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PubMed1985

Microassay for ammonium by determination of ammonia nitrogen in a nitrogen analyzer.

The method described comprises the transformation of ammonium into ammonia, the rapid and gentle liberation of the ammonia followed by the measurement of the nitrogen in a Dohrmann nitrogen analyzer. Untreated biological samples (1-50 microliters) were pipetted onto magnesium oxide tablets at 130 degrees C and the ammonia liberated was transferred by a continuous stream of nitrogen carrier gas into the nitrogen analyzer. There the ammonia was determined by oxidative pyrolysis and subsequent chemiluminescence measurement of the excited NO2. The result could be read in nanograms ammonia nitrogen within 6.5 min. Apart from volatile amines, which are usually negligible in biological samples, the method was specific for ammonia because under the given conditions of volatilization the labile groups of glutamine and asparagine did not interfere. The assay was sensitive in the range of 1.5-150 nmol ammonia and suitable for the routine analysis of small samples.

Ammonia↗
PubMed1992

Mechanism of gastric mucosal damage induced by ammonia.

The mechanism for Helicobacter pylori-induced gastric mucosal injury remains obscure. H. pylori has high urease activity to produce ammonia from urea in the stomach. In this study, the effects of ammonia on (a) gastric mucosal integrity, (b) gastric mucosal hemodynamics, (c) mucosal cellular viability, (d) mitochondrial respiration, and (e) energy metabolism of gastric mucosal were investigated. Ammonia (pH 10.3) at concentrations of greater than 125 mmol/L caused acute macroscopic gastric mucosal lesions in a dose-dependent manner, whereas glycine-NaOH buffer (pH 10.3) or ammonium chloride (pH 4.5) did not. The decrease in energy charge preceded the occurrence of gastric mucosal lesions, but ammonia caused no change in mucosal hemodynamics. Oxygen consumption of isolated cells and mitochondria of gastric mucosa was inhibited by ammonia dose-dependently. The present results indicate that ammonia impairs mitochondrial and cellular respiration and energy metabolism and that ammonia decreases mucosal cell viability, leading subsequently to mucosal damage.

Ammonia↗
PubMed1982

Biochemical bases for environmental adaptation in goldfish (Carassius auratus L.): resistance to ammonia.

Goldfish specimens were exposed for 24-48 hr to 20, 40, 600, and 2500 micrograms N/liter unionized ammonia (UIA). This treatment causes, in the brain, increases in total ammonia, glutamine, lactate, and succinate and decreases in glutamate, glucidic stores, total NADH, and ATP. Most of these effects have already been reported in ammonia-treated trout. It is therefore suggested that the cerebral biochemical mechanisms of ammonia toxicity in these two species are fundamentally the same. The most important metabolic alterations, however, appear for UIA concentrations which are higher than those necessary to produce the same effects in trout, in accordance with the greater resistance of goldfish to ammonia. Some of the physiological-biochemical adaptations which are at the root of this phenomenon have been pointed out and discussed. In the liver of the ammonia-treated goldfish total ammonia, glutamine, glutamate, and succinate all increase, while lactate, glycine, and taurine decrease; liver glucidic stores remain unaltered. These results indicate a difference in the metabolic responses of goldfish and trout liver.

Adaptation, Physiological↗
PubMed1996

Response of rat cerebral somatostatinergic system to a high ammonia diet.

It has been reported that ingestion of an ammonium-containing diet produces hyperammonemia without encephalopathy, thus permitting the study of the specific effects of ammonia toxicity. The present study investigated the rat cerebral somatostatinergic system using this experimental model of hyperammonemia. Wistar rats were fed a high ammonia diet prepared by mixing a standard diet with ammonium acetate (20% w/w); in addition, 5 mM of ammonium acetate was added to their water supply. Control rats were fed with a standard diet. The animals were sacrificed at 3, 7 and 15 days of ammonia ingestion. Ammonia levels in blood had increased approximately 3-fold at 7 days of ammonia ingestion. These changes were associated with a significant decrease in the specific binding of somatostatin (SS) to putative receptors sites in the frontoparietal cortex and hippocampus at 7 and 15 days after starting the high ammonia diet. Scatchard analysis shows that the decrease in SS binding resulted from a decrease in the number of available SS receptors rather than a change in receptor affinity. No changes in the somatostatin-like immunoreactivity content (SSLI) were detected in either brain area at the three study times. These results suggest that hyperammonemia alone can affect the rat brain somatostatinergic system. However, the animal model of hyperammonemia used here is insufficient to produce encephalopathy despite the significant increase in serum ammonia.

