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:1.4.1.2 (glutamate dehydrogenase)
4,380 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in blood chemistry were examined in vitamin B12 deficient lambs which developed ovine white-liver disease (OWLD), and were compared with values of cobalt/B12 supplemented lambs on the same pastures, as well as clinically healthy, but sometimes B12 deficient, lambs on other pastures (H). In the OWLD group, signs of hepatic damage were seen concurrently with reduction in weight gain, or 1-3 weeks before, and comprised elevation of serum glutamate dehydrogenase (GLDH) and decrease of phospholipid and cholesterol. Drop of plasma glucose and elevation of gamma GT also came in the earlier phase of the disease. All other blood changes developed later, and were partly regarded as reflections of the inappetence or hepatic injury. The changes included a drop in packed cell volume (PCV) and mean corpuscular volume (MCV), elevation of serum iron, and reduction of total serum protein and urea. Generally Co/B12 supplementation prevented hepatic damage and normalized blood values. The clinically healthy H lambs also showed signs of hepatic damage, especially one year when they were B12 deficient, indicating that simple B12 deficiency causes a moderate liver damage as well. For diagnostic purposes, clinical pathology is recommended mainly on a flock basis.
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PMID:Ovine white-liver disease (OWLD). Changes in blood chemistry. 208 Jul 72

Ammonia in food samples was determined by its reaction in an immobilised enzyme reactor containing glutamate dehydrogenase (GIDH) in a flow injection system, by measuring the decrease in the absorbance of ultraviolet radiation by reduced nicotinamide adenine dinucleotide (NADH). There was a linear relationship (r = 0.9995) between peak height and ammonia concentration over the range 0.05-0.6 mM. The detection limit was 0.005 mM for an injection volume of 19 microliters. Sampling frequency was 60 h-1 and the precision was better than 1.09% for 11 successive assays. The interference effect of urea and ascorbic acid at concentrations greater than 100 mg per 100 g of product should be taken into account. The interference caused by glycine, creatinine and amino acids is negligible. Only a 20% loss in the activity of the GIDH column was observed after 500 determinations during a 3-month period.
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PMID:Enzymic determination of ammonia in food by flow injection. 209 94

The effect of fatty infiltration on liver function was studied in 29 dairy cows aged 6 +/- 0.4 (SEM) years with primary acetonaemia, secondary acetonaemia or the fat cow syndrome. The average interval from calving at diagnosis was 16.4 +/- 2.0 days and the animals had been anorexic for a mean of 5.6 +/- 0.8 days. Fatty infiltration of the liver occurred well before calving and was associated with severe clinical illness and intercurrent infections. The percentage of fatty infiltration in the liver (mean 53.1 +/- 2.8 per cent) was significantly correlated with both the degree of clinical illness (P less than 0.001) and the period of anorexia (P less than 0.05). Alterations in uptake, conjugation and excretion at the hepatocyte level were determined by measuring bromsulphthalein clearance, and plasma total bilirubin and total bile acid concentrations. Values for all three were positively correlated with the extent of fatty infiltration. Plasma albumin, urea and glucose concentrations were reliable indicators of the liver's synthetic function and together with plasma aspartate aminotransferase, iditol and glutamate dehydrogenase were correlated with the degree of hepatic lipidosis.
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PMID:Effect on liver function of acetonaemia and the fat cow syndrome in cattle. 233 29

The infusion of ether anesthaetized rats with 0.2 M (1 mmols in total) ammonium acetate or glutamine were compared with the infusion of 0.2 M NaCl. The levels of circulating glucose, amino acids, lactate, urea and ammonium were measured as well as liver glycogen and tissue amino acids and the liver and muscle activities of carbamoyl phosphate synthetases I and II, glutamate dehydrogenase, glutamine synthetase and adenylate deaminase. Neither treatment altered the glucose and glycogen homeostasis. The infusion of ammonium did not result in increases in circulating ammonium, but resulted in increased circulating urea after a short delay; the infusion of glutamine resulted also in urea production but much later on. Glutamine infusion also resulted in increased tissue free amino-acid levels. There was little alteration in enzyme activities, except for decreased glutamine synthetase and adenylate deaminase activity in muscle of glutamine-infused rats and higher tissue carbamoyl phosphate synthetase II. The results agree with a fast removal of infused ammonium, and maintenance of glutamine, with their channeling towards urea production at a rate comparable with that of infusion, that did not alter significantly the homeostasis of the experimental animals.
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PMID:Glutamine and ammonium handling by anaesthetized rats. 247 81

