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PubMed2003

Nitrification with high nitrite accumulation for the treatment of wastewater with high ammonia concentration.

The objective of this paper was to determine the best conditions for partial nitrification with nitrite accumulation of simulated industrial wastewater with high ammonia concentration, lowering the total oxygen needed in the nitrification step, which may mean great saving in aeration. Dissolved oxygen (DO) concentration and pH were selected as operational parameters to study the possibility of nitrite accumulation not affecting overall ammonia removal. A 2.5L activated sludge reactor was operated in nitrification mode, feeding a synthetic wastewater simulating an industrial wastewater with high ammonia concentration. During the start-up a pH of 7.85 and a DO of 5.5mg/L were used. The reactor was operated until stable operation was achieved at final nitrogen loading rate (NLR) of 3.3kgN- NH(4)(+)/m(3)d with an influent ammonia concentration of 610mg N-NH(4)(+)/L. The influence of pH was studied in continuous operation in the range of 6.15-9.05, changing the reactor pH in steps until ammonia accumulation (complete nitrification inhibition) took place. The influence of DO was studied in the same mode, changing the DO in steps from 5.5 to 0.5mg/L. The pH was not a useful operational parameter in order to accumulate nitrite, because in the range of pH 6.45-8.95 complete nitrification to nitrate occurs. At pH lower than 6.45 and higher than 8.95 complete inhibition of nitrification takes place. Setting DO concentration in the reactor at 0.7mg/L, it was possible to accumulate more than 65% of the loaded ammonia nitrogen as nitrite with a 98% ammonia conversion. Below 0.5mg/L of DO ammonia was accumulated and over a DO of 1.7mg/L complete nitrification to nitrate was achieved. In conclusion, it is possible under the conditions of this study, to treat high ammonia synthetic wastewater achieving an accumulation of at least 65% of the loaded nitrogen as nitrite, operating at a DO around 0.7mg/L. This represents a reduction close to 20% in the oxygen necessary, and therefore a considerable saving in aeration.

Ammonia↗
PubMed2003

Removal of ammonia solutions used in catalytic wet oxidation processes.

Ammonia (NH(3)) is an important product used in the chemical industry, and is common place in industrial wastewater. Industrial wastewater containing ammonia is generally either toxic or has concentrations or temperatures such that direct biological treatment is unfeasible. This investigation used aqueous solutions containing more of ammonia for catalytic liquid-phase oxidation in a trickle-bed reactor (TBR) based on Cu/La/Ce composite catalysts, prepared by co-precipitation of Cu(NO(3))(2), La(NO(3))(2), and Ce(NO(3))(3) at 7:2:1 molar concentrations. The experimental results indicated that the ammonia conversion of the wet oxidation in the presence of the Cu/La/Ce composite catalysts was determined by the Cu/La/Ce catalyst. Minimal ammonia was removed from the solution by the wet oxidation in the absence of any catalyst, while approximately 91% ammonia removal was achieved by wet oxidation over the Cu/La/Ce catalyst at 230 degrees C with oxygen partial pressure of 2.0 MPa. Furthermore, the effluent streams were conducted at a liquid hourly space velocity of under 9 h(-1) in the wet catalytic processes, and a reaction pathway was found linking the oxidizing ammonia to nitric oxide, nitrogen and water. The solution contained by-products, including nitrates and nitrites. Nitrite selectivity was minimized and ammonia removal maximized when the feed ammonia solution had a pH of around 12.0.

Ammonia↗
PubMed1988

Adrenergic control of the glucagon response to ammonia in the perfused rat pancreas.

