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)

The influence of different levels of dietary pyridoxine-HC1 (1.2, 2.4, 4.8, 9.6, 19.2, 38.4, 76.8 and 153.6 mg/kg diet) fed to dams on certain parameters of developing and mature brain was studied in rats. Brain weights and alanine aminotransferase (ALAT) activities (initial and following in vitro addition of pyridoxal phosphate, PLP) were significantly reduced in brains of 12-day-old pups of dams fed the lowest level of pyridoxine compared to other treatments; in vitro addition of PLP significantly stimulated the activities of glutamic acid decarboxylase (GAD) and ALAT. Vitamin B-6 concentrations in brain were higher for 2-day-old pups of dams fed 38.4 or 76.8 mg vitamin/kg diet and for 12-day-old pups of dams fed 2.4 to 153.6 mg compared to the 1.2 mg groups; at weaning, values were greater in groups fed 76.8 or 153.6 mg compared to the 1.2 mg group. As brain developed during the suckling period, the content of bitamin B-6 and protein increased in all groups, except the 1.2 mg group in which values remained the same. The vitamin and protein content in brain had not reached chemical maturity at weaning as evidenced by greater concentrations of each in brains of dams as compared with values for 21-day-old progeny. As brain developed, ALAT activity increased about 30 times from age 2 to 21 days when activities were similar to those observed in mature brains of dams. Activity of GAD in brain increased about four times from age 12 to 21 days.
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PMID:Influence of different levels of dietary pyridoxine on certain parameters of developing and mature brains in rats. 126 75

Several hepatotoxic agents damage Ca++ regulation and produce toxic cell death in a manner consistent with a cause-and-effect relationship; however, vital targets of Ca++ remain unidentified. Recent results show that DNA may be the chief Ca++ target during apoptosis, a form of cell death considered distinct from toxic cell death or necrosis. The present studies explored whether nuclear Ca++ regulation is lost before dimethylnitrosamine-induced necrosis, whether DNA is attacked by Ca(++)-dependent endonucleases and whether inhibitors of Ca(++)-endonuclease activity and the DNA repair enzyme poly(ADP-ribose)polymerase affect necrosis. Adult male ICR mice received 100 mg/kg of dimethylnitrosamine i.p. By 2 to 4 hr, total nuclear Ca++ reached 150 to 180% of control and DNA fragmentation was 140 to 170% of control. Electrophoresis of DNA revealed a sharp decline in genomic DNA with the appearance of DNA fragments in a ladder-like pattern. Ca++ elevation and DNA fragmentation preceded toxic cell death by 4 hr or more and reached peak values at 18 to 24 hr, coincident with maximal alanine aminotransferase leakage. Aurintricarboxylic acid, a Ca(++)-endonuclease inhibitor, reduced toxicity 67%. 3-Aminobenzamide, nicotinamide adenine dinucleotide and theophylline, inhibitors of poly(ADP-ribose)polymerase-mediated DNA repair, potentiated liver damage 2-fold. These results support the hypothesis that DNA fragmentation plays a contributing role in toxic cell death induced by dimethylnitrosamine. Furthermore, the findings suggest that new opportunities may exist to moderate the toxicity of alkylating hepatotoxins by altering DNA regulation.
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PMID:Ca(++)-activated DNA fragmentation and dimethylnitrosamine-induced hepatic necrosis: effects of Ca(++)-endonuclease and poly(ADP-ribose) polymerase inhibitors in mice. 132 12

