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PubMed1997

Ammonia mediates communication between yeast colonies.

Under certain growth conditions unicellular organisms behave as highly organized multicellular structures. For example, the fruiting bodies of myxobacteria and of the slime mould Dictyostelium discoideum form structures composed of non-dividing motile cells. Although non-motile, yeasts can create organized structures, colonies in which cells communicate and act in a coordinated fashion. Colony morphologies are characteristic for different species and strains. Here we describe that, in addition to short-range intracolony cell-cell communication, yeasts exhibit long-distance signals between neighbouring colonies. The volatile alkaline compound ammonia, transmitted by yeast colonies in pulses, has been identified as a substance mediating the intercolony signal. The first alkaline pulse produced by neighbouring colonies is non-directed and is followed by acidification of the medium. The second pulse seems to be enhanced and is oriented towards the neighbour colony. Ammonia signalling results in growth inhibition of the facing parts of both colonies. This phenomenon is observed in different yeast genera. The presence of amino acids in the medium is required for ammonia production. Colonies derived from the yeast Saccharomyces cerevisiae shr3 mutant, defective in localization of amino-acid permeases, do not produce detectable amounts of ammonia and do not exhibit asymmetric growth inhibition.

Amino Acids↗
PubMed2004

Hydrogenation and cleavage of dinitrogen to ammonia with a zirconium complex.

Molecular nitrogen is relatively inert owing to the strength of its triple bond, nonpolarity and high ionization potential. As a result, the fixation of atmospheric nitrogen to ammonia under mild conditions has remained a challenge to chemists for more than a century. Although the Haber-Bosch process produces over 100 million tons of ammonia annually for the chemical industry and agriculture, it requires high temperature and pressure, in addition to a catalyst, to induce the combination of hydrogen (H2) and nitrogen (N2). Coordination of molecular nitrogen to transition metal complexes can activate and even rupture the strong N-N bond under mild conditions, with protonation yielding ammonia in stoichiometric and even catalytic yields. But the assembly of N-H bonds directly from H2 and N2 remains challenging: adding H2 to a metal-N2 complex results in the formation of N2 and metal-hydrogen bonds or, in the case of one zirconium complex, in formation of one N-H bond and a bridging hydride. Here we extend our work on zirconium complexes containing cyclopentadienyl ligands and show that adjustment of the ligands allows direct observation of N-H bond formation from N2 and H2. Subsequent warming of the complex cleaves the N-N bond at 45 degrees C, and continued hydrogenation at 85 degrees C results in complete fixation to ammonia.

Ammonia↗
PubMed2003

A passive sampling method to determine ammonia in ambient air.

Ambient ammonia concentrations, mainly originating from agricultural activities, have increased in the last few decades in Europe. As a consequence, critical loads on oligotrophic ecosystems such as forests and mires are greatly exceeded. Monitoring of ambient ammonia concentrations is necessary in order to investigate source-receptor relationships. Measuring ambient ammonia concentrations continuously with high time resolution is very expensive and cost-efficient systems are required. Where time resolution is of minor importance, several cost-effective systems, mainly dry denuder and passive samplers, can be applied. In this paper the Zürcher passive sampler, a diffusive sampling system, is presented. It is a Palmes type sampler with an acidic solution as absorbent and is easy to handle. It was tested at 46 sites in Switzerland over one year. The average concentration in ambient air was 2.5 microg m(-3) +/- 0.4 microg m(-3). The average of the blank values were 0.21 microg m(-3). The detection limit (double the standard deviation of the blank values) was 0.36 microg m(-3). Three passive samplers were exposed at each site and each period. The mean standard deviation of these triplicate measurements was 9.5%. Compared with a discontinuous tubular denuder system and a continuous annular denuder system, the deviation was less than 10%. The Zürcher passive sampler is a useful and cost-efficient tool to determine long-term average ammonia concentrations (one- to four-week periods) in ambient air for mean concentrations above 1 microg m(-3).

Agriculture↗
PubMed2004

The coordination chemistry of copper(I) in liquid ammonia, trialkyl and triphenyl phosphite, and tri-n-butylphosphine solution.