The isolated perfused rat pancreas was used to investigate how adrenergic influences within the pancreas might mediate ammonia-induced glucagon secretion. The addition of 2 mM ammonia to the perfusate increased norepinephrine release and glucagon secretion in the effluent. Upon cessation of ammonia addition, a pronounced burst of glucagon release was observed. Alpha-adrenergic blockade with phentolamine (10 microM) blocked the glucagon response to ammonia. Beta-adrenergic blockade with propranolol (10 microM) had no significant effect on the amount of glucagon release induced by ammonia. Depletion of norepinephrine from sympathetic nerve terminals by pretreatment with 6-hydroxydopamine lowered the pancreatic norepinephrine content to less than 16% of the control value and diminished the glucagon and norepinephrine response to ammonia almost completely. The burst of glucagon release after the removal of ammonia was inhibited to 2% of the control value by phentolamine and to 57% by propranolol. Pretreatment with 6-hydroxydopamine reduced the burst of glucagon secretion to 28% of the control value. Neither phentolamine nor propranolol reduced the magnitude of the ammonia-induced suppression of insulin secretion. We conclude that the effect of ammonia on glucagon release from the isolated rat pancreas is mediated by intrapancreatic adrenergic control.

Ammonia↗
PubMed1989

Ammonia production and secretion by the proximal tubule.

Ammonia production and secretion by the proximal tubule accounts for most of the ammonia that appears in the urine. Rates of ammonia production and net luminal ammonia secretion were measured in isolated perfused mouse proximal tubule segments. This approach combines the in vitro microperfusion technique with a sensitive bioluminescence assay for total ammonia and permits the determination of ammonia production and secretion rates in specific proximal tubule segments bathed and perfused with defined solutions. Luminal perfusion stimulates ammonia production by proximal tubule segments in a flow-related manner. The effect of perfusion is not dependent on intact Na+-H+ exchange. In contrast, the rate of net luminal secretion of ammonia is largely dependent on Na+-H+ exchange but not markedly dependent on an acid luminal fluid pH. These results suggest an important role of Na+-NH4+ exchange in the mechanism by which the Na+-H+ exchanger facilitates net ammonia secretion.

Ammonia↗
PubMed2000

Long-term results of ammonia removal and transformation by biofiltration.

In this paper, long-term (>8 month) results of ammonia removal in biofilters was studied. Compost was used as the biofilter medium and activated carbon as an added material. The ammonia removal was normally >95% at influent ammonia concentrations of 20-500ppmv. According to the test results, the influent ammonia concentration should be <200ppmv (0.1570g ammonia/kg media per day) so that the effluent concentration of ammonia is <1.0mg/m(3) (the emission standard of China), and the biofiltration system can achieve good long-term performance. In the biofiltration system utilized in this study, the shortest retention time that the system could attain was 0.532min. However, the retention time can be decreased further without decreasing the ammonia removal efficiency. Countercurrent flow is favorable, as it enhances the moisture retention ability of the media. In the bioreactors, ammonia can be converted into the nitrate. The bioreactors have a stratification phenomenon for ammonia removal over the biofiltration depth, which implies that different parts of the bioreactor play different roles in the ammonia removing process.

Air Pollution↗
PubMed1999

Effects of ammonia in vitro on endogenous taurine efflux and cell volume in rat cerebrocortical minislices: influence of inhibitors of volume-sensitive amino acid transport.

Rat cerebrocortical minislices were incubated with physiological saline in the absence or presence of 5 mM ammonium acetate ("ammonia") and/or inhibitors of osmosensitive amino acid transport: 50 microM niflumic acid and 100 microM N-ethyl-maleimide for 60 min, with medium changes after 20 min and 40 min. The efflux of endogenous taurine, glutamate and glutamine was assayed by high-performance liquid chromatography, and steady-state cell volumes were monitored in the slices with the [14C]inulin method. In the absence of ammonia, niflumic acid abolished taurine efflux but did not affect glutamate or glutamine efflux at all time-points, and increased cell volume at 20 min and 60 min. N-Ethyl-maleimide increased taurine, glutamine and glutamate efflux at 20 min and 40 min, inhibited taurine and glutamine efflux at 60 min, and increased cell volume at 20 min. Ammonia strongly stimulated taurine (by 380% at 20 min), and only moderately glutamate (30% at 20 min) or glutamine efflux (76% at 20 min). Ammonia increased cell volume above the control level at all time-points. Niflumic acid inhibited, but did not abolish ammonia-dependent taurine and glutamine efflux, and did not change glutamate efflux. The effects of ammonia + niflumic acid on cell volume did not differ from the effects of each compound separately. N-Ethyl-maleimide inhibited ammonia-dependent efflux of all three amino acids except for stimulation of glutamate efflux at 20 min. N-Ethyl-maleimide + ammonia decreased the cell volumes more than did each compound separately. It is concluded that although ammonia-induced taurine efflux is accompanied by an increase in cell volume, the underlying mechanism is not simply a cell volume regulatory response normally observed in hypoosmotic stress. Increased efflux of taurine, which is an inhibitory amino acid and a cell membrane protectant, may serve to counteract the deleterious effects of increased excitatory transmission accompanying acute hyperammonemic insult.