Response characteristics are presented for a dual-enzyme fiber-optic biosensor for glutamate. An enzyme layer composed of glutamate dehydrogenase (GDH) and glutamate-pyruvate transaminase (GPT) is used to produce reduced nicotinamide adenine dinucleotide (NADH) at the tip of a fiber-optic probe. NADH luminescence is monitored through this probe and the measured fluorescence intensity is related to the concentration of glutamate. GDH catalyzes the formation of NADH, and GPT drives the GDH reaction by removing a reaction product and regenerating glutamate. Optimal response is obtained in a pH 7.4 Tris-HCl buffer maintained at 25 degrees C in the presence of 4 mM NAD+ and 10 mM L-alanine. The temperature profile reveals a strong negative temperature effect which is attributed to the temperature dependency of NADH luminescence. Under optimal conditions, the sensor sensitivity is 0.127 nA/microM over the 1-10 microM concentration range, the detection limit is 0.13 microM, and response times range from 4 to 8 min. The sensor response is stable for 12 days when stored at 4 degrees C. Selectivity for glutamate is excellent over most of the common amino acids as well as ascorbic acid, uric acid, taurine, and GABA. Only slight responses were observed for glutamine and lysine. The effect of ammonia on the glutamate response was found to be minimal at total ammonia nitrogen concentrations as high as 200 microM.
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PMID:Dual-enzyme fiber-optic biosensor for glutamate based on reduced nicotinamide adenine dinucleotide luminescence. 135 Apr 33

Several key enzymes related to carbohydrate metabolism were assayed in Setaria digitata. In the cytosolic fraction pyruvate kinase, phosphoenolpyruvate carboxykinase, malate dehydrogenase, malic enzyme, aspartate transaminase and alanine transaminase were found. Among the TCA cycle enzymes succinate dehydrogenase, fumarate reductase, fumarase (malate dehydration), malate dehydrogenase (malate oxidation and oxaloacetate reduction) and malic enzyme (malate decarboxylation) were detected in the mitochondrial fraction. Only reduced nicotinamide adenine dinucleotide (NADH) dehydrogenase, NADH oxidase and NADH-cytochrome c reductase were found in the mitochondrial fraction. The significance of these results with respect to the metabolic capabilities of the worm are discussed.
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PMID:Intermediary carbohydrate metabolism in the adult filarial worm Setaria digitata. 177 15

During operation, biopsies from the gastrocnemius muscle and, in some cases, from the sartorius muscle were taken from 32 patients with peripheral arterial occlusive disease and from 5 subjects with normal peripheral circulation. In patients with inadequate circulation only during exercise, when compared with the control group, increased activities of enzymes involved in oxidative metabolism (malate dehydrogenase, nicotinamide adenine dinucleotide phosphate-dependent isocitrate dehydrogenase, cytochrome C oxidase, creatine kinase), in amino acid metabolism (asparate aminotransferase, alanine aminotransferase), and in anaerobic glycoysis (lactate dehydrogenase) were found. In patients with circulatory disturbances that manifested themselves already at rest, enzyme activities were, with the exception of LDH, lower than those of patients with exclusively exercise-related insufficiency. By means of intraindividual comparisons with the corresponding enzyme activities in the sartorius muscle, the author was able to show that the changes found were not simply the result of differences in training conditions. The diminished concentrations of energy-rich phosphate are an expression of the anaerobic metabolic state in patients with inadequate circulation at rest. It is concluded that chronic ischemia of muscle leads to changes in the energy metabolism of the cell. In the presence of more nearly adequate circulation at rest, the portion of oxidative potential of the total energy metabolism increases. In contrast, if there is an inadequate circulation at rest, the mainly anaerobic glycolysis becomes quantitatively predominant.
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PMID:Investigations on the biochemical characteristics of chronically underperfused muscle. 201 45

The amount of L-lactate in biological fluids (serum, plasma and cerebrospinal fluid) was determined by monitoring the reduced form of nicotinamide adenine dinucleotide (NADH) produced by immobilised lactate dehydrogenase (LDH), with bacterial bioluminescent enzymes immobilised on a separate nylon coil. The LDH catalysed the reaction of L-lactate with NAD; this reaction took place in a nylon coil that preceded the coil for the bioluminescent detection. The co-immobilisation of alanine aminotransferase (ALT) with LDH improved the lactate transformation by 117-183%. The response was linear from 0.1 to 50 micron mol l(-1) at 25 degrees C for the LDH - ALT reactor. The intra- and inter-assay coefficients of variation were less than 5% and the recoveries ranged from 93 to 106%. The results agreed well with those obtained with a spectrophotometric method and with the normal reference values.
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PMID:Bioluminescent flow sensor for the determination of L-(+)-lactate. 222 97

