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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Double isotope procedures (3H and 14C) were used in vivo to investigate a) slow long-term gluconeogenic actions of adrenal glucocorticoids, and b) rapid stimulation of gluconeogenesis by glucagon. [U-14C,6-3H]Glucose was administered to normal and adrenalectomized rats. No effect was observed on the [6-3H]glucose half-life suggesting the dicarboxylic acid shuttle is unaffected by adrenalectomy; the Cori cycle is also not influenced. Loads of [14C]aspartate, [14C]glutamate, or [14C]alanine were given to normal and adrenalectomized rats. Simultaneously, in vivo transaminase activity was studied by measuring the appearance of 3H2O in body water after administration of [2-3H]aspartate, [2-3H]glutamate, or [2-3H]alanine, Adrenalectomy has no influence on the incorporation of glutamate or aspartate into glucose or on their in vivo transaminases. Diminution of incorporation of [14C]alanine into glucose and alanine transaminase activities occurs only when rats are given unphysiological loads. These studies support the contention that glucocorticoid rate-limiting actions occur in extrahepatic tissues to produce an increased flow of glucose precursors to the liver. [U-14C,3-3H]Glucose was used to investigate the effect of glucagon on the hepatic fructose-6-phosphate (F-6-P) cycle. Glucagon administration resulted in a rapid drop in the 3H/14C ratio of circulating glucose, suggesting an increase in F-6-P recycling caused by activation of FDPase with little or no decrease in phosphofructokinase. Such a change would direct substrate flux toward gluconeogenesis.
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PMID:Use of 3H and 14C doubly labeled glucose and amino acids in the study of hormonal regulation of gluconeogenesis in rats. 19 46

The sequential pattern of lipid accumulation and associated biochemical changes were studied in two commonly used experimental models of nutritional fatty liver in rats. Female rats were maintained for 8 weeks on high fat, low protein diets containing adequate methionine and choline, and drinking water ad libitum (Diet 1), or deficient in methionine and choline and containing 20% ethanol as a substitute for drinking water (Diet 2). Histologically, there was a progressive increase in liver lipids, mainly in the periportal areas. Occasional foci of liver cell necrosis with lipogranuloma formation occurred in areas of severe fatty change. These changes appeared earlier and were more marked in rats maintained on Diet 2. Electron micrographs revealed large lipid droplets in the liver cells, which sometimes contained myelin figures. The mitochondria were enlarged, distorted and appeared as amorphous structures with disorientated cristae in rats on Diet 1, whereas they had a condensed conformation in rats maintained on Diet 2. Rough endoplasmic reticulum was fragmented and degranulated particularly in rats on Diet 1, and smooth endoplasmic reticulum showed hyperplasia and vesiculation in rats on Diet 2. There was a progressive increase in the total liver lipids and triglycerides in both the groups of rats. This fatty change was accompanied by a significant increase in hepatic 3-hydroxybutyrate, acetoacetate, malate, 2-oxoglutarate, citrate, lactate, ammonia, glutamate, alanine and aspartate, and a significant decrease in oxaloacetate, urea and glucose concentrations. The mass action ratios for alanine aminotransferase, aspartate amino transferase, and glutamate dehydrogenase, generally moved in a parallel direction. Hepatic ATP content was considerably reduced accompanied by a decrease in [ATP]/[ADP] ratios and a significant increased in [lactate]/[pyruvate] and [3-hydroxybutyrate]/[acetoacetate] ratios. There was a corresponding decrease in the [NAD+]/[NADH] ratios both in the cytoplasmic and mitochondrial compartments. These biochemical changes were particularly severe in rats maintained on Diet 1 and Diet 2 for 8 weeks. There was a very good relationship between impaired mitochondrial and endoplasmic reticulum functions, redox and phosphorylation states, and the relevance of their changes to the fate of fatty liver cells.
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PMID:Lipid accumulation in the rat liver: a histological and biochemical study. 23

Male rats provided with a 5 or 15% (v/v) ethanol solution as the sole source of fluid consumed ethanol at a rate of 11.4 or 24.9% of total calories (4.2 or 8.3 g/kg daily). After ethanol consumption lasting 1, 2 and 3 weeks the hepatotoxicity of CCl4 (0.1 ml/kg i.p.) was elevated by determination of serum activities of glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase ( GPT), sorbitol dehydrogenase (SDH) and histological investigations. Carbon tetrachloride (CCl4)-induced liver damage was significantly greater in rats provided with ethanol than in the tap-water consuming controls. This potentiation of CCl4 hepatotoxicicty was fully developed already after a 1-week exposition to ethanol and was greater in the 15% than in the 5% ethanol group. Ethanol alone did not influence serum enzyme activities but increased microsomal aniline hydroxylation. There was, however, no clear-cut parallelism between potentiation of CCl4 hepatotoxicity and activation of aniline hydroxylation.
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PMID:Increased carbon tetrachloride hepatotoxicity after low-level ethanol consumption. 70

