Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effect of a herbicide, paraquat (1,1'-dimethyl-4,4'-bipyridilium-dichloride), the fungicide copper sulphate, and zinc chloride was studied on the histological structure of liver, kidney and gill of three fish species with different feeding habits, viz.: a herbivorous, silver carp (Hypophthalmichthys molitrix); an omnivorous, common carp (Cyprinus carpio L.) and a carnivorous, sheatfish (Silurus glanis L.). The organs were studied electron microscopically after fixation according to Karnovsky. The toxic effect manifested itself characteristically on the respective species, regardless of the type of the chemical applied and the species specificity. Upon the effect of the treatments applied the cytoplasm of the respiratory cells of the gill became electron transparent and the cytoplasmic organelles disappeared almost totally. In the chloride cells showing focal necrosis, residuals of nuclear, mitochondrial and endoplasmic origin were seen. Pillar cells and the pericytes remained intact. In the nucleus of the liver cells, electron dense heterochromatin was not present. The degree of the damage in the liver cells was indicated by swollen mitochondria with electron transparent matrix and by dilatation and vacuolation of the endoplasmic reticulum system. Epithelial cells decreased in electron density, the endoplasmic reticulum was vesiculated, mitochondria were swollen. Leucocytes increased in number, and empty vacuoles and vacuoles filled with dense granules appeared in them during toxicosis. Copper sulphate or paraquat increased serum transaminase enzyme activities (glutamic acid-oxalacetic acid transaminase, glutamic acid-pyruvic acid transaminase) in all the three fish species. These damages can cause serious disturbances in energy uptake and secretion processes of fish.
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PMID:Morphological and biochemical studies on liver, kidney and gill of fishes affected by pesticides. 623 May 60

The activity of certain key enzymes involved in glutamic acid metabolism was studied in purified brain mitochondria and in mitochondrial subfractions separated in a discontinuous 1.2--1.6 mol/l sucrose gradient. Alanine aminotransferase and glutamate dehydrogenase were found to be matrix enzymes and aspartate aminotransferase to be associated with the inner mitochondrial membranes. After the purified mitochondria had been separated into 5 subfractions, aspartate aminotransferase and NAD+-dependent isocitrate dehydrogenase were found to be bound to the lighter mitochondrial subfractions settling at the 1.4--1.5 mol/l sucrose boundary while alanine aminotransferase, 4-aminobutyrate transaminase and glutamate dehydrogenase were associated with the heavier subfractions settling below 2.4 mol/l sucrose. The highest specific activity of the given enzymes was found in the subfraction settling at the 1.4--1.5 mol/l sucrose boundary, the only exception being alanine aminotransferase activity, whose maximum was found in the subfractions settling in 1.5 and 1.6 mol/l sucrose. It was concluded that alanine aminotransferase, in conjunction with glutamate dehydrogenase, is linked to NH3 binding and to the oxidation of reduced adenine nucleotides; in addition, alanine aminotransferase is presumed to have the function of transporting glutamate from the mitochondria to the extramitochondrial space.
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PMID:Alanine aminotransferase and some other enzymes in different populations of free brain cortex mitochondria. 645 52

Pathophysiological concentrations of ammonia, both in vivo and in vitro, suppressed the oxidation of glutamate by rat cerebellar mitochondria. The transport of glutamate into mitochondria was either unaltered or enhanced during hyperammonemic states. Activities of mitochondrial enzymes, aspartate aminotransferase, alanine aminotransferase, glutamate dehydrogenase, glutaminase, and GABA-transaminase were suppressed during hyperammonemic states. Suppression of 14CO2 production with (aminooxy)acetic acid but not with glutamic acid diethyl ester indicated that transamination but not oxidative deamination of glutamate plays a major role in glutamate oxidation during normal and hyperammonemic states.
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PMID:Transport and metabolism of glutamate by rat cerebellar mitochondria during ammonia toxicity. 810 3