The influence of dopamine on liver metabolism in the state of brain death was assessed by measuring arterial ketone body ratio (AKBR) in dogs. Mean arterial blood pressure (MABP) was significantly decreased, from 137.4 +/- 3.7 to 64.7 +/- 2.8 mm Hg, 1 hour after completion of brain death (p less than 0.01). In the control group AKBR was maintained at the near control value of 1.07 thereafter, concomitant with a significant decrease in serum lactate levels, despite marked hypotension (p less than 0.05). Dopamine infusion at rates of 5 and 10 micrograms/kg/min sustained both AKBR and MABP at near control values. In contrast, dopamine given at doses greater than 15 micrograms/kg/min caused a significant reduction of AKBR, to less than 0.66 +/- 0.12 (p less than 0.01), although MABP was restored to near-normal levels. In addition, serum levels of alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase were significantly elevated, reflecting liver cell injury. It is suggested that the liver is primarily tolerant to hypotension in the state of brain death and that dopamine administered at a rate of 15 micrograms/kg/min or more impairs liver metabolism by reducing the redox state (free nicotinamide-adenine dinucleotide/reduced nicotinamide-adenine dinucleotide) of liver mitochondria.
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PMID:Influence of dopamine on the liver assessed by changes in arterial ketone body ratio in brain-dead dogs. 229 56

Activity of enzymes participating in metabolism of glutamate and content of nicotinamide nucleotides was studied in rat liver tissue within 24 hrs after intramuscular administration of alpha-tocopheryl acetate at doses of 30 mg and 300 mg per kg of body mass. Excess of the vitamin was responsible for a decrease in the ratio NAD+/NADH in cytosol, for stimulation of glutamate dehydrogenase reaction, for a decrease of aspartate aminotransferase activity in mitochondria and of alanine aminotransferase activity in cytosol as well as for an increase of NADPH content.
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PMID:[Effect of alpha-tocopherol on glutamic acid metabolism and nicotinamide coenzyme levels in hepatocytes]. 287 84

Vitamin B-6 status was assessed by measuring erythrocyte glutamic-pyruvic transaminase (EGPT) indices in 122 pregnant Hispanic teenagers. Seventeen percent were vitamin B-6 deficient (EGPT indices greater than 1.25) at the initial interview (first or second trimester). A daily supplement of 5 mg vitamin B-6, beginning at initial interview, did not reduce prevalence of vitamin B-6 deficiency at final interview (third trimester). No association was found between EGPT indices greater than 1.25 and the outcome of pregnancy. The activity of diamine oxidase (DAO), a vitamin B-6-dependent enzyme produced by the placental decidua, was measured in maternal plasma. At initial and final interviews, plasma-DAO activity was increased by in vitro addition of pyridoxal-5'-phosphate. The activity in early pregnancy was positively associated with dietary vitamin B-6 intake and was lower in teenagers with EGPT indices greater than 1.25 at the final interview. Findings suggest that plasma-DAO activity is influenced by vitamin B-6 status.
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PMID:Vitamin B-6 nutriture and plasma diamine oxidase activity in pregnant Hispanic teenagers. 309 85

The vitamin B-6 status of 62 black and 50 white adolescent girls living in Virginia and Alabama was assessed in 1981 and again in 1983, using the parameters coenzyme stimulation of erythrocyte alanine aminotransferase activities and dietary intakes of the vitamin. The subjects were 12 or 14 years old in 1981. The height and weight measurements of the subjects were within normal ranges. The mean daily vitamin B-6 intake of the girls from food was 1.25 mg both years, as estimated by two nonsequential 24-hour food recalls. Approximately half of the girls reported consuming less than 0.02 mg vitamin B-6 per gm protein during both years. Almost half of the girls had coenzyme stimulation values indicative of marginal or deficient status. Coenzyme stimulation and dietary values of the race, age, and income groups were similar. Changes in the status grouping of the girls between the 2 years as reflected by the coenzyme stimulation measurement were associated with changes in their vitamin B-6 intakes in 70% of the cases. Vitamin B-6 inadequacy seems to be prevalent among both black and white adolescent girls.
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PMID:Longitudinal assessment of vitamin B-6 status in southern adolescent girls. 381 49


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