Urethral obstruction induced in adult male cats caused clinical signs identical with those observed in naturally occurring disease. Central nervous system depression, anorexia, dehydration, vomiting, muscle weakness, and hypothermia occurred. Weight loss (due to water loss and catabolism), metabolic acidosis, mild hyponatremia, hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia, hyperglycemia, azotemia, and hyperproteinemia were also observed. Serum amylase, alkaline phosphatase, and alanine aminotransferase activities were normal. Ten of 13 cats (group 1), with 72 hours' induced obstruction but not treated with parenteral fluids, died either before the obstruction was relieved or within 8 days afterward. Eight cats (group 2) with induced obstruction for 49 to 98 hours developed severe clinical and biochemical alterations. Treatment with a multiple-electrolyte solution, in addition to relief of urethral obstruction, resulted in favorable clinical and biochemical responses. These cats survived and were clinically healthy at 9 to 10 days after relief of obstruction. It was concluded that use of a multiple-electrolyte solution to correct acidosis, restore circulatory volume, and enhance renal excretion of potassium was effective supportive therapy after urethral obstruction was removed.
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PMID:Characterization and treatment of water, electrolyte, and acid-base imbalances of induced urethral obstruction in the cat. 87 80

Effects of 3 hours of methoxyflurane anesthesia in 20 dogs were determined by blood urea nitrogen (BUN), serum creatinine (SC), serum alanine aminotransferase (ALT), serum alkaline phosphatase (ALP). sulfobromphthalein (BSP), phenosulfonphthalein (PSP) clearance test, 24-hour water intake and urine excretion, and serum inorganic fluoride (SIF) evaluation. Values for BUN, SC, serum ALT, BSP, and PSP after the anesthetic were not significantly different (P less than 0.05) from the base-line values. The serum ALP values were significantly increased (P less than 0.001). Water intake and urine excretion showed a peak increase 48 hours after anesthesia. Serum inorganic fluoride concentration increased significantly (P less than 0.001) compared with the base line. The SIF 20 minutes before anesthesia was 4.54 +/- 0.82 mumol/L, at 90 minutes of surgical anesthesia 92.35 +/- 8.91 micronmol/L, at 20 minutes after anesthesia 132 +/- 12.55 micronmol/L, and at 1, 3, and 6 days after anesthesia they were 105.60 +/- 8.93, 42.10 +/- 6.90, and 12.65 +/- 1.32 micronmol/L. Clinical signs of renal or hepatic failure were not detected in any of the treated dogs during 7 day post-anesthetic observation period.
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PMID:Serum fluoride concentration, renal, and hepatic function test results in dogs with methoxyflurane anesthesia. 88 22

Male mice treated with nicotine hydrochloride either acutely (5 mg/kg i.p.) or subchronically (5 mg/kg i.p. daily for 3 weeks; 25 mg/liter in drinking water for 2-3 months) showed no evidence of hepatic dysfunction, as measured by serum glutamic-pyruvic transaminase or serum alkaline phosphatase activities. Neither acute nor subchronic administration modified the hepatotoxic response to a potent hepatotoxin (carbon tetrachloride), nor that of less potent hepatotoxins chloroform or 1, 1, 1-trichloroethane, nor was the cholestatic effect of alpha-naphthylisothiocyanate modified.
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PMID:Hepatic function after acute of subchronic nicotine administration in untreated mice and mice treated with hepatotoxic chemicals. 99 92

Because of the difficulties in drawing blood for clinical chemistry in small laboratory animals there exist many methods for sampling blood and the preparation of serum, none of which is generally accepted or well standardised. It was the aim of this study to investigate the effects of sampling techniques on normal values of enzyme activities in the serum of rat and mouse. The activities of the following enzymes were determined: sorbitol dehydrogenase, lactate dehydrogenase, malate dehydrogenase, glutamate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, pyruvate kinase, creatine kinase, myokinase, alkaline phosphatase and leucine aminopeptidase. In addition plasmaproteins, urea and inorganic phosphorus were measured. In rats blood was obtained from the following sites: retroorbital venous plexus, jugular vein, heart and ventral aorta. In mice blood was sampled from the jugular vein and the ventral aorta. Shifts of water from the interstitial to the intravascular space due to hypovolemia occurring during the experimental procedure were followed up by measuring the hematocrit and the distribution of radioiodide labelled albumin. In rats the activities of lactate dehydrogenase, malate dehydrogenase, aspartate aminotransferase, pyruvate kinase, creatine kinase and myokinase found in blood serum obtained from the retroorbital venous plexus and the ventral aorta were too high compared to the other sampling sites. Activities of alkaline phosphatase and alanine aminotransferase were slightly elevated when blood was sampled from the punctured retroorbital venous plexus. Small differences in plasmaproteins and hematocrit values were found to be due to acute shifts of water within the extracellular space. In mice the activities of lactate dehydrogenase, malate dehydrogenase, aspartate aminotransferase and myokinase were found to be too high in blood serum obtained from the ventral aorta. Efflux of enzymes from damaged cells and the interstitial space ive caused erroneous results too, but only to a minor extent. The most reliable method for blood sampling in rat and mouse is the cannulation of the jugular vein. The heart puncture can be recommended too. Attention should be paid, however, to the possibility of aspirating disrupted muscle cells through the inserted needle.
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PMID:[Effects of blood sampling on enzyme activities in the serum of small laboratory animals (author's transl)]. 108 84