In a chronic toxicity study in the rat, bidisomide administered as a dietary admixture produced a dose-related lowering of reticulocytes and leucocytes. Plasma alanine aminotransferase activity was increased at 300 mg/kg and decreased at 900 mg/kg. The potential mechanisms of these effects were investigated by comparing the responses in groups of male Sprague-Dawley rats receiving a control diet, or 300 or 1200 mg/kg/day bidisomide. Subsets of these groups were co-treated subcutaneously with folinic acid or with a vitamin B1, B6, B12 complex. Subsets of control and 300 mg/kg groups were maintained on a 20-25% feed restriction regimen for 3 months, to mimic the depression in body weight gain observed in animals receiving 1200 mg/kg. Body weight gains were significantly reduced at 1200 mg/kg and in all feed-restricted animals. Plasma and liver alanine aminotransferase (ALT) and plasma aspartate aminotransferase (AST) levels were also reduced at this dose level. At 300 mg/kg, plasma transaminases, glutamate dehydrogenase (GLDH) and sorbitol dehydrogenase (SDH) activities were increased. These changes were prevented in animals receiving folinic acid supplementation. Plasma glucose, triglycerides, and unsaturated and total iron binding capacities were decreased, while plasma iron levels tended to increase, mainly at the high dose. Vitamin supplementation prevented a decrease in reticulocyte counts at 300 mg/kg. Bidisomide increased urinary formimino-glutamic acid (FIGLU) excretion but did not affect methylmalonic acid (MMA) or taurine excretion. The effect on FIGLU at 1200 mg/kg was prevented by folinic acid co-treatment. Absolute liver weight was lowered at both dose levels and in feed-restricted animals. However, the relative liver weights were unaffected. Thymidine kinase and thymidylate synthase activity of the bone marrow cells were not altered by the bidisomide treatment. Except for the increase in plasma transaminase, GLDH and SDH levels at 300 mg/kg, changes in clinical chemistry parameters are considered to result mainly from nutritional restrictions. Changes in hematologic parameters appear to be related to the combination of decreased feed consumption (leukocytes) and decreased availability or utilization of folates (reticulocytes). This alteration, however, did not affect DNA synthesis in bone marrow. The prevention by folinic acid, but not by feed restriction, of the elevation of liver enzymes at 300 mg/kg is an intriguing, yet unexplained finding. There was no evidence that bidisomide affected B6 and B12 availability.
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PMID:Effect of folate supplementation on clinical chemistry and hematologic changes related to bidisomide administration in the rat. 858 20

Fatigue of night duty workers in different divisions of a newspaper office was investigated by physiological methods such as the Blinker, Flicker and grip methods. The relationship between fatigue and hematological parameters such as hemoglobin (Hb), the hematocrit (Ht), serum-free amino acid levels, and indices of liver function such as the GOT and GPT levels were also examined. The composing and press room workers mainly complained of the subjective symptom of muscle fatigue, while workers in the photo-engraving and editorial departments mainly complained of mental fatigue. The overall rate of fatigue in the newspaper office was about 38.1%, but varied from one division to another, being especially high in the photo-engraving and editorial departments. The subjects with fatigue had low levels of serum GOT and GPT and high levels of serum-gluconeogenic amino acids, such as aspartic acid, glutamic acid, prolin, glycine, and alanine. These altered levels of serum-free amino acids and GOT and GPT seemed to be due to increased secretion of adrenal corticoid hormone caused by the stress of fatigue.
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PMID:Studies on fatigue of night duty workers at a newspaper office. 885 78

The protective effect of dietary L-glutamine against the hepatotoxic action of D-galactosamine (GaIN) was investigated by model experiments with rats. Rats fed with 20% casein diets containing 10% free amino acids were injected with GaIN, and the serum aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase activities and the hepatic glycogen content were assayed 20 hours after the injection. These enzyme activities in the group fed with 10% L-glutamine diet for 8 days were lower than those in the groups fed with the control, 10% L-glutamic acid and 10% L-alanine diets for 8 days. The more prolonged the feeding period with the 10% L-glutamine diet was, the more the serum activity levels of such enzymes were decreased. Although neomycin also lowered these enzyme activities, its simultaneous ingestion with neomycin did not show any additive or synergistic effect. The hepatic glycogen content in the 10% glutamine group still remained high after the GaIN treatment. It is therefore assumed that the effectiveness of glutamine intake would have been mediated by glycogen metabolism rather than by uridine metabolism.
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PMID:Effect of dietary L-glutamine on the hepatotoxic action of D-galactosamine in rats. 898 89

Effects of tranquilizing agents on neurotransmitters in the heart have not been widely studied. Thus, the effect of intraperitoneal injection of reserpine, (2.5 mg/kg bw) on the concentrations of excitatory (glutamic acid, glutamine, aspartic acid, asparagine), inhibitory (GABA, glycine, alanine, taurine), neurotransmitters as well as the enzymes (GOT and GPT) and total protein were measured in both heart and serum chicks at different ages (1, 7, 30, 90 and 180 days). Reserpine induced a decrease in the excitatory amino acids and an increase in GABA in both heart and serum in most ages. Glycine and alanine increased in the heart and decreased in serum. Taurine increased in the heart of young ages (1 and 7 days) and decreased in older ones (90 and 180 days), however, it decreased in serum of most ages. Both GOT and GPT increased in heart but, in serum, GOT increased and GPT decreased in most ages. Total protein increased in the heart of young chicks and decreased in the 90- and 180-day-old chicks. In conclusion, reserpine induced a parallel decrease in the ratio glutamate, glutamine, aspartate/GABA in both myocardial tissue and serum of the different age groups. Changes observed in neurotransmitters of the heart suggest that these amino acids may play a similar role in the myocardial tissue, as is described in the central nervous system.
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PMID:Reserpine effects on neurotransmitters in chick heart during growth. 932 36