Ammonia↗
PubMed1999

13N-ammonia myocardial blood flow and uptake: relation to functional outcome of asynergic regions after revascularization.

OBJECTIVES: In this study we determined whether 13N-ammonia uptake measured late after injection provides additional insight into myocardial viability beyond its value as a myocardial blood flow tracer. BACKGROUND: Myocardial accumulation of 13N-ammonia is dependent on both regional blood flow and metabolic trapping. METHODS: Twenty-six patients with chronic coronary artery disease and left ventricular dysfunction underwent prerevascularization 13N-ammonia and 18F-deoxyglucose (FDG) positron emission tomography, and thallium single-photon emission computed tomography. Pre- and postrevascularization wall-motion abnormalities were assessed using gated cardiac magnetic resonance imaging or gated radionuclide angiography. RESULTS: Wall motion improved in 61 of 107 (57%) initially asynergic regions and remained abnormal in 46 after revascularization. Mean absolute myocardial blood flow was significantly higher in regions that improved compared to regions that did not improve after revascularization (0.63+/-0.27 vs. 0.52+/-0.25 ml/min/g, p < 0.04). Similarly, the magnitude of late 13N-ammonia uptake and FDG uptake was significantly higher in regions that improved (90+/-20% and 94+/-25%, respectively) compared to regions that did not improve after revascularization (67+/-24% and 71+/-25%, p < 0.001 for both, respectively). However, late 13N-ammonia uptake was a significantly better predictor of functional improvement after revascularization (area under the receiver operating characteristic [ROC] curve = 0.79) when compared to absolute blood flow (area under the ROC curve = 0.63, p < 0.05). In addition, there was a linear relationship between late 13N-ammonia uptake and FDG uptake (r = 0.68, p < 0.001) as well as thallium uptake (r = 0.76, p < 0.001) in all asynergic regions. CONCLUSIONS: These data suggest that beyond its value as a perfusion tracer, late 13N-ammonia uptake provides useful information regarding functional recovery after revascularization. The parallel relationship among 13N-ammonia, FDG, and thallium uptake supports the concept that uptake of 13N-ammonia as measured from the late images may provide important insight regarding cell membrane integrity and myocardial viability.

Adult↗
PubMed1999

Blocking NMDA receptors prevents the oxidative stress induced by acute ammonia intoxication.

Acute ammonia intoxication diminishes the activities of antioxidant enzymes and increases superoxide formation in brain. These effects could play a role in the mechanism of ammonia toxicity. It has been shown that ammonia toxicity is mediated by activation of NMDA receptors. The aim of this work was to assess whether ammonia-induced changes in antioxidant enzymes and in superoxide formation are mediated by activation of NMDA receptors. It is shown that MK-801, an antagonist of NMDA receptors prevents ammonia-induced changes in superoxide dismutase, glutathione peroxidase and catalase. Ammonia intoxication also induces a depletion of glutathione and an increase in lipid peroxidation. Both effects, as well as ammonia-induced increase in superoxide formation are prevented by MK-801. These results indicate that ammonia-induced oxidative stress in brain is mediated by excessive activation of NMDA receptors and support the idea that oxidative stress can play a role in the mechanism of ammonia toxicity.

Acute Disease↗
PubMed2002

Reactivity differences of indomethacin solid forms with ammonia gas.

