Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMMONIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,171 records · Page 65Linked to original sources

[Spectroscopic study on the high voltage fast pulsed discharge of nitrogen, ammonia or their mixture].

The emission spectra from the pulsed discharge plasma of nitrogen, ammonia or their mixture were measured. In the discharge of pure nitrogen gas, as the pressure increased, the discharge volume decreased and more dissociation of nitrogen molecules occurred due to the higher energy density. In the discharge of ammonia, N,N+ and NH+ were observed, but no NH2 and NH3 were detected, indicating that ammonia, which has the lower dissociation and ionization energies as compared to nitrogen, was highly dissociated. The discharge of the mixture of N2 and NH3 was also studied. The dependence of the dissociation of nitrogen on the ratio of nitrogen to ammonia was investigated by emission spectra. The optimal ratio for nitrogen dissociation was obtained. The advantage of using the mixture of nitrogen and ammonia in the synthesis of nitrides was discussed.

Ammonia↗

[Acute toxicity of ammonia to Artemia sp].

The acute toxicity of total ammonia-N, (NH3 + NH4+), and un-ionized ammonia-N, NH3-N, on newly hatched Artemia nauplii and Artemia adults was measured in 24, 48, 72, and 96-h semi-static bioassays system. There was a significant difference (P < 0.05) in medial lethal concentrations (LC50) obtained during the tests. The LC50 values on nauplii ranged from 650 mg/l, in 24-h, to 399.1 mg/l total ammonia-N, in 96-h, while the LC50 values on adults ranged from 1290.4 mg/l to 600.5 mg/l total ammonia-N, in the same period. Two methods for calculations of un-ionized ammonia toxicity are analyzed and discussed.

Ammonia↗

Nitrite accumulation in the treatment of wastewaters with high ammonia concentration.

Different operational parameters of the nitritation process were investigated in both jar tests and pilot scale Sequencing Batch Reactors (SBRs). In the laboratory study, 100-1,200 mg N l(-1) of ammonia was used. The pH and temperature were varied. Batch experiments were done on municipal sludge, pectin industrial sludge and sludge from a reject water treatment unit. Ammonia oxidation was observed with relative nitrite accumulations from 2% to 100% and ammonia oxidation rates from 0.01 to 0.58 g N g VSS(-1) d(-1). The nitritation process and relative nitrite accumulation were highly affected by pH, temperature and the sludge type. pH 8.0-8.5 and temperature 30 degrees C were found favourable for the nitritation. Pilot SBR systems for treating reject water achieved 100% of nitrite accumulation under the operational conditions of pH 7.5-8.0, temperature 30 degrees C and dissolved oxygen (DO) 1.0 mg 1(-1). Six months of operation revealed that pH regulations were essential to avoid the inhibitions by either free ammonia or nitrous acid. At an unionized ammonia concentration of approximately 20 mg NH3-N l(-1), half of the normal nitritation ability still remained. Total inhibition occurred when the concentration of nitrous acid reached 3.0 mg HNO2-N l(-1). However, both types of inhibitions were reversible in the SBR with a proper operation control. Stable and controllable nitritation could be achieved in pilot scale.

Ammonia↗

Effect of three antibacterial drugs in lowering blood & stool ammonia production in hepatic encephalopathy.

Neomycin (700 mg/8 h), ampicillin (500/6 h) and metronidazole (400 mg/8 h), were compared for their effect, on oral administration for 4 days, in reducing blood ammonia in 27 patients with stable chronic liver disease. It was found that there was 38.2, 38.5 and 8.7 m mol/litre mean reduction in blood ammonia in the neomycin, ampicillin and metronidazole treated groups respectively. The difference in blood ammonia was statistically significant for both neomycin (P = 0.01) and ampicillin (P = 0.03) but there was no significant change after metronidazole treatment (P = 0.6). The total stool enzyme activity at optimum pH was maximally reduced by ampicillin and minimally with metronidazole. The reduction was noted to be 3.51 m mol/1 (P = 0.01), 3.87 m mol/1 (P = 0.08) and 2.8 m mol/1 (P = 0.02) of NH3/g dry weight of stool for neomycin, ampicillin and metronidazole respectively. The main bacterial gut enzymes responsible for ammonia production, urease and protease, were found to be very sensitive to stool pH. At pH 6 their activity was around 20 per cent of what was found in optimum pH of 7.4 and at pH 5 it is only about 8 per cent of optimum activity. None of the three antibacterial agents changed the stool pH significantly. It can be concluded that oral neomycin and ampicillin are superior to oral metronidazole in lowering blood ammonia.

