Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

AMP deaminase, the activity that catalyzes the deamination of AMP to form IMP and NH3 has been measured in Dictyostelium discoideum. A new procedure to assay the activity of this enzyme was developed using formycin 5'-monophosphate, a fluorescent analog of AMP as the substrate, and ion-paired reverse phase HPLC to separate the reactants and products. Quantitation of the formycin containing compounds was accomplished at 290 nm. At this wavelength adenosine containing compounds were not detected and activity could be monitored in the presence of its activator ATP. The AMP deaminase activity in vegetative cells was 7.4 nmols/min/mg proteins while the activity in cells measured at 2 and 6 hrs after starvation-induced growth-arrest was 376 nmols/min/mg protein...a 51-fold increase. When vegetative cells were treated with hadacidin, a drug that restricts de novo AMP synthesis and pinocytosis, the activity of the AMP deaminase was 511 nmols/min/mg protein...a 70-fold increase compared to that in untreated vegetative cells. Smaller increases were noted following the inhibition of growth with the drugs cerulenin and vinblastine, as well as after the inhibition of de novo GMP synthesis with the drug mycophenolic acid or the partial inhibition of de novo AMP synthesis with analogs of hadacidin, N-hydroxyglycine and N-formylglycine. In addition, when the activity of two other enzymes involved in purine metabolism, namely adenosine kinase and hypoxanthine-guanine phosphoribosyl transferase, was measured in vegetative cells, and the activity of both compared to that measured in starvation and hadacidin induced growth-arrested cells, showed no significant changes.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Cell Biochem 1986 Jun
PMID:AMP deaminase in Dictyostelium discoideum: increase in activity following nutrient deprivation induced by starvation or hadacidin. 301 11

The main nitrogen source for most higher plants is soil nitrate. Prior to its incorporation into amino acids, plants reduce nitrate to ammonia in two enzymatic steps. Nitrate is reduced by nitrate reductase to nitrite, which is further reduced to ammonia by nitrite reductase. In this paper, the complete primary sequence of the precursor protein for spinach nitrite reductase has been deduced from cloned cDNAs. The cDNA clones were isolated from a nitrate-induced cDNA library in two ways: through the use of oligonucleotide probes based on partial amino acid sequences of nitrite reductase and through the use of antibodies raised against purified nitrite reductase. The precursor protein for nitrite reductase is 594 amino acids long and has a 32 amino acid extension at the N-terminal end of the mature protein. These 32 amino acids most likely serve as a transit peptide involved in directing this nuclear-encoded protein into the chloroplast. The cDNA hybridizes to a 2.3 kb RNA whose steady-state level is markedly increased upon induction with nitrate.
Mol Gen Genet 1988 Apr
PMID:Isolation of cDNA clones coding for spinach nitrite reductase: complete sequence and nitrate induction. 316 66

Cyanase, an oligomeric enzyme of Escherichia coli that catalyzes the decomposition of cyanate to ammonia and bicarbonate, crystallizes in the space group P1 with unit cell parameters a = 85.96 A, b = 83.17 A, c = 83.28 A, alpha = 110.29 degrees, beta = 118.29 degrees and gamma = 72.40 degrees. Crystals diffract to a resolution of at least 2.5 A. The crystal data, in conjunction with a subunit molecular weight of 17,008, suggest that two oligomers are in the asymmetric unit of the crystal and that eight subunits comprise a single oligomer.
J Mol Biol 1987 Nov 05
PMID:Preliminary X-ray crystallographic study of cyanase from Escherichia coli. 332 28

Axenic culture amastigote-like forms of Trypanosoma cruzi, grown at 28 degrees C, reach a stationary phase after two generations, and differentiate to epimastigotes, which then resume growth. Axenic culture amastigotes readily ferment glucose to succinate and acetate, and do not excrete NH3; they have high activities of hexokinase and phosphoenolpyruvate carboxykinase, and very low citrate synthase activity; cytochrome o is absent, and cytochrome b-like is present at a very low level. Epimastigotes catabolize glucose and produce succinate and acetate at a considerably lower rate; they exhibit lower levels of hexokinase and carboxykinase, and much higher levels of citrate synthase and cytochromes o and b-like. They catabolize amino acids, as shown by excretion of NH3 to the medium. The results suggest that axenic culture amastigotes have an essentially glycolytic metabolism, and they acquire the ability to oxidize substrates such as amino acids only after differentiation to epimastigotes.
Mol Biochem Parasitol 1987 Nov
PMID:Aerobic glucose fermentation by Trypanosoma cruzi axenic culture amastigote-like forms during growth and differentiation to epimastigotes. 332 2