The present study deals with the acid-base reaction of three solid-state forms of the nonsteroidal antiinflammatory drug indomethacin with ammonia gas. X-ray powder diffraction, optical microscopy, gravimetry, and spectroscopic methods were employed to establish the extent of the reaction as well as the lattice changes of the crystal forms. The glassy amorphous form readily reacts with ammonia gas to yield a corresponding amorphous ammonium salt. In addition, the metastable crystal form of indomethacin (the alpha-form) also reacts with ammonia gas, but produces the corresponding microcrystalline ammonium salt. This reaction is anisotropic and propagates along the a-axis of the crystals. The stable crystal form (the gamma-form), however, is inert to ammonia gas. Amorphous indomethacin can react with ammonia gas because it has more molecular mobility and free volume. The reactivity differences between the alpha- and gamma-forms are dictated by the arrangement of the molecules within the respective crystal lattices. The recently determined crystal structure of the metastable alpha-form of indomethacin (monoclinic P2(1) with Z = 6, V = 2501.8 A(3), D(c) = 1.42 g.cm(-3)) has three molecules of indomethacin in the asymmetric unit. Two molecules form a mutually hydrogen-bonded carboxylic acid dimer, while the carboxylic acid of the third molecule is hydrogen bonded to one of the amide carbonyls of the dimer. The carboxylic acid groups of the alpha-form are exposed on the [100] faces and are accessible to attack by ammonia gas. After one layer of molecules reacts, the reactive groups in the subsequent layer are accessible to the ammonia gas. This process proceeds along the a-axis until the ammonia gas has penetrated the entire crystal. In contrast to the alpha-form, the gamma-form has a centrosymmetric crystal structure in which the hydrogen-bonded carboxylic acid dimers are not accessible to ammonia gas because they are caged inside a hydrophobic shield comprising the remainder of the indomethacin molecule. In view of the significantly lower density of the stable gamma-form as compared to the metastable alpha-form (1.37 and 1.42 g cm(-3), respectively), it became apparent that the reactivity of the crystal forms depends exclusively on the molecular arrangement and not on the packing density of the indomethacin crystals.

Ammonia↗
PubMed2007

Investigation of proton transport tautomerism in clusters of protonated nucleic acid bases (cytosine, uracil, thymine, and adenine) and ammonia by high-pressure mass spectrometry and ab initio calculations.

The energetics of the ion-molecule interactions and structures of the clusters formed between protonated nucleic acid bases (cytosine, uracil, thymine, and adenine) and ammonia have been studied by pulsed ionization high-pressure mass spectrometry (HPMS) and ab initio calculations. For protonated cytosine, uracil, thymine, and adenine with ammonia, the measured enthalpies of association with ammonia are -21.7, -27.9, -22.1, and -17.5 kcal mol-1, respectively. Different isomers of the neutral and protonated nucleic acid bases as well as their clusters with ammonia have been investigated at the B3LYP/6-31+G(d,p) level of theory, and the corresponding binding energetics have also been obtained. The potential energy surfaces for proton transfer and interconversion of the clusters of protonated thymine and uracil with ammonia have been constructed. For cytosine, the experimental binding energy is in agreement with the computed binding energy for the most stable isomer, CN01-01, which is derived from the enol form of protonated cytosine, CH01, and ammonia. Although adenine has a proton affinity similar to that of cytosine, the binding energy of protonated adenine to ammonia is much lower than that for protonated cytosine. This is shown to be due to the differing types of hydrogen bonds being formed. Similarly, although uracil and thymine have similar structures and proton affinities, the binding energies between the protonated species and ammonia are different. Strikingly, the addition of a single methyl group, in going from uracil to thymine, results in a significant structural change for the most stable isomers, UN01-01 and TN03-01, respectively. This then leads to the difference in their measured binding energies with ammonia. Because thymine is found only in DNA while uracil is found in RNA, this provides some potential insight into the difference between uracil and thymine, especially their interactions with other molecules.

Adenine↗
PubMed2001

Gaseous NO2 as a regulator for ammonia oxidation of Nitrosomonas eutropha.