Administration, Oral↗

Nitrification of ammonia nitrogen high concentration in membrane assisted bioreactor.

Use of the membrane-assisted bioreactors (MBR) in wastewater treatment can bring a lot of advantages. Usually COD removal achieves level 90% and nitrification of ammonia nitrogen concentrations typical for municipal wastewater performs without any disturbances, what was confirmed by large number of experiments. However, inhibition of nitrification of the high ammonia nitrogen concentration was noticed. In this study, the performance of ammonia-rich wastewater nitrification in membrane-assisted bioreactor (MBR) was examined. With SRT of 40, 32, 24 and 16 days any nitrification inhibition effect wasn't noticed. Ammonia nitrogen removal was around 98% and full nitrification was observed. At the sludge age equal to 12 d the first stage of nitrification was full, but the second stage of nitrification was incomplete. The variation in number and presence of the higher organisms were noticed at the all examined sludge ages. With SRT of 40, 32, 24 and 16 days the free ciliates were prominent organisms. At the sludge age of 12 days the domination of flagellates was observed The kinetic constants of the high-ammonia wastewater nitrification were calculated The average value of Vmax at the sludge age 12, 16 and 24 days was constant (4.7 mg NH4(+)-N/g MLSS h, 4.8 mg NH4(+)-N/g MLSS h and 4.8 mg NH4(+)-N/g MLSS, respectively), but the value of Km rose, when the sludge age increased (6.8 mg NH4(+)-N/L for 12 days, 11.3 mg NH4(+)-N/L for 16 days, 21.6 mg NH4(+)-N/L for 24 days). At the sludge age 32 and 40 days the increase of Vmax was observed (7.2 mg NH4(+)-N/g MLSS h and 12.5 mg NH4(+)-N/g MLSS h, respectively) and, also, changes of Km (6.8 mg NH4(+)-N/L and 44 mg NH4(+)-N/L, respectively. Concerning the second stage of nitrification value of Vmax decreased with the increase of the sludge age and the average Km varied from 20.3 to 31.3 mg NO2(-)-N/L.

Ammonia↗

[Nitrification and denitrification in BACF for treating high ammonia source water].

A high ammonia micropolluted source water advanced treatment for ammonia removal by biological activated carbon filter was tested. The removal rate of ammonia was high than 95% when influent concentration was under 1.0 mg/L. The removal rate decreased with the influent concentration increased when the ammonia concentration was in range of 1.5 - 4.9 mg/L and the influent DO was under 10 mg/L, and the minimum removal rate was about 30%. The key factor of restrict nitrification in BACF was the influent DO. When the influent ammonia concentration was high, the DO in water was depleted quickly by nitrify and hetetrophic bacteria in 0.4 m deep of filter and the filter layer was divided to aerobic zone and anoxic zone. The denitrification was occurred in the anoxic zone, and because of very low concentration of electron donor led to accumulation of the denitrification intermediates such as NO2-. Aerobic bacteria was existed in the anoxic zone.

Ammonia↗

Deamidation of glutamine by increased plasma gamma-glutamyltransferase is a source of rapid ammonia formation in blood and plasma specimens.

Owing to increased enzymatic hydrolysis of glutamine, additional ammonia is formed in blood and plasma specimens with increased gamma-glutamyltransferase activity (gamma-GT, EC 2.3.2.2.). The close correlation between gamma-GT and glutaminase (EC 3.5.1.2) activities (r = 0.97) in plasma, the inhibition with 6-diazo-5-oxo-L-norleucin or borate plus serine, and the activation with maleate clearly show that gamma-GT itself is the glutamine-deamidating enzyme in plasma. Under pathological conditions, increased gamma-GT activity can increase the rate of ammonia formation in plasma more than 30-fold the mean values of healthy subjects. Increased in vitro formation of ammonia caused by increased gamma-GT activity is an important source of false-positive findings in ammonia determination. Because of the high prevalence of pathological gamma-GT activities in clinical populations, blood specimens for ammonia analysis should be preserved by addition of borate plus serine.

Ammonia↗

Blood ammonia concentration in mice: normal reference values and changes during growth.

To establish normal reference values of blood ammonia concentration in mice, possible factors which may affect blood ammonia determination such as age, sex, strain and sampling site of blood, were investigated by the microdiffusion method. The ammonia concentration in blood collected from the tail (mixture of venous and arterial blood) and left ventricle was significantly higher than that in venous blood collected from the orbital sinus and right auricle. Neither strain nor sex differences were observed. Blood ammonia concentration in newborn pups was 92 +/- 19 micrograms/dl immediately after birth and increased to 184 +/- 22 micrograms/dl 24 hours after birth. This increased level was maintained for a week. By 15 days, it decreased to the level at birth. Thereafter, no significant variation with age was observed. Blood ammonia concentration in mice after weaning, irrespective of age, sex and strain, varied from 38 to 123 micrograms/dl, with a mean +/- SD of 79 +/- 18 micrograms/dl.