Ammonia↗
PubMed1976

Ammonia production and pathways of glutamine utilization in rat kidney slices.

Ammonia production from glutamine was studied in slices from non-acidotic and acidotic rat kidneys. Slices from non-acidotic kidneys made 53% as much ammonia from D-glutamine as from L-glutamine during the initial 15 min of incubation. Thereafter the production rate from the L-isomer accelerated while that from the D-isomer remained constant. The accelerated rate of ammonia production from L-glutamine was dependent upon tissue swelling since prevention of swelling reduced the production rate. Swelling activates the mitochondrial glutaminase I pathway as evidenced by the rise in ammonia produced per glutamine utilized ratio as well as by the accelerated rate of CO2 production derived from the oxidative disposal of glutamin's carbon skeleton. Cortical slice swelling activates the mitochondrial pathway in a manner not unlike that seen in vivo during chronic acidosis and may reflect increased permeability to glutamine. Acidotic rat kidneys are not swollen in vivo while cortical slices initially produce 4-fold more ammonia than do non-acidotic slices. After 15 min, this 4-fold difference in total ammonia production drops to only a 2-fold difference due to the swelling-induced activation of the mitochondrial pathway. Consequently, slice swelling obliterates the important fact that ammonia production by the mitochondrial pathway is 15-fold greater in acidotic than in non-acidotic kidneys.

Acidosis↗
PubMed1984

The hypokalemic, bowel, bladder, headache relationship; a new syndrome. The role of the potassium ammonia axis.

A conceptual approach that relates vascular headaches, bowel and bladder dysfunction to abnormalities of the "ammonia potassium axis" is presented. Hypokalemia alters smooth muscle function of both the bowel and bladder and results in the elaboration of an alkaline urine. The occurrence of an alkaline urine, along with bladder dysfunction and urinary stasis, predisposes to recurrent urinary tract infections. Hypokalemia and/or alkalosis increases the renal return of ammonia, exposes the brain to chronically higher concentration of ammonia and facilitates its passage into the central nervous system. Increased levels of blood ammonia predispose to hyperventilation which results in a superimposed respiratory alkalosis on a pre-existing hypokalemia and/or alkalosis therefore causing intense cerebral vasoconstriction. Varying degrees of cerebral ischemia and hypoxia occur and give rise to higher brain concentrations of ammonia. Vasodilatation occurs during the headache phase and may be a consequence of the sudden increase of brain ammonia and/or due to the release of other vasoactive mediators. As a consequence of increased blood ammonia, a reduction of protein intake may result in the alterations of amino acid precursors for brain uptake and therefore further interferes with the modulation of cerebral blood flow and brain function.

Adult↗
PubMed1993

Chronic hyperammonemia prevents changes in brain energy and ammonia metabolites induced by acute ammonium intoxication.

Acute ammonia toxicity has been attributed to the depletion of energy metabolite intermediates. Ingestion of an ammonium containing diet produces hyperammonemia and protects rats against acute ammonium intoxication. We have tested the effect of chronic hyperammonemia on the brain contents of energy and ammonia metabolite intermediates and on the effect on these contents of acute ammonia intoxication (i.p. injection of 7 mmol/kg of ammonium acetate). Chronic hyperammonemia was induced in rats by feeding them a diet containing 20% ammonium acetate. Control rat were fed the same diet without addition of ammonium acetate. It is shown that chronic hyperammonemia did not affect the content of most metabolites, the only remarkable changes are the increases of the contents of ammonia (46%), glutamine (81%), acetoacetate (31%) and of the mitochondrial NAD+/NADH ratio (32%) as well as the marked decrease of beta-hydroxybutyrate (by 86%). Chronic hyperammonemia prevents most changes in metabolites induced by acute ammonium intoxication (i.p. injection of 7 mmol/kg of ammonium acetate). In control rats it was a marked breakdown of glycogen and increased contents of glucose, lactate and pyruvate, with decreased cytosolic NAD+/NADH ratio and beta-hydroxybutyrate and ATP contents. These changes were nearly completely prevented in hyperammonemic rats. In controls, ammonia increased 12.8-fold while glutamate and aspartate decreased by approximately 40% and glutamine and alanine raised by 37% and 93%, respectively; in hyperammonemic rats ammonia increased 6.9-fold while glutamate, glutamine and alanine were not significantly affected. Also the mitochondrial NAD+/NADH ratio raised by 18-fold in controls and by 6-fold in hyperammonemic rats. These results indicate that chronic hyperammonemia markedly prevents the alterations of the contents of energy and ammonia metabolites induced by acute ammonium intoxication.