Cells of Nitrosomonas eutropha strain N904 that were denitrifying under anoxic conditions with hydrogen as electron donor and nitrite as electron acceptor were unable to utilize ammonium (ammonia) as an energy source. The recovery of ammonia oxidation activity was dependent on the presence of NO2. Anaerobic ammonia oxidation activity was observed in a helium atmosphere supplemented with 25 ppm NO2 after 20 h. Ammonia oxidation activity was detected after 2-3 days using an oxic atmosphere with 25 ppm NO2. In contrast, ammonia consumption started after 8-9 days under oxic conditions without the addition of NO2; in this case, small amounts of NO and NO2 were detected and their concentrations increased with increasing ammonia oxidation activities. Hardly any ammonia oxidation was detected when nitrogen oxides were removed by intensive aeration. It would seem, therefore, that NO2 is the master regulatory signal for ammonia oxidation in Nitrosomonas eutropha. Anaerobic ammonia oxidation activity was inhibited by the addition of NO. This inhibition was partly compensated by either increasing the NO2 concentration or by using 2,3-dimercapto-1-propane-sulfonic acid as a NO binding substrate. DMPS was inhibitory to nitrification under oxic conditions, while increased amounts of NO or NO2 led to increased oxidation activities.

Aerobiosis↗
PubMed2000

Inhibiting effect of ammonia on citric acid-induced cough in pigs: a possible involvement of substance P.

The effect of ammonia on the cough response to citric acid and on substance P release from C-fibers involved in this reflex was assessed. For a period from one to four days, piglets were exposed, in an inhalation chamber, to ammonia at a concentration of 15 or 30 ppm. During exposure, cough induction tests were done every two days. Recovery of the cough reflex after ammonia exposure was also determined. In a separate group of piglets exposed for 2 days to 30 ppm ammonia, substance P content was determined in bronchial and tracheal lavage fluids and in the tracheal and bronchial mucosa. Ammonia (30 ppm) was found to inhibit coughing significantly (the cough frequency was reduced by 64%) after a two-day exposure. In animals exposed for 4 days to this ammonia concentration, the recovery ranged from 3 to 7 days (mean: 5 days). The same ammonia concentration also caused the substance P content to increase significantly in bronchoalveolar lavage fluid (to 432% of its initial value) and tracheal lavage fluid (to 149%) and to decrease significantly in the tracheal mucosa (-58%), however the content in bronchial mucosa was not significantly affected (-43%). Exposure to 15 ppm ammonia had no effect on the frequency of citric acid-induced coughing. In conclusion, ammonia inhibits citric acid-induced coughing in pigs at concentrations that can be detected in piggeries. This inhibitory effect may be related to substance-P depletion in C-fiber endings.

Ammonia↗
PubMed1994

Renal ammonia in autosomal dominant polycystic kidney disease.

Recent studies have suggested that defective medullary trapping of ammonia underlies the acidosis associated with renal failure and sets in motion maladaptive compensatory mechanisms that contribute to the progression of renal disease. Since a renal concentrating defect is an early functional abnormality in autosomal dominant polycystic kidney disease (ADPKD), defective medullary trapping and urinary excretion of ammonia may also occur early and have important pathophysiological consequences. The urinary pH and excretions of ammonia, titratable acid, and bicarbonate, were measured during a 24-hour baseline period and following the administration of ammonium chloride (100 mg/kg body wt) in ADPKD patients with normal glomerular filtration rate and in age- and gender-matched healthy control subjects. The distal nephron hydrogen ion secretory capacity was assessed during a bicarbonate infusion. Ammonia, sodium, pH, C3dg, and C5b-9 were measured in cyst fluid samples. The excretion rates of ammonia during the 24-hour baseline period and following the administration of ammonium chloride were significantly lower, and the relationship of ammonia excretion to urinary pH was significantly shifted downward in ADPKD. No difference in the increment of urinary pCO2 (delta pCO2) or the peripheral blood-urine pCO2 gradient (U-B pCO2) between ADPKD patients and control subjects was detected during a sodium bicarbonate infusion. Calculated concentrations of free-base ammonia in cyst fluid samples exceeded those calculated from reported concentrations of ammonia in renal venous blood of normal subjects. C3dg and C5b-9 were detected in some cyst fluids. The urinary excretion of ammonia is reduced in ADPKD patients with normal glomerular filtration rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1990

Metabolism of branched-chain amino acids and ammonia during exercise: clues from McArdle's disease.