Ammonia↗

Ammonia production and secretion by isolated perfused proximal tubule segments.

The heterogeneous nature of renal ammonia production and transport necessitated the adaptation of the in vitro microperfusion technique to study ammonia production and transport by specific segments of the proximal tubule. Specific proximal tubule segments were dissected from mouse kidneys and microperfused in vitro with physiologic buffer solutions. This approach has demonstrated the important effects of luminal perfusion and luminal flow rate, in vitro and in vivo metabolic acidosis and in vitro potassium concentration on total ammonia production rates in proximal tubule segments. Studies examining net luminal ammonia secretion have suggested an important role of the Na(+)-H+ exchanger in the mechanism of ammonia secretion by the proximal tubule.

Acidosis, Renal Tubular↗

Value of rest-stress myocardial positron tomography using nitrogen-13 ammonia for the preoperative prediction of reversible asynergy.

To determine the predictive value of stress [13N]ammonia positron emission tomography (PET) for reversible ischemia, 31 patients with coronary artery disease underwent rest-stress [13N]ammonia PET before and after coronary artery bypass surgery. The circumferential profile analysis was applied to determine the presence of transient defect (TD) and persistent defect (PD) preoperatively, and the fate of perfusion abnormality and asynergy after the surgery was assessed. Preoperative PET demonstrated 100 segments with perfusion abnormalities, including 69 TD and 31 PD. Fifty-six of the 69 TD (81%) improved in regional perfusion, while only four of 31 PD (13%) improved in perfusion postoperatively (p less than 0.001). Of 75 segments showing regional asynergy on contrast or radionuclide ventriculography preoperatively, 34 of 48 segments with TD (71%) improved in asynergy, while only five of 27 segments with PD (19%) improved in asynergy postoperatively (p less than 0.001). Stress-delayed 201TI tomography was performed in 22 of them. The predictive values for improvement in perfusion (77%) and asynergy (65%) were similar as those by [13N]ammonia PET (81% and 71%, respectively). However, the predictive values for no improvement in perfusion and asynergy by 201TI tended to be low (66% and 58%, respectively), as compared to those in 13N ammonia PET (87%; p less than 0.05 and 81%; p = 0.09, respectively). We conclude that an accurate prediction of reversible ischemia and asynergy can be achieved with rest-stress [13N]ammonia PET. Particularly, it can identify irreversible areas more accurately than the commonly performed stress-delayed 201TI imaging.

Adult↗

Effects of somatostatin on plasma ammonia and amino acid profile during fasting and after protein feeding in cirrhotic patients.

The effects of somatostatin on fasting and absorptive plasma ammonia and amino acids were studied in 12 cirrhotic patients. They received a 6 h intravenous infusion of somatostatin (500 micrograms/h) or saline, starting 90 min before protein feeding. During the fasting period somatostatin significantly reduced plasma ammonia (-18%) and total tryptophan (-39%), increased plasma leucine (+19%), isoleucine (+17%), glutamine (+22%), glycine (+13%), arginine (+14%) and lysine (+12%), and prevented the significant fall of phenylalanine (-8%), tyrosine (-6%), alanine (-8%) and threonine (-9%) seen with saline. The percent changes in ammonia and glutamine concentrations were inversely correlated (r = -80; p less than 0.001) After protein ingestion, somatostatin slowed the maximal plasma increase in ammonia and alpha-nitrogens by at least two hours, but their total 5 h plasma response was not reduced, and even, in some instances, significantly increased (valine, leucine, glutamine, alanine and serine) with respect to saline. The results suggest that in fasting cirrhotics somatostatin reduces plasma ammonia, probably through an impaired intestinal ammoniogenesis from circulating precursors, and inhibits the disposal of branched chain, aromatic (except tryptophan) and gluconeogenic amino acids. Furthermore, it delays, but does not reduce, the plasma increase in nitrogen after protein ingestion.

Adult↗

Ammonia assimilation in Bacillus polymyxa. 15N NMR and enzymatic studies.

