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)

The kinetics of the interaction between deionized supernatant aspartic aminotransferase and various anions (cacodylate, phosphate and chloride) were studied by the temperature-jump technique. The anion concentration in the range covered by our experiments does not affect the transamination rate. On the other hand the conformational transition, recently observed at the active site of the enzyme, is hindered by an excess of anions. A single relaxation effect was observed at the enzyme chromophore wavelength in systems containing the aldimine form of the enzyme and the above anions. It is shown that this effect corresponds to the protonation of the chromophore. The relaxation times were of about 10 mus with phosphate, 20-100 mus with cacodylate and 1-2 ms with chloride. The pH and concentration dependence of this effect were studied. The fits of experimental data to a rate equations for various models were tested by a chi2 analysis. The best fit was obtained with models where anions bind rapidly to a site close to the chromophore, so that the pK of the chromophore is affected by anions binding. The rate of the observed relaxation considerably increased when the anion has buffering capacities; this indicates, in the case of cacodylate and phosphate, that the acidic component of the buffer directly exchanges a proton with the enzyme chromophore.
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PMID:Kinetics of the interaction between aspartic aminotransferase and anions. 1 67

The acute oral LD50 in Sprague-Dawley rats was determined to be 171 mg/kg (100-295) for males and 268 mg/kg (205-344) for females. 2. A 1 ppm dietary supplement of Vancide KS for 90 days did not induce any abnormalities in weanling Sprague-Dawley rats. The parameters evaluated were serum glutamic-oxaloacetic transaminase (SGOT), hematocrit, differential white blood cell count, food consumption, and weight gain, along with histologic studies of the myocardium, spleen, liver, kidney, stomach, and small intestine. A 500 ppm diet was lethal. Weanling and older rats subjected to 1000 and 10,000 ppm diets died within 5 days. 3. Vancide KS induced no acute dermal toxicity, nor did it exhibit percutaneous absorption in New Zealand strain albino rabbits. 4. Vancide KS induced no chronic dermal toxicity in New Zealand strain albino rabbits. 5. Vancide KS was not shown to be teratogenic. It exhibited an antifertility action, especially in Sprague-Dawley rats dosed on day 1 through day 7 of timed-pregnancy. 6. Vancide KS was shown to be an eye irritant which induces corneal opacity. 7. Acute oral toxicity studies in Sprague-Dawley rats indicate that Vancide KS should be classified as a toxic substance as defined in the regulations under the Federal Hazardous Labeling Act. 8. The intravenous administration of 25 mg/kg of Vancide KS to New Zealand strain albino rabbits induced death preceded by topic convulsions. 9. Vancide KS did not induce skin sensitization in male adult guinea pigs.
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PMID:Acute and subacute toxicology and safety evaluation of triphenyl tin hydroxide (Vancide KS). 31 Jul 51

Laboratory studies are an essential aspect in the management of children with grave diseases, helping to plan the therapeutic measures and to identify the disease. The most acute syndromes in pediatric emergency care are: coma, convulsions, dehydration, metabolic disequilibrium, hypovolemic or anaphylactic shock, a grave infection, chemical or drug poisoning. The laboratory tests that should be available within few minutes are blood cell count, blood and gas analysis, sodium, potassium, calcium, glucose measurements. The results of total proteins, serum creatinine and urea measurements, bleeding tests, analysis of blood smear, sedimentation rate, ALT, AST, osmolality, urinary electrolytes, creatinine and cerebrospinal fluid examinations should be available within sixty min. New accurate and rapid techniques and instruments facilitate the diagnostic and therapeutic approach to pediatric emergency.
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PMID:[A rapid response laboratory in a pediatric clinic]. 172 94

The laboratory contribution in the care of a seriously ill child is essential to plan and organize the therapy after the first-step emergency care and to know the aethiology of the illness. The most acute syndromes in pediatric emergency care are: coma, convulsions, dehydration, metabolic disequilibrium, hypovolemic or anaphylactic shock, serious infectious diseases and chemical or drug poisoning. The laboratory tests which have to be available within few minutes are blood cell count, hemogasanalysis, sodium, potassium and calcium, glucose. Total proteins, serum creatinine and urea, bleeding tests, blood smear, sedimentation rate, ALT, AST, osmolality, urinary electrolytes and creatinine and cerebrospinal fluid examination should be available within sixty minutes. New accurate and rapid techniques and instrumentations make easier the diagnostic and therapeutical approach to pediatric emergency.
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PMID:Pediatric emergency laboratory. 189 92