The coordination chemistry of the solvate complexes of the relatively soft electron-pair acceptor copper(I) has been studied in solution and solid state in seven solvents with strong electron-pair donor properties, liquid ammonia, trimethyl, triethyl, triisopropyl, tri-n-butyl and triphenyl phosphite, and tri-n-butylphosphine. The solvate complexes have been characterised by means of EXAFS and 63Cu NMR spectroscopy, and in some cases also by 65Cu NMR spectroscopy. The copper(I) ion is three-coordinated, most probably in a coplanar trigonal fashion, in liquid ammonia with a mean Cu-N bond distance of 2.00(1) Angstroms. No 63Cu NMR signal has been detected from the ammonia solvated copper(I) ion in liquid ammonia, which supports a three-coordination. The phosphite and phosphine solvated copper(I) ions are tetrahedral with Cu-P bond distances in the range 2.24-2.28 Angstrom in both solution and solid state as determined by EXAFS spectroscopy. The tetrahedral configuration of these complexes has been confirmed by 63Cu and 65Cu NMR spectroscopy through the J(63Cu-31P) and J(65Cu-31P) couplings. The fact that two of the investigated complexes, [Cu(P(OC6H5)3)4]+ and [Cu(P(C4H9)3)4]+, are 63Cu and 65Cu NMR silent is probably caused by a significantly angular distorted tetrahedral configuration.

Ammonia↗
PubMed1984

Potentiation by ammonia of the metabolic effects of pent-4-enoate in isolated rat hepatocytes.

The metabolic effects of pent-4-enoate were studied in isolated rat hepatocytes; 1 mM-pent-4-enoate did not significantly inhibit gluconeogenesis from lactate, alanine and glycerol, but significantly decreased glucose synthesis from pyruvate. The addition of 1 mM-NH4Cl led to a drastic inhibition of glucose synthesis from all these substrates. In hepatocytes incubated with 10 mM-alanine and 1 mM-oleate, pent-4-enoate at 0.05-1 mM slightly inhibited glucose synthesis and ketogenesis. The addition of ammonia resulted in a dramatic potentiation of the metabolic effects of pent-4-enoate. Half-maximum effect of ammonia was observed at 0.2 mM concentration. Concomitant cellular concentrations of ATP and acetyl-CoA were also decreased by the addition of ammonia, as were lactate/pyruvate ratio and beta-hydroxybutyrate/acetoacetate ratio. These data suggest that ammonia seriously interferes with the cellular metabolism of pent-4-enoate and leads to a dramatic potentiation of its effects.

Acetyl Coenzyme A↗
PubMed1985

Suicidal inactivation and labelling of ammonia mono-oxygenase by acetylene.

Acetylene brings about a progressive inactivation of ammonia mono-oxygenase, the ammonia-oxidizing enzyme in Nitrosomonas europaea. High NH4+ ion concentrations were protective. The inactivation followed first-order kinetics, with a rate constant of 1.5 min-1 at saturating concentrations of acetylene. If acetylene was added in the absence of O2, the cells remained active until O2 was re-introduced. A protective effect was also demonstrated with thiourea, a reversible non-competitive inhibitor of ammonia oxidation. Incubation of cells with [14C]acetylene was found to cause labelling of a single membrane polypeptide. This ran on dodecyl sulphate/polyacrylamide-gel electrophoresis with an Mr value of 28 000. It is concluded that acetylene is a suicide substrate for the mono-oxygenase. The labelling experiment provides the first identification of a constituent polypeptide of ammonia mono-oxygenase.

Acetylene↗
PubMed1975

The distribution of ammonia between extracellular and intracellular compartments of the rat brain.

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.

Ammonia↗
PubMed2000

A possible role of alanine for ammonia transfer between astrocytes and glutamatergic neurons.