Pathways of ammonia assimilation into glutamic acid and alanine in Bacillus polymyxa were investigated by 15N NMR spectroscopy in combination with measurements of the specific activities of glutamate dehydrogenase, glutamine synthetase, glutamate synthetase, alanine dehydrogenase, and glutamic-alanine transaminase. Ammonia was found to be assimilated into glutamic acid predominantly by NADPH-dependent glutamate dehydrogenase with a Km of 2.9 mM for NH4+ not only in ammonia-grown cells but also in nitrate-grown and nitrogen-fixing cells in which the intracellular NH4+ concentrations were 11.2, 1.04, and 1.5 mM, respectively. In ammonia-grown cells, the specific activity of alanine dehydrogenase was higher than that of glutamic-alanine transaminase, but the glutamate dehydrogenase/glutamic-alanine transaminase pathway was found to be the major pathway of 15NH4+ assimilation into [15N]alanine. The in vitro specific activities of glutamate dehydrogenase and glutamine synthetase, which represent the rates of synthesis of glutamic acid and glutamine, respectively, in the presence of enzyme-saturating concentrations of substrates and coenzymes are compared with the in vivo rates of biosynthesis of [15N]glutamic acid and [alpha,gamma-15N]glutamine observed by NMR, and implications of the results for factors limiting the rates of their biosynthesis in ammonia- and nitrate-grown cells are discussed.

Alanine↗

Mechanism of formation of bound alpha-iminoglutarate from alpha-ketoglutarate in the glutamate dehydrogenase reaction. A chemical basis for ammonia recognition.

Two mechanisms have been postulated for the formation of bound alpha-iminoglutarate intermediate during the glutamate dehydrogenase-catalyzed reductive amination of alpha-ketoglutarate; one involves the nucleophilic attack of ammonia on a covalently bound Schiff base in the enzyme-NADPH-alpha-ketoglutarate complex, and the other involves the reaction of ammonia with the carbonyl group of alpha-ketoglutarate in the ternary complex. We have measured the rates of carbonyl oxygen exchange in the complex to unambiguously distinguish between these two mechanisms. We find that the loss of label in the carbonyl oxygen-labeled ternary complex is at least 10(5) times slower than the rate of the reductive amination reaction. Therefore, the former mechanism cannot be operative. We also find that (i) the carbonyl oxygen exchange in free alpha-ketoglutarate proceeds without any significant catalysis by its gamma-carboxylate group; (ii) this exchange reaction has energy parameters which are comparable to those observed for the hydration of simple aliphatic ketones; and (iii) the carbonyl oxygen exchange in bound alpha-ketoglutarate is slower than that in the free keto acid over a wide pH range. We conclude that the oxygen exchange in the free and bound alpha-ketoglutarate must occur via a gem-diol intermediate. The observation that the enzyme inhibits the reaction of water with alpha-ketoglutarate while it catalyzes the reaction of ammonia with the same keto acid points to an extraordinary recognition of ammonia by the enzyme. We interpret this observation by assuming that the enzyme-NADPH-alpha-ketoglutarate complex exists in two forms, a predominant form which is produced rapidly upon mixing the components together and an unstable form which is produced in trace amounts from the predominant form via a gem-diol intermediate. These two forms are presumed to differ in the spatial relationship of the carbonyl group to the enzyme functional groups. The carbonyl group in the unstable form is assumed to be surrounded by the same enzyme groups as the iminium ion is in the bound iminoglutarate complex. We ascribe the remarkable catalysis of the ammonia reaction and the inhibition of the water reaction by the enzyme to the opposing interactions of the iminium and carbonyl groups with these surrounding enzyme groups.

Algorithms↗

Urea and glucose formation in ovine liver after ammonia and lactate loading in vivo.

Ammonium chloride (30 mumol/min/kg bw), lactate (50 mumol/min/kg bw) or ammonium chloride plus lactate were infused for two hours into the mesenteric vein of sheep. Blood samples were taken before, during, and two hours after infusion from portal, hepatic and jugular veins for estimation of ammonia, urea, lactate and glucose. Average portal and hepatic blood flow was 59 +/- 35 and 89 +/- 48 ml/min/kg bw respectively without any regular changes when ammonium chloride or lactate alone were administered. The treatment with ammonium chloride increased the hepatic ammonia fixation from 9.1 +/- 2.1 to 25.2 +/- 5.7 mumol/min/kg bw and urea formation from 17.6 +/- 14.2 to 56.4 +/- 43.2 mumol/min/kg bw. The infusion of ammonium chloride alone provoked a peripheral hyperammonaemia and it increased the endogenous sources of ammonia for urea production. Both lactate and ammonia caused an increase of hepatic glucose release. It was suggested that lactate stimulated mainly gluconeogenesis, and ammonium-glucogenolysis. The effect of ammonia in the last reaction as well as an increased net urea formation in the liver, was probably mediated by the hypoinsulinaemia and/or an increase of adrenaline secretion.

