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)

Tryptophanase (tryptophan: indole-lyase) from Escherichia coli has been isolated in the holoenzyme form and its absorption spectra and acid-base chemistry have been reevaluated. Apoenzyme has been prepared by dialysis against sodium phosphate and L-alanine and molar absorptivities of the coenzyme bands have been estimated by readdition of pyridoxal 5'-phosphate. The spectrophotometric titration curve, whose midpoint is at pH 7.6 in 0.1 M potassium phosphate buffers, indicates some degree of cooperativity in dissociation of a pair of protons. Resolution of the computed spectra of individual ionic forms of the enzyme with lognormal distribution curves shows that band shapes are similar to those of model Schiff bases and of aspartate aminotransferase. Using molar areas from the latter we estimated amounts of individual tautomeric species. In addition to ketoenamine and enolimine or covalent adduct the high pH form also appears to contain approximately 18% of a species with a dipolar ionic ring (protonated on the ring nitrogen and with phenolate -O-). We suggest that this may be the catalytically active form of the coenzyme in tryptophanase. The equilibrium between tryptophanase and L-alanine has also been reevaluated.
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PMID:Equilibria and absorption spectra of tryptophanase. 203 39

Viable toadfish hepatocytes were separated into distinct subpopulations by gradient centrifugation. Although 3-5 density subpopulations were obtained for each fish, only two metabolically and enzymatically different subpopulations could be discerned. In all cases, hepatocytes with the lowest density (less than 1.040 g ml-1) were more oxidative in scope, as judged by the activities of mitochondrial enzymes (citrate synthase, aspartate aminotransferase, glutamate dehydrogenase); activities of these enzymes (normalised to cell protein) were on average two- to threefold higher than in subpopulations with higher densities. Lower-density hepatocytes also contained higher levels of the urea cycle enzymes arginase and ornithine carbamoyltransferase. The higher-density subpopulations showed no significant differences from each other in enzymatic activities. Compared with lower-density cells, these hepatocytes had higher activities of two cytosolic enzymes, malate dehydrogenase and glutathione-S-transferase. There was no distinct distribution pattern for alanine aminotransferase and glutamine synthetase. Despite generally lower oxidative enzyme content, higher-density hepatocytes were metabolically more active, with 2.5- to fourfold higher rates of urea synthesis, gluconeogenesis and oxidation of lactate. We conclude that, although the toadfish liver shows distinct enzymatic and metabolic heterogeneity, this heterogeneity is dissimilar to the zonation pattern in the livers of mammals, in that separated toadfish hepatocyte types did not appear to possess exclusive metabolic functions. Notably, all cells were capable of metabolic functions that are strictly localised in mammalian liver. In nitrogen metabolism, glutamine synthetase displays a distribution pattern commensurate with its unique metabolic function in the liver of the ureogenic toadfish. Further, all subpopulations possessed detoxification capabilities as indicated by high levels of glutathione-S-transferase, a 'phase II' conjugation enzyme.
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PMID:Metabolic and enzymatic heterogeneity in the liver of the ureogenic teleost Opsanus beta. 205 Nov 31

We have recorded 1H NMR spectra in H2O for exchangeable protons of four pyridoxal phosphate-dependent enzymes: D-serine dehydratase, aspartate aminotransferase, tryptophan: indole-lyase and glutamate decarboxylase. The molecular masses range from 48-250 kDa. In every case there are downfield peaks which are lost when the apoenzyme is formed. In most cases some peaks shift in response to interactions with substrates and inhibitors and with changes in pH. We associate one downfield resonance with the proton on the ring nitrogen of the coenzyme and others with imidazole groups that interact with coenzyme or substrates. The chemical shift for the coenzyme-bound proton differs for free enzyme, substrate Schiff base or quinonoid forms.
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PMID:NMR spectra of exchangeable protons of pyridoxal phosphate-dependent enzymes. 206 76

Safety data have been gathered in US clinical trials of nabumetone on 1912 patients from August 1981 to May 1988. Dosing in the double-blind trials was 100 mg at bedtime, but in open-label trials patients could increase the dosage of nabumetone to 1500 or 2000 mg if required. Adverse experiences reported in the double-blind and open-label studies that were considered related to nabumetone treatment, or of unknown origin, occurred most commonly in two body systems: the body as a whole, and the digestive system. Incidence rates greater than 10% for adverse experiences categorised by preferred term occurred in the 'body as a whole' category for abdominal pain, and in the digestive system for diarrhoea and dyspepsia. Dosage increases to 2000 mg appeared to cause a dose-related increase in diarrhoea. In the long term studies, gastrointestinal ulcers have been confirmed in 13 (0.7%) patients. Hepatic and renal function was well preserved in patients treated with nabumetone. Overall, only 7 nabumetone-treated patients (0.4%) showed a marked elevation in both ALT (SGPT) and AST (SGOT). Two nabumetone-treated patients showed marked elevations in renal parameters, serum creatinine and blood urea nitrogen. Overall, nabumetone was well tolerated, and the adverse experience profile was clinically acceptable and presented no unusual or unexpected patterns.
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PMID:An overview of the long-term safety experience of nabumetone. 208 90