The four half-transamination reactions [the pyridoxal form of Escherichia coli aspartate aminotransferase (AspAT) with aspartate or glutamate and the pyridoxamine form of the enzyme with oxalacetate or 2-oxoglutarate] were followed in a stopped-flow spectrometer by monitoring the absorbance change at either 333 or 358 nm. The reaction progress curves in all cases gave fits to a monophasic exponential process. Kinetic analyses of these reactions showed that each half-reaction is composed of the following three processes: (1) the rapid binding of an amino acid substrate to the pyridoxal form of the enzyme; (2) the rapid binding of the corresponding keto acid to the pyridoxamine form of the enzyme; (3) the rate-determining interconversion between the two complexes. This mechanism was supported by the findings that the equilibrium constants for half- and overall-transamination reactions and the steady-state kinetic constants (Km and kcat) agreed well with the predicted values on the basis of the above mechanism using pre-steady-state kinetic parameters. The significant primary kinetic isotope effect observed in the reaction with deuterated amino acid suggests that the withdrawal of the alpha-proton of the substrates is rate determining. The pyridoxal form of E. coli AspAT reacted with a variety of amino acids as substrates. The Gibbs free energy difference between the transition state and the unbound state (unbound enzyme plus free substrate), as calculated from the pre-steady-state kinetic parameters, showed a linear relationship with the accessible surface area of amino acid substrate bearing an uncharged side chain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pre-steady-state kinetics of Escherichia coli aspartate aminotransferase catalyzed reactions and thermodynamic aspects of its substrate specificity. 220 6

The activity of glutamate related enzymes and the concentration of glutamine, glutamate and gamma-amino n-butyric acid (GABA) were investigated in the cerebral cortex of rats, in different stages of insulin-induced hypoglycemia. Hypoglycemia was produced by intraperitoneal injection of insulin 0.05-100 units per kg body weight. The minimum required dose to produce irreversible severe hypoglycemia was 0.5 units/kg. In 85% of the cases an insulin induced hypoglycemic convulsion, was achieved 130-150 minutes after injection. Blood glucose levels during insulin induced seizures ranged between 8-15 mg%. In the range of 0.5-100 u insulin/kg the degree of hypoglycemia and the onset of convulsions were identical. The concentration of glutamine was significantly reduced during convulsive and postconvulsive stages. Glutamate and GABA concentrations were reduced significantly in all stages of insulin-induced hypoglycemia. The decrease in glutamine concentration was concurrent with an increase in the activity of its degradative enzyme, glutaminase. This was apparent at the preconvulsive, convulsive and postconvulsive stages. The activity of other enzymes related to energy production such as glutamate dehydrogenase (GDH), glutamate transaminase (GPT) and aspartate aminotransferase (AAT) were also increased. The activity of glutamine synthase (GS) was unaffected by hypoglycemia. Insulin induced changes in glutamine, glutamate and their related enzymes could not be attributed to convulsion since a similar pattern of changes was observed in the preconvulsive and postconvulsive stages, and no changes were detected following picrotoxin-induced seizures.
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PMID:Changes in the activity of glutamate related enzymes in cerebral cortex, during insulin-induced seizures. 257 18

Physiological haematological and blood biochemical parameters were studied in Canaan dogs (n = 8) as possible indices of fitness. These parameters were then used to distinguish between fit and unfit dogs and to monitor the changes in these parameters during training and detraining periods. Fitness was defined as the ability to run for one hour on a motorised treadmill (speed 8.65 km h-1, inclination 10 degrees) while maintaining rectal temperature and heart rate below 41 degrees C and 250 beats min-1 respectively. Fit dogs showed consistently lower values of heart rate and rectal temperature during exercise and recovery, and significantly lower increases for post exercise plasma creatine kinase activity and plasma lactate concentration. Significantly higher values for haemoglobin concentration were found immediately post exercise. There were no significant differences between fit and unfit dogs for post exercise plasma concentrations of aspartate aminotransferase, white blood cell count or total protein, although the unfit dogs showed a tendency towards higher values. Similarly, unfit dogs tended to have lower values for plasma glucose concentration, haematocrit and red cell count. Values for heart rate and rectal temperature during exercise differed significantly between various dogs until numbers fell, due to the inability of certain dogs to complete the exercise test. Dogs were consistent according to whether their values lay above or below the mean value for all dogs. These differences disappeared after 8 weeks of training. Fitness deteriorated after 3 to 5 weeks of detraining. According to these results, heart rate and rectal temperature appear to be the most suitable and sensitive indicators of fitness in tracking dogs. The haematological and blood biochemical parameters tested were found to be of limited use. It is suggested that apparent inherent superiority of dogs should be accounted for in prospective breeding programmes.
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PMID:Physiological and blood biochemical responses to submaximal treadmill exercise in Canaan dogs before, during and after training. 260 37

