophoretic variation of enzymes in five Eimeria spp. of the domestic fowl, including nine strains, ten single-sporocyst clones and two single-sporozoite clones of E. acervulina, three strains each of E. maxima and E. tenella, two strains of E. praecox and one strain of E. necatrix, were assayed using cellulose acetate electrophoresis. Ten enzymes [aldehyde oxidase (AO), alkaline phosphatase (ALP), amylase (AMY), fumarate hydratase (FUM), glucose-6-phosphate dehydrogenase (G6PDH), glucose phosphate isomerase (GPI), glutamate-oxaloacetate transferase (GOT), isocitrate dehydrogenase (IDH), malate dehydrogenase (MDH) and phosphoglucomutase (PGM)] were analyzed for their ability to distinguish between these species and strains. Enzymatic activity of G6PDH, GPI, IDH, MDH and PGM was detected in all the Eimeria spp. examined. Strains within each species were characterized by the same electrophoretic variant of G6PDH. Electrophoretic variants of GPI and PGM were the most valuable in the identification of inter- and intra-specific variation, particularly in the field strains of E. acervulina and E. tenella. These two enzymes were used to examine single-sporocyst and single-sporozoite clones derived from two strains of E. acervulina. The enzymes in E. maxima appeared to be conserved, showing no variation among strains with the five enzymes detected. Relative mobilities, calculated as described in this paper, were found to be consistent between different electrophoresis runs and may serve as a reference when this medium is used.
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PMID:Isoenzymes of Eimeria from the domestic fowl: electrophoretic variants among species, strains and clones. 919 94

Hepatotoxic effects of chromium have been studied on the liver function enzymes of male New Zealand white rabbits, Oryctolagus cuniculus, with and without pretreatment with phenobarbitone (PB) and promethazine (PM). The total body weight was decreased under all experimental conditions. After PB administration (5 mg/kg body wt/day for 5 days), the serum glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), lactate dehydrogenase (LDH), and isocitrate dehydrogenase (ICDH) activities decreased 21%, 65%, 25%, and 37%, respectively, whereas the alkaline phosphatase (AP) activity increased 70%. After PM treatment (5 mg/kg body wt/day for 5 days) the serum GPT was inhibited 73%, whereas LDH activity was increased 37%. The hepatic GPT and AP activities decreased after PB (52% and 31%, respectively), and PM (48% and 44%, respectively) treatments, whereas the activities of LDH and ICDH increased (after PB: 817% and 109%, respectively, and after PM: 136% and 44%, respectively). Potassium dichromate, administered at a dose of 8 mg/kg body wt/day for 5 days, decreased serum GOT (44%), GPT (61%), LDH (63%), and AP (44%) activities. The hepatic GOT, GPT and AP activities were likewise decreased (86%, 51%, and 46%, respectively), whereas hepatic LDH and ICDH activities increased 667% and 193%, respectively. When administered to PB-pretreated animals, the serum GOT and AP activities were decreased (50% and 68%), whereas ICDH was increased (29%). The hepatic GOT, LDH, and ICDH activities increased 79%, 221%, and 130%, respectively. In the PM-pretreated animals, the chromium treatment inhibited the activities of serum GOT (48%), GPT (44%), and LDH (43%). The hepatic GPT, LDH, and ICDH activities increased 90%, 133%, and 52%, respectively.
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PMID:Sublethal effects of hexavalent chromium on the body growth rate and liver function enzymes of phenobarbitone-pretreated and promethazine-pretreated rabbits. 925 33

Syntheny and localization of the following genes in common shrew Sorex araneus were determined: isocitrate dehydrogenase 2 (IDH2), acid phosphatase 2 (ACP2), glutamine--pyruvate--oxo-acid transaminase (GPT), and inorganic pyrophosphatase (PP) on chromosome ik; adenylate kinases 1 and 3 (AK1 and AK3) on chromosome af; and enolase 1 (ENO1) on chromosome jl. Two genes were assigned to definite arms: aminoacylase 1 (ACY1) to arm p of chromosome mp and glutamic-oxaloacetic transaminase 1 (GOT1) to arm q of chromosome qr. Thus, 26 genes marking eight out of ten chromosomes are present now on the cytogenetic map of common shrew. These include previously described localizations.
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PMID:[Chromosomal localization of nine genes in common shrew (Sorex araneus)]. 958 66


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