The metabolism of [U-(13)C]lactate (1 mM) in the presence of unlabeled glucose (2.5 mM) was investigated in glutamatergic cerebellar granule cells, cerebellar astrocytes, and corresponding co-cultures. It was evident that lactate is primarily a neuronal substrate and that lactate produced glycolytically from glucose in astrocytes serves as a substrate in neurons. Alanine was highly enriched with (13)C in the neurons, whereas this was not the case in the astrocytes. Moreover, the cellular content and the amount of alanine released into the medium were higher in neurons than astrocytes. On incubation of the different cell types in medium containing alanine (1 mM), the astrocytes exhibited the highest level of accumulation. Altogether, these results indicate a preferential synthesis and release of alanine in glutamatergic neurons and uptake in cerebellar astrocytes. A new functional role of alanine may be suggested as a carrier of nitrogen from glutamatergic neurons to astrocytes, a transport that may operate to provide ammonia for glutamine synthesis in astrocytes and dispose of ammonia generated by the glutaminase reaction in glutamatergic neurons. Hence, a model of a glutamate-glutamine/lactate-alanine shuttle is presented. To elucidate if this hypothesis is compatible with the pattern of alanine metabolism observed in the astrocytes and neurons from cerebellum, the cells were incubated in a medium containing [(15)N]alanine (1 mM) and [5-(15)N]glutamine (0.5 mM), respectively. Additionally, neurons were incubated with [U-(13)C]glutamine to estimate the magnitude of glutamine conversion to glutamate. Alanine was labeled from [5-(15)N]glutamine to 3.3% and [U-(13)C]glutamate generated from [U-(13)C]glutamine was labeled to 16%. In spite of the modest labeling in alanine, it is clear that nitrogen from ammonia is transferred to alanine via transamination with glutamate formed by reductive amination of alpha-ketoglutarate. With regard to the astrocytic part of the shuttle, glutamine was labeled to 22% in one nitrogen atom whereas 3.2% was labeled in two when astrocytes were incubated in [(15)N]alanine. Moreover, in co-cultures, [U-(13)C]alanine labeled glutamate and glutamine equally, whereas [U-(13)C]lactate preferentially labeled glutamate. Altogether, these results support the role proposed above of alanine as a possible ammonia nitrogen carrier between glutamatergic neurons and surrounding astrocytes and they show that lactate is preferentially metabolized in neurons and alanine in astrocytes.

Alanine↗
PubMed2002

L-arginine reduces exercise-induced increase in plasma lactate and ammonia.

To investigate the effect of L-arginine supplementation (L-ARG) on physiological and metabolic changes during exercise, we determined in a double-blind study the cardiorespiratory (heart rate, oxygen consumption (VO(2)) and carbon dioxide production (VCO(2)) and the metabolic (lactate and ammonia) responses to maximal exercise after either an intravenous L-ARG hydrochloride salt or placebo load in 8 healthy subjects. Exercise-induced increases in heart rate, VO(2) and VCO(2) were not significantly different after L-ARG or placebo. By contrast, peak plasma ammonia and lactate were significantly decreased after L-ARG load (60.6 +/- 8.2 vs. 73.1 +/- 9.1 micro mol x l(-1), p < 0.01 and 7.1 +/- 0.7 vs. 8.2 +/- 1.1 mmol x l(-1), p < 0.01, for ammonia and lactate, respectively). Plasma L-citrulline increased significantly during exercise only after L-ARG load, despite a concomitant decrease in plasma L-ARG. Furthermore, a significant inverse relationship was observed between changes in lactate and L-citrulline concentrations after L-ARG load (r = -0.84, p = 0.009). These results demonstrate that intravenous L-ARG reduces significantly exercise-induced increase in plasma lactate and ammonia. Taken together, the specific L-citrulline increase and the inverse relationship observed between L-citrulline and plasma lactate after L-ARG might support that L-ARG supplementation enhances the L-arginine-nitric oxide (NO) pathway during exercise.

Adult↗
PubMed1990

Blood ammonia determination in a specific field test as a method supporting talent selection in runners.