The hemlocks, Conium maculatum (poison-hemlock) and Cicuta spp. (waterhemlock), are poisonous plants that cause sizeable losss to the livestock industry. Clinical signs of poisonhemlock toxicosis are similar in all species of livestock and include muscular weakness, incordination, trembling, initial central nervous system stimulation, depression and death from respiratory paralysis. Poison-hemlock also causes skeletal defects in the offspring of cattle, pigs and sheep and cleft palate in pigs when ingested during specific periods of gestation. The primary toxicants in poison-hemlock are coniine and gamma-coniceine. Coniine predominates in mature plants and seed, whereas gamma-coniceine predominates in early growth of the plant. Waterhemlock is the most violently toxic poisonous plant known. The toxicant is cicutoxin, which acts on the central nervous system, causing violent convulsions and death. Clinical signs of poisoning appear within 15 min after ingestion of a lethal dose and include excessive salivation, nervousness, tremors, muscular weakness and convulsive seizures interspersed by intermittent periods of relaxation and a final paralytic seizure resulting in anoxia and death. Elevated activities of lactic dehydrogenase, aspartate aminotransferase and creatine kinase in blood are observed, indicative of muscular damage. Toxicoses from poisonhemlock and waterhemlock generally occur in early spring when both plants emerge before other, more palatable plants begin to grow. All parts of the poison-hemlock plant are toxic. The root or tubers of waterhemlock are toxic; however, experimental evidence concerning the toxicity of other plant parts is inconclusive.
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PMID:Toxicoses in livestock from the hemlocks (Conium and Cicuta spp.). 304 97

The mechanism by which pentylenetetrazole provokes convulsions in animals has been investigated by measuring its influence in vitro on the activities of several enzymes of glutamate metabolism in rat brain homogenates. Pentylenetetrazole does not affect the specific activities of glutamine synthetase, glutaminase, or glutamate decarboxylase; it inhibits those of glutamate dehydrogenase and aspartate aminotransferase, and stimulates that of gamma-aminobutyric acid (GABA) aminotransferase. The overall consequence of the action of pentylenetetrazole on the activities of these enzymes should be an increase in the concentration of glutamate and a decrease in that of GABA. This modulation of glutamate and GABA metabolism by pentylenetetrazole could contribute to the triggering of convulsions.
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PMID:Pentylenetetrazole inhibits glutamate dehydrogenase and aspartate aminotransferase, and stimulates GABA aminotransferase in homogenates from rat cerebral cortex. 321 59

A male born to first cousins presented at 12 months with hypocalcemic convulsions, rickets, epistaxis due to vitamin K deficiency, and extremely low serum levels of beta-carotene and vitamin A. Liver function was altered moderately (glutamic-oxaloacetic transaminase, 55 U/L; glutamic-pyruvic transaminase, 37 U/L; lactate dehydrogenase, 255 U/L; alkaline phosphatase, 437 U/L). To correct the deficiencies, 8,000 IU vitamin D/day, 10,000 IU vitamin A/day, and intramuscular administration of vitamin K1 were required. At 9 years, he presented signs of neuromuscular affection, and the serum vitamin E level (measured for the first time) was extremely low. Classic lipid malabsorption syndromes (abetalipoproteinemia, chronic cholestasis, mucoviscidosis, coeliac disease, Whipple's disease) were excluded by appropriate examinations. Composition of duodenal bile acids was characterized by undetectable levels of cholic acid metabolites, and only chenodeoxycholic acid metabolites were present. Serum total bile acid concentration was normal, with an atypical low cholic acid/chenodeoxycholic acid ratio and abnormal presence of 3 beta-OH-delta 5-cholenic acid and 6-OH-bile acids. Urinary bile acid composition was also characterized by elevated 6-OH-bile acids. Known enzymopathies of the bile acid synthetic pathway were excluded (cerebrotendinous xanthomatosis, cerebro-hepato-renal syndrome of Zellweger, coprostanic acidemia). Bile acid pool sizes were determined by using stable isotopes: cholic acid pool size [2.90 (N, 32 +/- 16) microM/kg] and chenodeoxycholic acid pool size [10.8 (N, 32.6 +/- 9.9) microM/kg] were extremely low; fractional turnover rates of both bile acids were in a normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malabsorption of liposoluble vitamins in a child with bile acid deficiency. 379 31


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