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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The dark and light reduction of nitrate and nitrite by cell-free preparations of the blue-green alga Anacystis nidulans has been investigated. The three following methods have been successfully applied to the preparation of active particulate fractions from the alga cells: (a) shaking with glass beads, (b) lysozyme treatment and lysis of the resulting protoplasts, and (c) sonication. The two enzymes of the nitrate-reducing system-namely, nitrate reductase and nitrite reductase-are firmly bound to the isolated pigment-containing particles, and can be easily solubilized by prolonging the vibration or sonication time. Both enzymes-whether solubilized or bound to the particles-depend on reduced ferredoxin as the immediate electron donor. In its presence, the alga particles catalyze the gradual photoreduction of nitrate to nitrite and ammonia, a process that can thus be considered as one of the most simple and relevant examples of Photosynthesis. Some of the properties of nitrate reductase have been studied. Nitrate reductase as well as nitrite reductase are adaptive enzymes repressed by ammonia.
Mol Cell Biochem 1976 Feb 25
PMID:Ferredoxin-dependent photosynthetic reduction of nitrate and nitrite by particles of Anacystis nidulans. 0 27

Se-Carboxymethyl-DL-selnocysteine (CMSeC) has been prepared in a pure crystalline form from selenocysteine and monochloracetic acid. It has been shown that CMSeC is a substrate for the L-aminoacid oxidase form snake venom and for the D-aspartate oxidase from beef kidney. Oxygen consumption and ammonia production indicate that only the L or the D form of CMSeC ar acted upon respectively by one or the other of the above enzymes. No noticeable differences were shown in the oxidation rate of CMSeC and S-carboxymethylcysteine, an indication that the substitution of a selenium for a sulfur atom in the molecule does not greatly affect the substrate specificity of the two enzymes. Data have been obtained suggesting that the product of the oxidative deamination of CMSeC Is Se-carboxymethyl-selenopyruvic acid.
Mol Cell Biochem 1976 Aug 30
PMID:Oxidation of S-e-carboxymethyl-selenocysteine by L-aminoacid oxidase and by D-aspartate oxidase. 0 3

1. A 25% faecal suspension in sodium chloride solution, incubated anaerobically at 37 degrees C for 48 h, showed excellent survival of all the main groups of faecal bacteria. 2. All faecal incubation systems studied generated large amounts of ammonia, particularly those in which bacterial counts fell during incubation. As normal faeces contain negligible amounts of urea this ammonia must have been generated from sources other than urea. 3. Ammonia was also generated by faeces delivered by sodium chloride enema, and by ileostomy fluid, indicating that the phenomenon is not confined to distal colonic contents. 4. Ammonia generation by incubated faeces was inhibited by prior autoclaving of the sample, but not by sterilization with gamma-irradiation. 5. Generation of ammonia by incubated stool was accompanied by release of large amounts of organic anion and a fall in pH. 6. These observations are interpreted as evidence that ammonia generated within the colon in situ is not derived exclusively from urea, but also from bacterial deamination of amino acids, peptides and proteins. Simultaneously bacterial activity generates large amounts of organacid. The presence of living bacteria is not essential for ammonia generation, provided that bacterial enzymes are present. 7. Bacterial generation of organic solute in faeces which have left the body is sufficiently rapid to cast serious doubts on the validity of faecal centrifugation, or other time-consuming techniques involving lengthy handling of faeces, as methods of obtaining extracellular faecal fluid for measurements of organic constituents or ammonia.
Clin Sci Mol Med 1976 Sep
PMID:Generation of ammonia from non-urea sources in a faecal incubation system. 0 21

High protein dietary content stimulates urea formation in ureotelic animals but does not exert almost any effect on ammonia production from L-amino acids in vitro. L-histidine and L-threonine are the only amino acids which are most actively deaminated by ureotelic animals fed on a high protein diet. All the steps of L-histidine metabolism have been studied: it has been found that both the histidine transaminase pathway and the histidase pathway are stimulated. Glutamic acid is also a product of histidine catabolism through the histidase pathway, but its catabolism is unaffected by the dietary protein content. These data suggest the existence of independent mechanism controlling the catabolism of the two amino acids.
Mol Cell Biochem 1979 Jan 26
PMID:Histidine degradation enzymes in rat liver: induction by high protein intake. 3 41

In Saccharomyces cerevisiae, the presence or absence of NADP-specific glutamate dehydrogenase does not affect inhibition of sporulation by ammonia, suggesting that the inhibition is not mediated by this enzyme.
Mol Gen Genet 1979 Oct 03
PMID:NADP-specific glutamate dehydrogenase is not involved in repression of yeast sporulation by ammonia. 4 57