Effects of repeated administration of benthiocarb on the nitrogen metabolism of hepatic and neuronal systems have been studied. Repeated benthiocarb treatment was associated with significant decrease in proteins with a concomitant increase in free amino acids (FAA) and specific activity levels of proteases suggesting impaired protein synthesis or elevated proteolysis. The glycogenic aminotransferases showed a significant elevation in both the tissues indicating high feeding of ketoacids into oxidative pathway for efficient operation of TCA cycle to combat energy crisis during induced benthiocarb stress. However, the activity levels of branched-chain aminotransferases decreased suggesting their reduced contribution of intermediates to TCA cycle. A comparative evaluation of the activity levels of ammonogenic enzymes, AMP deaminase, adenosine deaminase and glutamate dehydrogenase (GDH) indicated that ammonia was mostly contributed by nucleotide deamination rather than by oxidative deamination. GDH exhibited reduced activity due to low availability of glutamate. In accordance with increased levels of urea, the activity levels of arginase, a terminal enzyme of urea cycle was increased suggesting increased urea cycle operation in order to combat the increased ammonia content. As the presence of urea cycle in the brain is rather doubtful, the conversion of ammonia to glutamine for the synthesis of GABA is envisaged in brain whereas in liver, excess ammonia was converted to urea through ornithine-arginine reacting system. The increased glutaminase activity observed during benthiocarb intoxication is accounted for counteracting acidosis or maintenance of metabolic homeostasis. Arginase, a terminal enzyme of ornithine cycle showed increased activity denoting the efficient potentiality of tissues to avert ammonia toxicity. The changes observed in tissues of rat administered with benthiocarb reflects a shift in nitrogen metabolism for efficient mobilization of end products of protein catabolism.
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PMID:Perturbations in nitrogen metabolism of brain and liver of rat following repeated benthiocarb administration. 266 46

Effects of coenzyme (NADH) and substrate (2-oxoglutarate) on the urea-induced dissociation and inactivation of immobilized phosphopyridoxyl derivative of bovine liver glutamate dehydrogenase (L-glutamate-NAD(P)-oxidoreductase, EC 1.4.1.3) have been studied. Urea at concentration 3.0 to 4.0 M in the presence of NADH induced dissociation of the enzyme's hexamer to catalytically inactive immobilized dimer. In the presence of both NADH and 2-oxoglutarate at the urea concentration 1.0 to 2.0 M the hexamer dissociated to the conformationally stable immobilized trimer possessing 60% catalytic activity of the hexamer. Studies of regulatory properties of the immobilized trimer showed that the allosteric inhibition of glutamate dehydrogenase by GTP was realized on the level of trimers, where the subunits interact through identical heterological contacts.
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PMID:[Structural organization of a hexamer of glutamate dehydrogenase. 3. Effect of the coenzyme and substrate on the urea-induced dissociation and inactivation of the hexamer]. 274 8

Rats were fed a standard diet or the standard diet supplemented with ammonium acetate (20% w/w) for up to 100 days. The effect of the ingestion of the high-ammonium diet on some aspects of nitrogen metabolism in rats was studied. Ammonia levels in blood increased approximately 3-fold; in brain, liver and muscle the increases were 36, 34 and 50%, respectively. Urea levels in blood and urea excretion increased approximately 2-fold. There was no increase of carbamyl phosphate synthase. Liver glutamine synthase activity increased by 58% and glutamate dehydrogenase by 40%, whereas glutaminase was not affected. Glutamine content in brain was twice that of controls. This new animal model to study hyperammonemia offers several advantages over others: it is simpler, is bloodless, requires no animal manipulation and permits long-term studies.
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PMID:A simple animal model of hyperammonemia. 275 49