Patients with McArdle's disease (myophosphorylase deficiency) cannot use muscle glycogen as an energy source during exercise. They therefore are an ideal model to learn about the metabolic adaptations which develop during endurance exercise leading to glycogen depletion. This review summarizes the current knowledge of ammonia and amino acid metabolism in these patients and also adds several new data. During incremental exercise tests in patients with McArdle's disease, forearm venous plasma ammonia concentration rises to a value between 200 and 500 microM. Femoral arteriovenous difference studies show that muscle produces the ammonia. The leg release of both ammonia and glutamine (in mumol/min) has been estimated to be five- to tenfold larger in one of these patients than in healthy individuals exercising at comparable relative work load. Patients with McArdle's disease have a larger uptake of branched-chain amino acids (BCAA) by exercising leg muscles and show a more rapid activation of the muscle branched-chain 2-oxo acid dehydrogenase complex, a key enzyme in the degradation of the BCAA. In general, supplements of BCAA taken before the exercise test lead to a deterioration of exercise performance and a higher increase in heart rate and plasma ammonia during exercise, whereas supplements of branched-chain 2-oxo acids improve exercise performance and lead to a smaller increase in heart rate and plasma ammonia. At constant power output, patients with McArdle's disease show a rapid increase in heart rate and exertion perceived in the exercising muscles, which peak within 10 min after the start of exercise and then fall again ("second wind"). Peak heart rate and peak exertion coincide with a peak in plasma ammonia. Ammonia production during exercise in these patients is estimated to exceed the reported breakdown of ATP to IMP and therefore most likely originates from the metabolism of amino acids. Deamination of amino acids via the reactions of the purine nucleotide cycle and glutamate dehydrogenase are possible pathways. Deamination of glutamine, released by muscle, by glutaminase present in the endothelial cells of the vascular system may also contribute to the ammonia production. The observations made in these patients have led to the hypothesis that excessive acceleration of the metabolism of BCAA drains 2-oxoglutarate in the primary aminotransferase reaction and thus reduces flux in the citric acid cycle and impedes aerobic oxidation of glucose and fatty acids. This draining effect is normally counteracted by the anaplerotic conversion of muscle glycogen to citric acid cycle intermediates, a reaction which is severely hampered in these patients due to the glycogen breakdown defect.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acids, Branched-Chain↗
PubMed2001

Correlation of breath ammonia with blood urea nitrogen and creatinine during hemodialysis.

We have spectroscopically determined breath ammonia levels in seven patients with end-stage renal disease while they were undergoing hemodialysis at the University of California, Los Angeles, dialysis center. We correlated these measurements against simultaneously taken blood samples that were analyzed for blood urea nitrogen (BUN) and creatinine, which are the accepted standards indicating the level of nitrogenous waste loading in a patient's bloodstream. Initial levels of breath ammonia, i.e., at the beginning of dialysis, are between 1,500 ppb and 2,000 ppb (parts per billion). These levels drop very sharply in the first 15-30 min as the dialysis proceeds. We found the reduction in breath ammonia concentration to be relatively slow from this point on to the end of dialysis treatment, at which point the levels tapered off at 150 to 200 ppb. For each breath ammonia measurement, taken at 15-30 min intervals during the dialysis, we also sampled the patient's blood for BUN and creatinine. The breath ammonia data were available in real time, whereas the BUN and creatinine data were available generally 24 h later from the laboratory. We found a good correlation between breath ammonia concentration and BUN and creatinine. For one of the patients, the correlation gave an R(2) of 0.95 for breath ammonia and BUN correlation and an R(2) of 0.83 for breath ammonia and creatinine correlation. These preliminary data indicate the possibility of using the real-time breath ammonia measurements for determining efficacy and endpoint of hemodialysis.

Ammonia↗
PubMed2000

Restricted passage of reaction intermediates through the ammonia tunnel of carbamoyl phosphate synthetase.