Through the present delta value check used in quality control programs is a powerful tool for detecting random errors in clinical chemistry analysis, it has some problems, such as missed true errors and delays in reporting time, because it also has the potential of showing erroneous positive results. Recently, new calculation methods for delta check with delta difference, delta percent change, rate difference, and rate percent change have been suggested by Lacher and Connelly (Clin Chem 34:1966-1970, 1988). Based on this new delta check method, we made the new criteria of which calculation method is applied to the clinical chemistry tests, i.e., the differential application of rate and delta check, and selectively applied the new method to 17 chemistry tests in order to solve the above problems. The applied criteria were the time dependence of the test item and the coefficient of variation of the absolute delta difference. Calcium, inorganic phosphorus, total protein, albumin, sodium, potassium, and chloride were classified as delta difference calculation method group; glucose and cholesterol as delta percent change group; creatinine, total and direct bilirubin as rate difference group; and urea nitrogen, uric acid, ALP, ALT, and AST as rate percent change group. With the previous criteria by Whitehurst et al. (Clin Chem 221:87-92) for 5045 specimens, the check-out rate was 47.8% (2,411 out of 5,045), and the positive predictive value was 0.41% (10 out of 2,411). For the new criteria, the check-out rate was 12.7% (621 out of 5,045), and the positive predictive value was 1.8% (nine out of 621).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential application of rate and delta check on selected clinical chemistry tests. 210 Jan 25

Indoxyl sulfate is a metabolite of tryptophan. Indole is synthesized in intestine from tryptophan by intestinal bacteria. The absorbed indole is converted to indoxyl sulfate through indoxyl in liver. Serum concentration of indoxyl sulfate is markedly increased as an inhibitor of drug-binding in uremic patients as compared with healthy subjects. Since indoxyl sulfate is bound to serum albumin, it cannot be removed efficiently by hemodialysis, and it tends to accumulate in uremic serum. To determine if oral sorbent, AST-120, could adsorb indole in intestine and then decrease serum concentration of indoxyl sulfate, it was administered to nephrectomized uremic rats. Serum concentration of indoxyl sulfate was markedly decreased in uremic rats fed with oral sorbent as compared with control uremic rats. However, serum concentrations of creatinine and urea nitrogen were not significantly decreased in the uremic rats fed with oral sorbent as compared with the control uremic rats. Serum concentration of tryptophan was not decreased but rather increased in the uremic rats fed with oral sorbent as compared with the control uremic rats. Concentration of indoxyl sulfate in bile of a uremic rat was much lower than that in the uremic serum, suggesting that the adsorption of indoxyl sulfate in intestine is not a major mechanism of decreasing the serum concentration of indoxyl sulfate. These results demonstrate that oral sorbent, AST-120, can decrease serum concentration of indoxyl sulfate in uremia due to adsorption of indole in intestine.
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PMID:[Effect of oral sorbent, AST-120, on serum concentration of indoxyl sulfate in uremic rats]. 212 Apr 92

The effects of soman poisoning on hematological (counts of red blood cells (RBC), white blood cells (WBC), and platelets and measurement of hematocrit) and coagulation parameters (prothrombin time, activated partial thromboplastin time, thrombin time and concentrations of fibrinogen, factor V, factor VII, and factor XI) and serum biochemistry (concentration of albumin, protein, calcium, cholesterol, triglycerides, blood urea nitrogen (BUN), magnesium, and creatinine and activities of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, cholinesterase, creatinine phosphokinase (CPK), hydroxybutyrate dehydrogenase, and amylase) were determined at 1, 2, 4, 24, and 48 hours after poisoning of rabbits. There were significant (p less than 0.05) decreases in the RBC counts in all treatment groups that were measured initially at 4 hours and were reflected by parallel decreases in the hematocrit values. These changes were probably due to an increase in the hemolysis of the RBC rather than a decrease in the production of RBC. There were minor changes in the coagulation parameters. Generally, the fibrinogen content increased. The activated partial thromboplastin time decreased significantly (p less than 0.05) 24 and 48 hours after soman (50 micrograms/kg) poisoning. Blood cholinesterase values were significantly reduced in all treatment groups at all time periods. The CPK activity was increased after 4 and 24 hours in the 20 and 50 micrograms/kg soman groups. There were minor changes in the other biochemistry values, but none that showed a dose-response relationship; thus, they were considered to be of limited significance with regard to the toxic manifestations of soman exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of soman poisoning on hematology and coagulation parameters and serum biochemistry in rabbits. 212 98