Twenty-six male runners aged 14-16 years not yet specifically trained for sprint or middle-distance running performed a field test with distances of 25 m, 75 m, and 1000 m. Before the field test they were designated as sprinters (n = 19) and middle-distance runners (n = 7) according to their self-assessment and the estimation of the coaches. Blood ammonia and lactate concentrations were measured before and after the runs, and heart rates as well as the perceived exertion were evaluated. The most remarkable finding was a significantly higher ammonia increase in the supposed sprinters after 75 m compared with the supposed middle-distance runners. The ammonia concentrations after 1000 m were considerably less pronounced in both groups and did not differ significantly. The ratio of the ammonia concentration after the 75-m and the 1000-m distance was defined as an index. A high index was typical for designated sprinters, whereas a low index was found in supposed middle-distance runners. The combination of this index and the assessment of the coaches makes it possible to recommend special training regimens.

Adenine Nucleotides↗
PubMed1990

Medical implications of the lactate and ammonia relationship in anaerobic exercise.

The genesis of the modern ischemic forearm exercise test (IFET) employing the measurement of lactate and ammonia as countervailing metabolites is briefly reviewed, along with the application of the lactate ammonia exercise ratio in the diagnosis of myoadenylate deaminase deficiency and disorders of glycolysis and glycogenolysis. Two cases are presented to illustrate the response patterns elicited, their reproducibility, the types of parameters that can be quantified, and the role the IFET may play in the differential diagnosis of fitness failures. The role of the ammonia measurement is emphasized here because the lactate response is more familiar. The roles of hypoxanthine responses and of muscle ammonia measurements in the evaluation of cases are examined, and some pertinent and recently introduced analytic methods are cited. The applications of newer approaches, such as aspiration biopsy and N-14 NMR spectroscopy, are discussed, along with an example of the new clinical defects in enzymes and membrane carriers that should be anticipated during the utilization of the IFET.

AMP Deaminase↗
PubMed1995

Blood ammonia response to treadmill and bicycle exercise in man.

Nine male healthy and physically active volunteers performed four different exercise tests: an incremental load exercise test to exhaustion and a constant load exercise test of 15 min at 65% VO2max, both on the bicycle ergometer and on the treadmill. During the incremental exercise test, blood ammonia levels were significantly higher on the bicycle ergometer as compared to the treadmill at the same submaximal VO2 (p < 0.05 at 80% of VO2max) and at the VO2max, which was identical in the two modes of exercise. Plasma lactate levels were also significantly higher on bicycle ergometer at high submaximal exercise intensity but not at VO2max. During the constant load exercise test blood ammonia levels increased continuously and showed no differences between cycling and running, in contrast to plasma lactate accumulation, which was higher on the bicycle ergometer. The finding that blood ammonia accumulation during exercise is critically dependent upon the test procedure has to be taken into account whenever blood ammonia measurements are used in the physiological monitoring of athletes.

Adult↗
PubMed2001

Measurement of ammonia in blood.

The measurement of ammonia, now known to be a normal constituent of all body fluids, is fraught with problems. An elevated ammonia level in blood (100 micromol/L or higher) is an indicator of an abnormality in nitrogen homeostasis. The collection, handling, storage, and analysis of blood samples, their limitations, and potential sources of error are discussed. New techniques that permit continuous or real-time estimates of systemic ammonia levels over a broad range are also discussed. The aim should always be to minimize the release of ammonia from the collected sample before analysis. Recommendations are made on the collection and processing of blood samples, for it is by standardization and rigid adherence to these techniques that the reliability of the test results will be improved.

Ammonia↗
PubMed2006

Point mutations in the aromatic/arginine region in aquaporin 1 allow passage of urea, glycerol, ammonia, and protons.