Canaline and gabaculine, inhibitors of gamma-aminotransferases and thus of ornithine aminotransferase (E.C. 2.6.1.13), decreased the flow through ornithine carbamoyl transferase (E.C. 2.1.3.3) in isolated rat hepatocytes incubated with 10 mM NH4Cl and ornithine. The levels of acetylglutamate, an essential activator of carbamoyl phosphate synthetase (ammonia) (E.C. 6.3.4.16), were also decreased, suggesting that the inhibitors had also caused a decrease in the rate of carbamoyl phosphate synthesis. Under these conditions, ornithine appears to be a precursor of acetylglutamate, via ornithine aminotransferase, possibly as a consequence of glutamate synthesis. The influence of aminooxyacetate, an aminotransferase inhibitor, has also been examined.
Mol Cell Biochem 1988 Feb
PMID:Effects of inhibition of ornithine aminotransferase or of general aminotransferases on urea and citrulline synthesis and on the levels of acetylglutamate in isolated rat hepatocytes. 339 32

SRI used the L5178Y mouse lymphoma cell forward mutation assay to determine the mutagenic activity of 63 coded chemicals from 16 chemical classes. Replicate experiments were performed to assess the reproducibility of the assay within the laboratory. The evaluations (positive or negative) of the first two repeat experiments with the chemicals were the same for 116 (87%) of 134 tests. Evaluational differences between the first two experiments were fewer in the presence of induced S9 (6 tests) than in the absence of S9 (12 tests). The most commonly observed variability was the magnitude of positive mutagenic responses; this may be attributed to factors such as compound solubilities, S9 activation conditions, and differential recovery of mutant cells. Some consistency was observed in the responses of compounds of various chemical classes. Generally, antibiotics (ABO) and the azo dyes, azoxy and hydrazo compounds, diazoalkanes, nitriles and azides (AZO), were mutagenic with S9; alkyl, acyl, and aryl halides, halogenated ethers, and halohydrins (HAL) were more strongly mutagenic with than without S9; and monofunctional polycyclic aromatic hydrocarbons and fluorenones (PAH) were mutagenic only with S9. Amine-1-oxides (AMO), alkyl and aryl epoxides (EPO), and nitroalkanes, nitroaromatics, nitroquinolines, nitrofurans, and nitroimidazoles (NIT) were mutagenic with and without S9; amides, sulfonamides, aromatic amines, aliphatic amines, hydroxylamines, and benzidine and its derivatives (AMI) were mutagenic without S9; and methyl carbamate (the only monofunctional carbamate) and thioureas (CBM) induced a negative response under both conditions.
Environ Mol Mutagen 1988
PMID:Evaluation of the L5178Y mouse lymphoma cell mutagenesis assay: intralaboratory results for sixty-three coded chemicals tested at SRI International. 341 41

Positron emission tomography allows the noninvasive assessment of regional myocardial blood flow and metabolism. The purpose of this study was to correlate N-13 ammonia uptake as a measure of regional blood flow and C-11 palmitate kinetics as a marker for fatty acid metabolism in ischemic canine myocardium using positron emission tomography. Furthermore, the metabolic results were compared with ultrastructural findings obtained in the same animal model. Regional ischemia was induced by balloon occlusion of the left anterior descending artery in a closed chest dog model. The three myocardial sites studied were the center and "border" of the ischemic segment as well as the control myocardium. C-11 palmitate uptake closely correlated with blood flow (r = 0.88). In the center of ischemia uptake of C-11 palmitate was decreased and clearance of C-11 activity significantly prolonged. In the "border" of the ischemic segment with only mild reduction of flow and C-11 palmitate uptake (approximately 20%) clearance halftime and residual activity were significantly different from control. The residual activity normalized for initial uptake of C-11 palmitate was highest in the "border" regions consistent with increased deposition of C-11 palmitate in lipid pools. The electron microscopic studies showed in 8 of 11 dogs lipid droplets as the only abnormality in corresponding segments with only mild reduction in microsphere blood flow. Thus, these data indicate the potential of metabolic imaging to characterize ischemia on a cellular level. Positron emission tomography provides a sensitive means to detect mild ischemia and to define extent and severity. Metabolic imaging may prove clinically useful to identify not only necrosis, but also myocardium at risk.
J Mol Cell Cardiol 1987 Mar
PMID:Metabolic and ultrastructural abnormalities during ischemia in canine myocardium: noninvasive assessment by positron emission tomography. 349 62