One intraperitoneal dose of Candida albicans (10(8) CFU) caused a chronic (longer than 2 months), significant elevation of plasma fibrinogen levels (Clauss method) in mice of strain C3H/HeN. Even a small dose (10(6) CFU) resulted in a significant increase in fibrinogen level for 5 days following injection, whereas other blood parameters (leukocytes, erythrocytes, platelets, hematocrit, hemoglobin, blood urea nitrogen, aspartate aminotransferase, albumin, alkaline phosphatase, antithrombin III, glucose, calcium, and total protein) measured by standard methods were normal. Blood taken during this period was negative for C. albicans. The role of tumor necrosis factor (TNF) in C. albicans infections was investigated by measuring the fibrinogen response after the administration of C. albicans or recombinant mouse TNF-alpha. Both challenges resulted in an elevated fibrinogen level. When polyclonal antibodies to mouse TNF-alpha were given prior to challenge with C. albicans or mouse TNF-alpha, the fibrinogen increase was significantly inhibited. C. albicans injections were found to significantly elevate endogenous TNF levels in mice (enzyme-linked immunosorbent assay). It was concluded that C. albicans induces TNF in the mouse. Furthermore, these data give evidence which supports a relationship between TNF and the fibrinogen increase induced by C. albicans.
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PMID:Tumor necrosis factor (TNF) is induced in mice by Candida albicans: role of TNF in fibrinogen increase. 220 37

Neurologic and myopathic complications of alcoholism are multiple and diverse, affecting both the central and peripheral nervous systems. In the ED, initial concern is for diagnosing readily reversible causes and ruling out possible life- or limb-threatening etiologies. A rapid assessment of the ABCs, a fingerstick blood glucose determination, and, in cases of AMS, the administration of intravenous naloxone is indicated. In almost every instance of a potential neurologic complication, intravenous thiamine replacement is indicated initially, along with the parenteral administration of folic acid and the other B vitamins, including nicotinic acid and pyridoxine. Metabolic screening with electrolytes, glucose, blood urea nitrogen, creatinine, calcium, magnesium, liver enzymes (AST, alkaline phosphatase), bilirubin, arterial blood gases with carboxyhemoglobin determination, and a complete blood count are often warranted. Special tests such as CT scan, CK, ammonia, or toxicologic screens are indicated in specific instances. In terms of physical examination, attention to the presence of focal neurologic findings is paramount because of the possibility of a subdural or epidural hematoma. It is important not to miss meningitis and a low threshold for treatment or lumbar puncture should be maintained. Specialized consultation and referral are needed only after stabilization and appropriate tests are performed. If an organized approach to the evaluation of an alcoholic with neurologic symptoms is undertaken, occult disease will not be missed and outcomes will be improved.
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PMID:Neurologic complications of alcoholism. 222 90

Effects of dietary aflatoxin (AF) and T-2 toxin, singly and in combination, were evaluated in growing crossbred (Yorkshire x Landrace x Hampshire) pigs. The experimental design consisted of 4 treatment groups of 6 barrows each fed diets containing 0 mg of AF and T-2/kg of feed (controls; group 1), 2.5 mg of AF/kg of feed (group 2), 10 mg of T-2/kg of feed (group 3), or 2.5 mg of AF plus 10 mg of T-2/kg of feed (AF + T-2; group 4) ad libitum for 28 days (7 to 11 weeks of age). Production performance, and serum biochemical, and hematologic evaluations were made weekly. Body weight and body weight gain were depressed by all toxin treatments, but the effect of AF and T-2 toxin in combination was less than additive. Liver and kidney weights, as a percentage of body weight, were increased by AF treatment, and heart weight, as a percentage of body weight, was increased by T-2 treatment. Treatment with T-2 toxin induced necrotizing contact dermatitis on the snout, buccal commissures, and prepuce. Consumption of AF resulted in increased serum activities of alkaline phosphatase, aspartate transaminase, cholinesterase, and gamma-glutamyltransferase, and decreased serum concentrations of urea nitrogen, cholesterol, albumin, total protein, calcium, potassium, magnesium, and phosphorus. Consumption of T-2 toxin resulted in increased serum triglyceride concentration and decreased serum iron concentration. Treatment with AF induced lower serum unsaturated iron-binding capacity and high RBC count, PCV, hemoglobin concentration, WBC count, and prothrombin time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of treatment of growing swine with aflatoxin and T-2 toxin. 224 Jul 92


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