Water-specific aquaporins (AQP), such as the prototypical mammalian AQP1, stringently exclude the passage of solutes, ions, and even protons. Supposedly, this is accomplished by two conserved regions within the pore, a pair of canonical asparagine-proline-alanine (NPA) motifs, the central constriction, and an aromatic/arginine (ar/R) constriction, the outer constriction. Here, we analyzed the function of three residues in the ar/R constriction (Phe-56, His-180, and Arg-195) in rat AQP1. Individual or joint replacement of His-180 and Arg-195 by alanine and valine residues, respectively (AQP1-H180A, AQP1-R195V, and AQP1-H180A/R195V), did not affect water permeability. The double mutant AQP1-H180A/R195V allowed urea to pass. In line with the predicted solute discrimination by size, replacement of both Phe-56 and His-180 (AQP1-F56A/H180A) enlarged the maximal diameter of the ar/R constriction 3-fold and enabled glycerol and urea to pass. We further show that ammonia passes through all four AQP1 mutants, as determined (i) by growth complementation of yeast deletion strains with ammonia, (ii) by ammonia uptake from the external solution into oocytes, and (iii) by direct recordings of ammonia induced proton currents in oocytes. Unexpectedly, removal of the positive charge in the ar/R constriction in AQP1-R195V and AQP1-H180A/R195V appeared to allow the passage of protons through AQP1. The data indicate that the ar/R constriction is a major checkpoint for solute permeability, and that the exquisite electrostatic proton barrier in AQPs comprises both the NPA constriction as well as the ar/R constriction.

Ammonia↗
PubMed2002

Carbamoyl-phosphate synthetase. Creation of an escape route for ammonia.

Carbamoyl-phosphate synthetase catalyzes the production of carbamoyl phosphate through a reaction mechanism requiring one molecule of bicarbonate, two molecules of MgATP, and one molecule of glutamine. The enzyme from Escherichia coli is composed of two polypeptide chains. The smaller of these belongs to the Class I amidotransferase superfamily and contains all of the necessary amino acid side chains required for the hydrolysis of glutamine to glutamate and ammonia. Two homologous domains from the larger subunit adopt conformations that are characteristic for members of the ATP-grasp superfamily. Each of these ATP-grasp domains contains an active site responsible for binding one molecule of MgATP. High resolution x-ray crystallographic analyses have shown that, remarkably, the three active sites in the E. coli enzyme are connected by a molecular tunnel of approximately 100 A in total length. Here we describe the high resolution x-ray crystallographic structure of the G359F (small subunit) mutant protein of carbamoyl phosphate synthetase. This residue was initially targeted for study because it resides within the interior wall of the molecular tunnel leading from the active site of the small subunit to the first active site of the large subunit. It was anticipated that a mutation to the larger residue would "clog" the ammonia tunnel and impede the delivery of ammonia from its site of production to the site of utilization. In fact, the G359F substitution resulted in a complete change in the conformation of the loop delineated by Glu-355 to Ala-364, thereby providing an "escape" route for the ammonia intermediate directly to the bulk solvent. The substitution also effected the disposition of several key catalytic amino acid side chains in the small subunit active site.

Adenosine Triphosphate↗
PubMed2005

Acute insult of ammonia leads to calcium-dependent glutamate release from cultured astrocytes, an effect of pH.

Hyperammonemia is a key factor in the pathogenesis of hepatic encephalopathy (HE) as well as other metabolic encephalopathies, such as those associated with inherited disorders of urea cycle enzymes and in Reye's syndrome. Acute HE results in increased brain ammonia (up to 5 mM), astrocytic swelling, and altered glutamatergic function. In the present study, using fluorescence imaging techniques, acute exposure (10 min) of ammonia (NH4+/NH3) to cultured astrocytes resulted in a concentration-dependent, transient increase in [Ca2+]i. This calcium transient was due to release from intracellular calcium stores, since the response was thapsigargin-sensitive and was still observed in calcium-free buffer. Using an enzyme-linked fluorescence assay, glutamate release was measured indirectly via the production of NADH (a naturally fluorescent product when excited with UV light). NH4+/NH3 (5 mM) stimulated a calcium-dependent glutamate release from cultured astrocytes, which was inhibited after preincubation with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester but unaffected after preincubation with glutamate transport inhibitors dihydrokainate and DL-threo-beta-benzyloxyaspartate. NH4+/NH3 (5 mM) also induced a transient intracellular alkaline shift. To investigate whether the effects of NH4+/NH3 were mediated by an increase in pH(i), we applied trimethylamine (TMA+/TMA) as another weak base. TMA+/TMA (5 mM) induced a similar transient increase in both pH(i) and [Ca2+]i (mobilization from intracellular calcium stores) and resulted in calcium-dependent release of glutamate. These results indicate that an acute exposure to ammonia, resulting in cytosolic alkalinization, leads to calcium-dependent glutamate release from astrocytes. A deregulation of glutamate release from astrocytes by ammonia could contribute to glutamate dysfunction consistently observed in acute HE.