Trichomonas vaginalis growing in complex medium produced volatile thiols at a rate of 0.7 nmol min-1 (mg protein)-1 and the parasite suspended in PBS with L-methionine excreted volatile thiols, including methanethiol, and alpha-keto acid. Cell-free extracts of the parasite also produced volatile thiols from L-methionine, at the rate of 5.4 nmol min-1 (mg protein)-1. Thiol production was not detectable with living cells or cell-free extracts of Tritrichomonas foetus, Trichomitus batrachorum or Pentatrichomonas hominis and homogenates of a range of trypanosomatids and mouse liver also failed to produce volatile thiols from L-methionine. Approximately equimolar concentrations of alpha-keto acid and volatile thiols were produced from L-methionine by cell-free extracts of Trichomonas vaginalis; the release of ammonia, however, was not detectable. The parasite enzyme catabolised a range of substrates and was inhibited by several compounds, including bithionol and DL-propargylglycine. Parasites grown in the presence of 10(-5) M DL-propargylglycine had no detectable L-methionine-catabolising enzyme activity. These findings indicate that T. vaginalis is significantly different from other trichomonads, a range of trypanosomatids and mouse liver in L-methionine catabolism, and that the parasite enzyme responsible for the breakdown of L-methionine in T. vaginalis appears to be similar in several ways to bacterial L-methionine-gamma-lyase (EC 4.4.1.11) and trichomonal homocysteine desulphurase (EC 4.4.1.2).
Mol Biochem Parasitol 1987 Apr
PMID:L-methionine catabolism in trichomonads. 349 35

Rates of 7-ethoxycoumarin O-deethylation were determined in periportal and pericentral regions of the liver lobule in livers from corn oil- and beta-naphthoflavone-treated rats by monitoring the conversion of nonfluorescent 7-ethoxycoumarin to fluorescent 7-hydroxycoumarin with micro-light guides. Rates of monooxygenation in livers from fed, corn oil-treated rats of 1.4 mumol/g/hr were increased markedly to around 21 mumol/g/hr in both regions of the liver lobule after treatment of rats with beta-naphthoflavone. Fasting or treatment with 6-aminonicotinamide diminished the generation of NADPH by the pentose cycle, whereas KCN decreased NADPH generation via mitochondria. Fasting and 6-aminonicotinamide treatment decreased monooxygenation about 0.5 mumol/g/hr in both regions of the liver lobule in livers from corn oil-treated rats and around 5 mumol/g/hr in livers from beta-naphthoflavone-treated rats. KCN decreased rates about 0.5 mumol/g/hr in both regions of the lobule in livers from fed, corn oil-treated rats and nearly completely in livers from fasted rats. Rates declined from 14 to less than 2 mumol/g/hr in livers from fasted, beta-naphthoflavone-treated rats following 30-40 min of perfusion with cyanide. These data indicate that mitochondrial oxidations are the predominant source of reducing equivalents for monooxygenation in both regions of the liver lobule in livers from beta-naphthoflavone-treated rats. Activation of urea synthesis by infusion of ammonia, a process requiring mitochondrial NADPH, inhibited the metabolism of 7-ethoxycoumarin by 30%. Malate, which is a substrate for the malic enzyme shuttle mechanism involved in the transfer of reducing equivalents from the mitochondria to the cytosol, increased 10-fold during infusion of 7-ethoxycoumarin in livers from beta-naphthoflavone-treated rats but less than 3-fold in livers from control rats. Taken together, these data indicate that high rates of 7-hydroxycoumarin production in livers from beta-naphthoflavone-treated rats are sustained by increased rates of NADPH generation from mitochondrial sources.
Mol Pharmacol 1987 Aug
PMID:Effect of beta-naphthoflavone on mitochondrial supply of reducing equivalents for monooxygenation in periportal and pericentral regions of the liver lobule. 349 33

The effects of 26 different cosmetic ingredients (e.g., permanent wave and hair dye compounds, emulsifiers, resins, and detergents such as quats) were assessed by four end points indicative for qualitatively and quantitatively different cytotoxicity: (1) neutral red uptake reduction after 24 h of treatment (NR-90 and NR-50); (2) cell detachment from culture dish after 4 h of treatment (CD-25); (3) growth inhibition after 48 h of treatment (GI-50); and (4) membrane permeability measured by fluorescent dye retention (fluorescence shift FS-25) and dye exclusion (viability ratio VR-25). The cytotoxicity potentials of the test agents were ranked for each in vitro test and compared with the in vivo eye irritation in guinea pigs (Draize test) after application of 5 or 2.5% (w/v) solutions of the same test batches. Strong irritants could be easily detected by most of the in vitro tests, but the neutral red uptake assay (especially NR-50) was the only one that was able to distinguish the minimally irritating test agents from strong irritants as well as from nonirritants. (I) All three extremely irritating quaternary ammonia compounds were identified as the strongest cytotoxic agents. (II) Nine out of 12 minimally irritating substances (mainly emulsifiers and resins) were ranked in the intermediate group. (III) Eight out of 11 non-or practically nonirritating chemicals (mainly permanent wave compounds) showed cytotoxic effects at very high concentrations only. The distinction of these three groups was better by means of NR-50 than by NR-90 data. At least two of the other cell tests (CD-25, GI-50, FS-25, and VR-25) had to be considered to allow an adequate interpretation of in vitro cytotoxicity.
Mol Toxicol
PMID:Comparison of in vitro cell toxicity with in vivo eye irritation. 350 2


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