1. Rats were given moderate-selenium (4-5 mg/kg) or low-Se (0-5 mg/kg) diets during gestation and lactation. Their young were given diets with high (10 mg/kg), moderate or low Se contents from weaning, and groups of rats were killed at intervals during the 14-week experimental peroid. 2. Compared with young rats which received the low-Se diet, those which received the moderate- or high-Se diets had a high incidence of liver lesions and there were changes in liver Se content, haemoglobin concentration, packed cell volume, prothrombin activity, fibrinogen content, spleen weight, body water and serum glutamic-oxaloacetic and glutamic-pyruvic transaminas (L-aspartate : 2-oxoglutarate aminotransferase; EC 2.6.1.1 and L-alanine : 2-oxoglutarate aminotransferase; EC 2.6.1.2 respectively) and alkaline phosphatase (EC 3.1.3.1) activities. In those rats which received the high-Se diet the changes were more pronounced than in those which received the moderate-Se diet. 3. In young rats from dams given moderate-Se diets, which were themselves given the moderate-Se diet, the liver Se content decreased continuously, whereas rats given the same diet but from dams which had received the low-Se diet, the liver Se content increased continuously. There was a slight improvement of symptoms of Se toxicity in all groups by the 5th week of the experimental peroid. 4. The results suggest that there was an adaptation to chronic Se intake.
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PMID:Effects of ingestion of organic selenium in adapted and non-adapted rats. 112 69

The hydrogen exchange at the Beta-carbon of L-alanine, L-glutamate and L-asparate with water has been examined during transamination catalyzed by glutamic-oxaloacetic transaminase and by glutamic-pyruvic transaminase. A significant hydrogen exchange at the Beta-carbon has been demonstrated during incubation of L-[3-3H]alanine + glutamic-pyruvic transaminase, L-[3-3H]alanine + alpha-oxo-glutarate + glutamic-pyruvic transaminase, L-[3-3H]glutamate + glutamic-oxaloacetic transaminase, L-[3-3H]glutamate + oxaloacetate +glutamic-oxaloacetic transaminase, and L-[3-3H]glutamate + pyruvate + glutamic-pyruvic transaminase as shown by the appearance of 3H2O. No hydrogen exchange at the Beta-carbon of L-glutamate occurred during incubation of L-[3-3H]-glutamate with glutamic-pyruvic transaminase alone. The hydrogen exchaned at the Beta-carbon of L-glutamate coincides with transamination as demonstrated by nuclear magnetic resonance studies of 2H2O-L-glutamate exchange during transamination by glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase. No hydrogen exchange at the Beta-carbon occurred during transamination of L-aspartate by glutamic-oxaloacetic transaminase as shown by nuclear magnetic resonance spectroscopy and confirmed by nuclear magnetic resonance simulation studies. The results are discussed with special reference to the different equilibria between the pyridoxal form and the pyridoxamine form of glutamic-oxaloacetic transaminase and of glutamic-pyruvic transaminase.
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PMID:Hydrogen exchane at the beta-carbon of amino acids during transamination. 120 22

Hematograms, platelet function, and blood-enzyme chemistry were compared in two similar saturation-excursion dives, one conducted in a hyperbaric chamber and the other in the open sea. The chamber dive was more stressful in that it was preceded by a series of bounce decompression dives (one of which produced a 100% incidence of cutaneous pruritus in four subjects) and in that the excursions from saturation depth (60 fsw or 2.818 ATA) were longer and deeper (producing one case of O2 convulsions, one of confirmed decompression sickness, and several of Doppler-detected vascular bubbles). The chamber dive was associated with a marked and significant reduction in circulating platelet count; significant increases in plasma enzyme activities in the victim of O2 toxicity (LDH, CPK) and in one subject with Doppler bubbles and questionable bends symptoms (LDH, GOT, GPT) but not in another; and mild but significant anemia. In the open-water dive, one subject, who developed symptoms of gastroenteritis, showed moderate elevation of LDH, GOT, and GPT activity. No significant change in platelet counts occurred. Both dives were associated with elevated white-cell counts, apparently as a result of numerous minor infections, and reduced sensitivity of platelets of ADP-induced aggregation.
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PMID:Hematology and blood chemistry in saturation diving: II. Open-sea vs. hyperbaric chamber. 122 83


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