Ethanol or acetaldehyde orally administered (15% and 2% respectively in drinking water) to male Wistar rats for three months induced alterations in the main liver enzymes responsible for ethanol metabolism, aspartate and alanine aminotransferases and NAD glutamate dehydrogenase. Ethanol produced a significant decrease in the activity of soluble alcohol dehydrogenase, while acetaldehyde induced alterations both in soluble and mitochondrial aldehyde dehydrogenases: soluble activity was significantly higher than in the control and ethanol-treated groups, and mitochondrial activity was significantly diminished. Both soluble aspartate and alanine aminotransferases showed pronounced increases by the chronic effect of acetaldehyde, while mitochondrial activities were practically unchanged by the effect of ethanol or acetaldehyde. Mitochondrial NAD glutamate dehydrogenase showed a rise in its activity both by the effect of chronic ethanol and acetaldehyde consumption. The level of metabolites assayed in liver extracts showed marked differences between ethanol and acetaldehyde treatment which indicates that ethanol produced a remarkable increase in glutamate, aspartate and free ammonia together with marked decrease in pyruvate and 2-oxoglutarate concentrations. Acetaldehyde consumption induced a significant decrease in 2-oxoglutarate and pyruvate concentrations. These observations suggest that ethanol has an important effect on the urea cycle enzymes, while the effect of acetaldehyde contributes to the impairment of the citric acid cycle.
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PMID:Effect of chronic ethanol or acetaldehyde on hepatic alcohol and aldehyde dehydrogenases, aminotransferases and glutamate dehydrogenase. 286 Jul 5

Proline-producing strains of Serratia marcescens were more osmotolerant than wild-type strains. Growth inhibition by proline analogs was significantly enhanced by increasing the osmotic stress of the medium. Mutants resistant to azetidine-2-carboxylate were derived from a proline-producing strain, SP126, under a high osmotic condition. One of the mutants, strain SP187, produced 56 mg of L-proline per ml of medium containing sucrose and urea. This amount was ca. 3 times larger than that produced by strain SP126. The intracellular glutamate content which decreased in strain SP126 was restored in strain SP187. The glutamate dehydrogenase level of strain SP187 was 5 times higher than that of strain SP126.
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PMID:Proline-hyperproducing strains of Serratia marcescens: enhancement of proline analog-mediated growth inhibition by increasing osmotic stress. 286 Aug 49

Sheep received a single intragastric dose of 0.5, 1.0, 1.5, or 2.0 mmol F-/kg. Mild signs occurred at 1.5 mmol F-/kg and the animals recovered 2 days later. With the 2.0 mmol F-/kg dose all animals showed dullness, anorexia, and mild diarrhea which decreased from the third day. Dose-related congestion of duodenum, liver, kidney, and lung was observed in all animals. For the two higher doses kidney degeneration and tubular necrosis were associated with glomerular inflammation. Serum fluoride had a dose-related increase and was still significantly elevated on Day 7 for sheep given doses higher than or equal to 1.0 mmol F-/kg. Serum calcium and glucose levels were significantly lowered for all doses on the first day and the decrease was dose-related. In sheep given 2.0 mmol F-/kg total proteins and sodium were significantly lowered, whereas potassium and urea were increased (p less than 0.05); alkaline phosphatase (ALP) and lactic dehydrogenase (LDH) were both lowered (p less than 0.01) on the first day and ALP was still lowered on Day 7. For the highest dose glutamate dehydrogenase (GDH) was increased on Days 1 and 7 and gamma-glutamyl transferase (GGT) was increased on Day 1 and lowered on Day 7. Diuresis was increased for the two higher doses in Day 3 or 4 following dosage. A dose-related increase of daily fluoride excretion occurred for all doses on Day 1 and fluoride excretion was still significantly elevated on Day 7 except for the lowest dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experimental acute sodium fluoride poisoning in sheep: renal, hepatic, and metabolic effects. 286 58


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