The x-ray crystal structure of the heterodimeric carbamoyl phosphate synthetase from Escherichia coli has identified an intermolecular tunnel that connects the glutamine binding site within the small amidotransferase subunit to the two phosphorylation sites within the large synthetase subunit. The tunneling of the ammonia intermediate through the interior of the protein has been proposed as a mechanism for the delivery of the ammonia from the small subunit to the large subunit. A series of mutants created within the ammonia tunnel were prepared by the placement of a constriction via site-directed mutagenesis. The degree of constriction within the ammonia tunnel of these enzymes was found to correlate to the extent of the uncoupling of the partial reactions, the diminution of carbamoyl phosphate formation, and the percentage of the internally derived ammonia that is channeled through the ammonia tunnel. NMR spectroscopy and a radiolabeled probe were used to detect and identify the enzymatic synthesis of N-amino carbamoyl phosphate and N-hydroxy carbamoyl phosphate from hydroxylamine and hydrazine. The kinetic results indicate that hydroxylamine, derived from the hydrolysis of gamma-glutamyl hydroxamate, is channeled through the ammonia tunnel to the large subunit. Discrimination between the passage of ammonia and hydroxylamine was observed among some of these tunnel-impaired enzymes. The overall results provide biochemical evidence for the tunneling of ammonia within the native carbamoyl phosphate synthetase.

Binding Sites↗
PubMed2003

Effect of ammonia on Na+ transport across isolated rumen epithelium of sheep is diet dependent.

The cellular uptake of ammonia affects the intracellular pH (pHi) of polar and non-polar cells. A predominant uptake of NH3 and its intracellular protonation tend to alkalinise the cytoplasm, whereas a predominant uptake of NH4(+) acidifies the cytoplasm by reversing this reaction. Hence, the well-known absorption of ammonia across the rumen epithelium probably causes a change in the pHi. The magnitude and direction of this change in pHi (acid or alkaline) depends on the relative transport rates of NH3 and NH4(+). Consequently, the intracellular availability of protons will influence the activity of the Na(+)-H(+) exchanger, which could affect transepithelial Na(+) transport. The aim of the present study has been to test this possible interaction between ruminal ammonia concentrations and Na(+) transport. The term ammonia is used to designate the sum of the protonated (NH4(+)) and unprotonated (NH3) forms. Isolated ruminal epithelium of sheep was investigated by using the Ussing-chamber technique in vitro. The present results indicate that ammonia inhibits Na(+) transport across the rumen epithelium of hay-fed sheep, probably by binding intracellular protons and thus inhibiting Na(+)-H(+) exchange. By contrast, ammonia stimulates Na(+) transport in concentrate-fed and urea-fed sheep, which develop an adaptation mechanism in the form of an increased metabolism of ammonia in the rumen mucosa and/or an increased permeability of rumen epithelium to the charged ammonium ion (NH4(+)). Intracellular dissociation of NH4(+) increases the availability of protons, which stimulate Na(+)-H(+) exchange. This positive effect of ruminal ammonia on Na(+) absorption may significantly contribute to the regulation of osmotic pressure of the ruminal fluid, because intraruminal ammonia concentrations up to 40 mmol/l have been reported.

Ammonia↗
PubMed2003

Metabolism of inorganic N compounds by ammonia-oxidizing bacteria.

Ammonia oxidizing bacteria extract energy for growth from the oxidation of ammonia to nitrite. Ammonia monooxygenase, which initiates ammonia oxidation, remains enigmatic given the lack of purified preparations. Genetic and biochemical studies support a model for the enzyme consisting of three subunits and metal centers of copper and iron. Knowledge of hydroxylamine oxidoreductase, which oxidizes hydroxylamine formed by ammonia monooxygenase to nitrite, is informed by a crystal structure and detailed spectroscopic and catalytic studies. Other inorganic nitrogen compounds, including NO, N2O, NO2, and N2 can be consumed and/or produced by ammonia-oxidizing bacteria. NO and N2O can be produced as byproducts of hydroxylamine oxidation or through nitrite reduction. NO2 can serve as an alternative oxidant in place of O2 in some ammonia-oxidizing strains. Our knowledge of the diversity of inorganic N metabolism by ammonia-oxidizing bacteria continues to grow. Nonetheless, many questions remain regarding the enzymes and genes involved in these processes and the role of these pathways in ammonia oxidizers.

Ammonia↗