Adenosine Triphosphate↗
PubMedDate not supplied

Efficacy and permanency of ammonia treatment in reducing aflatoxin levels in corn.

Naturally contaminated yellow corn containing 12500 ng/g of aflatoxin B1 (AFB1) was ground and blended with non-contaminated corn to obtain various levels of AFB1 (7500, 6300, 400, 354, and 17 ng AFB1/g). All samples were exposed to ammonia treatment under various conditions for 60 min. Treatment variables included ammonia concentration, moisture level of the corn, temperature, and pressure applied. The moisture content of the corn (8%) was adjusted to 12% and 16%, respectively. Four ammonia treatments were conducted for each moisture level: (a) 1.5% and 2.0% gaseous NH3 at 40-45 degrees C and 55 psi; (b) aqueous NH4OH (2.0% as NH3) at 121 degrees C and 17 psi; (c) sequential treatment of (a) and (b); and (d) aqueous NH4OH (2.0% as NH3) at 25 degrees C and 55 psi. For the treatment with 2% gaseous NH3, the reduction in levels of AFB1 in samples containing 12% moisture ranged from 52.7 to 67.7%, while in samples containing 16% moisture, the reduction ranged from 79.4 to 93.1%. Treatment with NH4OH alone at elevated temperatures (b) or following gaseous NH3 treatment (c) resulted in a reduction of the AFB1 content by greater than 99%. Treatment with NH4OH at 25 degrees C (d) showed a lower efficiency in reducing AFB1 levels. The permanency of the process, i.e. reversion of inactivated AFB1 to the parent compound, was studied by exposing the ammonia-treated corn to HCl (pH = 2.0 at 37 degrees C for 2 h) to simulate stomach acidity. The results showed no significant reversion of aflatoxin (reversibility less than 0.05%). These findings suggest that at high temperature aqueous NH4OH or gaseous NH3 can be used effectively to reduce AFB1 in corn. The present study also revealed that the moisture level of the product and holding temperature were the crucial factors that influenced the efficacy of aflatoxin decontamination by ammoniation.

Aflatoxins↗
PubMed2001

A pre- and post-denitrification system treating a very high ammonia landfill leachate: effects of pH change on process performance.

The prime objective of this research was to investigate the nitrogen removal capabilities of a pre- and post-denitrification process, when treating landfill leachate containing an ammonia concentration of over 2,200 mg N l(-1). The treatment system, also known as a 4-Stage Bardenpho process, was operated with an external recycle ratio of 3:1 and an internal recycle ratio of 4:1. The first anoxic reactor actual hydraulic retention time was 1.5 hours, while the first aerobic retention time was 3 hours. The very high ammonia concentration was simulated by pumping ammonium chloride into the first anoxic reactor of the system. Methanol was used as the organic carbon source for denitrification. At an influent ammonia concentration of about 2,200 mg N l(-1), the anoxic pH levels stabilized at about 8.6 within the first reactor, and at about 9.8 within the second reactor. These high anoxic pH levels were partially responsible for decreased denitrification and, hence, residual NO concentrations in the effluent. By decreasing the pH in the anoxic basins, the overall performance of the system immediately improved; the effluent NOx concentration decreased rapidly over a period of about six days, from an average 80 mg N l(-1) to about 60 mg N l(-1), with some samples as low as 40 mg N l(-1). Subsequently, increased leachate toxicity resulted in an unexpected system failure; although the treatment system eventually recovered and stabilized, denitrification in each anoxic reactor remained at only about 55%, with final effluent NOx concentrations of over 100 mg N l(-1). Despite this reduced level of performance, the decrease in anoxic pH resulted in enhanced nitrification performance, complete ammonia removal in the first aerobic reactor, and a more stable, overall performance in the 4-Stage Bardenpho process.

Ammonia↗