Total superoxide dismutase (SOD, EC 1.15.1.1) and catalase (CAT, EC 1.11.1.6) activities in erythrocytes and the glutamic acid-oxalacetic acid-transaminase (GOT, EC 2.6.1.1) and glutamic acid-pyruvic acid-transaminase (GPT, EC 2.6.1.2) activities in the plasma were measured in experimental groups of carps (Cyprinus carpio L.) exposed to cadmium in a concentration of 20 mg Cd/l water under aquarium conditions for 6, 12, 18 and 24 hours and in control fishes. It was shown that the total activity of SOD in the erythrocytes is significantly decreased after 12, 18 and 24 hours of cadmium exposure. Increased activities of CAT (after 24 hours) in the erythrocytes and GOT and GPT in the plasma were found in cadmium-treated fishes. At the same time the concentration of blood haemoglobin and haematocrit values were significantly diminished. These results indicate that cadmium causes oxidative stress and tissue damage in the exposed fishes.
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PMID:Activities of superoxide dismutase and catalase in erythrocytes and transaminases in the plasma of carps (Cyprinus carpio L.) exposed to cadmium. 972 86

Chronic occupational exposure to organophosphorus and carbamate-type pesticides significantly inhibits acetylcholinesterase activity and causes morbidity. This study on mice was designed to evaluate their amino profile and to identify signs of hepatic dysfunction following their chronic exposure to mixtures of organophosphorus pesticides. Laboratory mice were exposed to a formulated mixture of the six organophosphorus pesticides (Dimethoate, Chlorpyrifos, Profenofos, Pirimiphos methyl, Triazophos and Dimethoate) most commonly used in agriculture in this region of the Middle East. Doses (10% of LD50 of the mixture) were given once a week by gavage in corn oil for 7 weeks; the control group was given only corn oil. At the end of the exposure period, mice were culled and blood samples were collected to determine erythrocyte acetylcholinesterase activity, biochemical markers of liver function and concentrations of serum amino acids. Erythrocyte acetylcholinesterase activity and total serum proteins decreased significantly in the exposed group. Serum concentrations of alanine aminotransferase and aspartate aminotransferase, alanine, glutamic acid, glycine, isoleucine, leucine, methionine, ornithine, proline, serine, threonine and valine were significantly increased in the exposed mice, while serum levels of cystine were decreased significantly. There were also non-significant increases in serum alkaline phosphatase, gama-glutamyl transpeptidase and some of the other amino acids. Chronic exposure to mixtures of organophosphorus pesticides is associated with decreased acetylcholinesterase activity, hepatic dysfunction and disturbance of amino acids profile. Biochemical indices of hepatocellular injury and disturbed amino acid metabolism may be of value as markers of chronic exposure to such pesticides.
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PMID:Hepatic injury and disturbed amino acid metabolism in mice following prolonged exposure to organophosphorus pesticides. 1002 66

Based on the relationship between in vivo disposition of macromolecules and their physicochemical and biological characteristics obtained through clearance concept-based pharmacokinetic analysis, polymeric prodrugs of prostaglandin E(1)(PGE(1)) were designed stepwise and evaluated on their targeting and therapeutic efficiencies. First poly-L-lysine (PLL) and poly-L-glutamic acid (PLGA) with an ethylenediamine (ED) spacer were modified with 2-imino-2-methoxyethyl 1-thiogalactoside to obtain galactosylated derivatives. After intravenous injection in mice, Gal-ED-PLGA was selectively taken up by the liver parenchymal cells via receptor-mediated endocytosis, while Gal-PLL accumulated in the liver as well as PLL mostly due to electrostatic interaction. Although Gal-ED-PLGA showed good targeting efficacy, its PGE(1) conjugate synthesized with activated PGE(1) by carbonyldiimidazole method failed to show therapeutic effects probably due to inactivation of PGE(1) during conjugation and lack of release in the tissue. In order to overcome these problems, we next conjugated PGE(1) to galactosylated poly-(L-glutamic acid) hydrazide (Gal-HZ-PLGA) in which PGE(1) was easily coupled to Gal-HZ-PLGA via a hydrazone bond in weak acidic solution (pH 5) at room temperature. The PGE(1)-Gal-HZ-PLGA conjugate labeled with [(111)In] or [(3)H]PGE(1) rapidly accumulated in the liver parenchymal cells. In addition, the PGE(1) conjugate effectively inhibited the increase of the GPT level in plasma, while free PGE(1) indicated no therapeutic efficacy even at more than ten times higher doses, in carbon tetrachloride-induced hepatitis mice. These findings suggest potentials of polymeric targeting systems of PGE(1) to hepatocyte utilizing galactose recognition.
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PMID:Design of polymeric prodrugs of prostaglandin E(1) having galactose residue for hepatocyte targeting. 1051 58


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