Ammonia↗

Urea and ammonia excretion into gastric juice in regularly dialyzed patients and patients after renal transplantation. I. Dialyzed patients.

In regularly dialyzed patients in basal gastric juice and after stimulation with pentagastrin the volume of titrable acidity, urea and ammonia were assessed. It was revealed that in relation to the plasma urea concentration in basal juice the mean urea and ammonia concentration is roughly half and in stimulation juice roughly one third. The urea concentration in gastric juice is negatively correlated to the ammonia concentration. Urea excretion into the stomach depends on the plasma urea level and on the secretory gastric activity. The decisive factor of gastric secretion is probably parietal cell secretion. From the results ensues that gastric juice of dialyzed patients contains a quantitatively significant amount of urea and ammonia. Ammonia due to its neutralizing action distorts the examination of gastric acidity assessed by titration. The findings call for a revision of hitherto known data concerning gastric secretion of uraemic patients.

Ammonia↗

Cerebral acetylcholine and energy metabolism changes in acute ammonia intoxication in the lower primate Tupaia glis.

Ammonia levels are elevated in many patients with hepatic encephalopathy. This observation, coupled with animal studies showing an encephalogenic role for ammonia, has led to the concept that ammonia is an important toxin in the production of neurologic symptoms. Studies in rodents have shown that ammonia alters cerebral energy metabolism in the reticular formation, an area important in the modulation of consciousness. Our study was undertaken to extend these observations to the lower primate Tupaia glis, the tree shrew. The energy metabolites glucose, glycogen, lactate, adenosine triphosphate, and phosphocreatine were measured in the reticular formation by microanalytic techniques and enzymatic cycling. Acetylcholine was measured in brain regions by gas chromatography. Acetylcholine levels were increased significantly only in the medulla-pons and diencephalon in the coma stage. The energy metabolites glucose, glycogen, and phosphocreatine were decreased in reticular formation cells during the coma, whereas lactate was increased. During the precoma, glycogen and phosphocreatine were decreased. It appears, therefore, that the tree shrew has a metabolic response to ammonia similar to that of mice. A lowering of energy metabolism in the area of brain-regulating consciousness may act to place the animal in a coma. This coma in turn acts to decrease overall metabolic demand, which allows the animal an opportunity to conserve its threatened energy reserves.

Acetates↗

Effects of plasma sample storage on blood ammonia, bilirubin, and urea nitrogen concentrations: cats and horses.

Ten horses, a pony, and 13 cats were used to evaluate base-line blood ammonia, bilirubin, and urea nitrogen concentrations and to determine The effects of prolonged cold storage (-20 degrees C) before assay. Base-line plasma ammonia concentrations in cats (0.992 +/- 0.083 [SE] micrograms/ml) did not change significantly after 48 hours of storage (0.871 +/- 0.073 micrograms/ml); however, they were increased 4.2- and 13-fold after 168 and 216 hours of storage, respectively. In contrast to base-line plasma-ammonia values in cats, those of horses were significantly (0.265 +/- 0.044 micrograms/ml) lower, and significantly increased from base-line values after 48 hours of storage (0.861 +/- 0.094 micrograms/ml) and continued to increase 25.6-fold at 168 hours and 18.4-fold at 216 hours. Plasma urea nitrogen concentrations in cats (25.8 +/- 1.06 mg/dl) and horses (11.2 +/- 0.749 mg/dl) did not change significantly during 168 hours of storage. Total plasma bilirubin values from both cats (0.19 +/- 0.049 mg/dl) and horses (0.75 +/- 0.064 mg/dl) also did not change significantly during storage. These results indicate that feline plasma samples for ammonia determinations may be stored at -20 degrees C for up to 48 hours, whereas equine plasma ammonia values tend to increase during that time. The reason for the increase remains unexplained. Both feline and equine plasma urea nitrogen and total bilirubin are stable for at least 168 hours of storage at -20 degrees C.

Ammonia↗

[Origin of ammonia excreted by trout gill (Salmo gairdneri)].

In the perfused head of Trout the gills are the site of ammonia clearance which corresponds exactly to the appearance rate of ammonia in the external medium. Thus metabolic production of ammonia by the gill apparently does not participate to its excretion. Under ammonia-free Ringer perfusion however, endogenous production is observed and ammonia is excreted in both external and internal media.

Ammonia↗