Neurospora crassa can utilize various purine bases such as xanthine or uric acid and their catabolic products as a nitrogen source. Four classes of mutants which affect the purine degradative pathway were isolated and studied. Mutants of the aln-1 class specifically lack allantoinase, while alc-1 mutants lack allantoicase. Mutants designated as xdh-1 cannot utilize hypoxanthine as a nitrogen source and are presumed to be deficient in xanthine dehydrogenase activity. A regulatory mutant, amr, was found to have only very low, uninduced levels of uricase, allantoinase, and allantoicase. None of these genes are closely linked to each other. The three initial enzymes involved in the catabolism of uric acid are controlled in a complex manner by both induction and repression. Several lines of evidence indicate that the true inducer of uricase and allantoicase is uric acid. The use of the newly isolated mutant strains made it possible to demonstrate that neither allantoin nor allantoic acid could act as inducers. Furthermore, hypoxanthine itself was shown to be ineffective as an inducer although it can be metabolized to form an inducer. A non-metabolizable analogue of uric acid, 8-azaxanthine, is a gratuitous inducer of these enzymes. Uricase and allantoicase were found to be synthesized coordinately, but they were not coordinately regulated with allantoinase. Both uricase and allantoicase are stable enzymes and do not undergo turnover; nor are they subject to feedback inhibition by ammonia. Allantoinase, however, is quite labile both in vivo and in vitro. This enzyme was found to turnover in vivo in the presence of cycloheximide with a half-life of approximately 20 minutes. The amr (for ammonia regulation) mutant cannot utilize a wide range of compounds, including purines, nitrate, and many amino acids as a nitrogen source and also displays a multiple enzyme loss. The amr gene appears to play a major role in the control of nitrogen metabolism. It is postulated that the amr locus encodes a regulatory protein which is required to activate transcription of the structural genes for a group of related enzymes involved in nitrogen metabolism.
Mol Gen Genet 1975 Aug 05
PMID:Genetic and metabolic control of the purine catabolic enzymes of Neurospora crasse. 12 63

Wild type and mutant strains of Neurospora crassa excrete hypoxanthine, xanthine, and uric acid, but not adenine or inosine, when exogenous adenine is added to growing cultures. No detectable excretion occurs in the absence of adenine. The de novo pathway of purine biosynthesis was found to influence the excretion, in that a metabolic block immediately prior to IMP significantly decreased the excretion, while a metabolic block immediately after IMP significantly increased the excretion over that of wild type. The purine catabolic pathway, which is sensitive to ammonia regulation, was found to be a key determinant in the amount and type of excretion. Recently, it was suggested that hypoxanthine accumulation is the result of a mechanism to regulate the adenylate pool size (Leung and Schramm, 1978). In this report, the possibility that hypoxanthine excretion controls adenylate and guanylate pool sizes is discussed and the role of the purine nucleotide cycle in hypoxanthine excretion is examined.
Mol Gen Genet 1979 May 23
PMID:Role of purine base excretion in regulation of purine pools. 15 18

1. The distribution of ammonia between extra-and intra-cellular compartments of the brain was evaluated in anaesthetized rats exposed to sustained hyperammonaemia and superimposed acute hypo- or hyper-capnia. 2. It is concluded that the concentration gradient for ammonia between arterial plasma and cerebro-spinal fluid (CSF) cannot be explained by pH-dependent non-ionic diffusion of ammonia. A continuous uptake by the brain tissue of ammonia from the CSF is postulated and possible mechanisms are discussed.
Clin Sci Mol Med 1975 Jan
PMID:The distribution of ammonia between extracellular and intracellular compartments of the rat brain. 23 16

1. Ammonia and urea transport across the colonic mucosa was studied by a perfusion technique in four subjects with colonic exclusion for chronic hepatic encephalopathy. 2. Reduction of luminal pH inhibited net and unidirectional transport of ammonia from lumen to plasma, but net absorption from high luminal concentrations persisted at low pH. 3. Neither addition of urea to the perfusate nor intravenous infusion of urea produced a consistent increase in the colonic excretion of ammonia when ammonia-free solutions were perfused. 4. In one subject intravenous infusion of (15N)-ammonium chloride produced rapid labelling of colonic effluent ammonia and within 60 min the specific enrichments of ammonia in effluent and in arterial plasma were approximately equal. 5. During perfusion of nitrogen-free solutions, only small amounts of urea appeared in the effluent, suggesing limited permeability of the colonic mucosa to urea. 6. These results are discussed in relation to the equilibration of ammonia across the colonic mucosa by both ionic and non-ionic diffusion. The lack of evidence of 'juxtamucosal' (as opposed to luminal) ureolysis is in contrast to other observations on the intact colon. The possible reasons for and implications of this discrepancy are discussed.
Clin Sci Mol Med 1975 Apr
PMID:Ammonia and urea transport by the excluded human colon. 23 10

Two sheep with a ruminal fistula and an isolated small rumen were studied for the secretion of ammonia nitrogen, urea nitrogen, and amino nitrogen into the isolated rumen at different levels of volatile fatty acids (VFA) (50, 133-97, and 97-66 M Mol 1(-1)) in the rumen. The VFA level in the rumen was found to exert a great influence on the quantitative secretion of endogenous nitrogen from the blood through the rumen wall into rumen content. When the VFA level in the rumen was increased by administration of a single dose of acetic, propionic, and butyric acid, the secretion of ammonia nitrogen and amino nitrogen abruptly dropped and the secretion of urea into the isolated rumen slightly increased. The over-all amount of nitrogen (NH3-N + urea-N + amino-N) that had passed into the isolated rumen in the course of an hour showed a highly significant correlation with the passage of nitrogen in the form of ammonia and amino nitrogen and was greatest before the application of VFA to the rumen, i.e. at the level of 50 m mol 1-1. Of the metabolites under study, which were passing to the isolated rumen, amino nitrogen shared the greatest proportion (45.38-46.54%). When the VFA level in the rumen was raised, the proportion of ammonia secreted to the isolated rumen decreased and the proportion of urea in the total amount of nitrogen increased.
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PMID:[Relationship between the volatile fatty acids (VFA) in the rumen and nitrogen secretion into isolated sheep's rumen]. 41 43


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