Ammonia↗
PubMed2005

The effects of acute and chronic ammonia exposure during early life stages of the gulf toadfish, Opsanus beta.

The gulf toadfish (Opsanus beta) is unusual among teleosts in that it is facultatively ureotelic and adults and juveniles have a particularly high tolerance to environmental ammonia. Male toadfish brood their offspring in confined nests. It has been hypothesized that the potential accumulation of ammonia in nests from the male and the offspring, coupled with suspected low ammonia tolerance in offspring would provide the selective pressure necessary for excretion of the less toxic urea by adult toadfish. This study examines this so-called 'nest-fouling' hypothesis through acute and chronic ammonia toxicity testing on early life stages of O. beta. In addition, nitrogen elimination was examined among embryos, yolk-sac larvae and juveniles where we found an ontogenic shift from ammonotely to ureotely with advancing life history stages. The acute ammonia 96 h LC50 values for embryos and larvae were 63.6 and 5.45 mmol-Nl(-1) total ammonia (TAmm), respectively. Thus, these early life stages are more tolerant to ammonia than either juveniles or adults and LC50 values are at least 2 orders of magnitude greater than concentrations naturally occurring at nest sites. Furthermore, 40 days exposures at mean and maximum NH3 concentrations normally found within nests revealed no observable detrimental effects. In fact, growth in terms of wet or dry weight was greatest at the maximum NH3 concentration. We therefore conclude that the nest-fouling hypothesis is not a viable explanation for ureotely in the gulf toadfish.

Age Factors↗
PubMed2005

A rapid and simple respirometric biosensor with immobilized cells of Nitrosomonas europaea for detecting inhibitors of ammonia oxidation.

As obligate chemolithotrophs, ammonia-oxidizing bacteria (AOB) grow very slowly and are known to be extremely sensitive to a wide variety of inhibitors. Since it is generally accepted that inhibition of ammonia oxidation by AOB results in a total failure of nitrogen removal, it is necessary to develop a method to detect inhibitors of ammonia oxidation in wastewater. Since ammonia oxidation accompanies oxygen consumption, ammonia oxidation can be easily evaluated by measuring oxygen consumption rate using a dissolved oxygen (DO) probe. In this study, a rapid and simple respirometric biosensor using the pure culture of Nitrosomonas europaea was developed. N. europaea was cultivated in a continuous fermentor operating at the dilution rate of 0.008 h(-1) to obtain physiologically constant cells and was immobilized onto the dialysis membrane through filtration. DO, determined by the biosensor, started to increase 30 s later after ammonia oxidation inhibitor was fed, and a new steady-state DO was obtained in 10-30 min. For this DO profile, steady-state kinetics was applied to evaluate ammonia oxidation efficiency. The concentration of a toxic compound causing 50% decrease of oxygen-consumption activity (EC50) was determined for different chemicals. The EC50 values obtained with the biosensor (0.018 mg l(-1) for allylthiourea, 0.027 mg l(-1) for thioacetamide, 1.10 mg l(-1) for phenol and 0.0 1mg l(-1) for thiourea) indicated that the developed biosensor was highly sensitive to a variety of the inhibitors. It was also shown that the biosensor is applicable for on-line real time monitoring.

Ammonia↗
PubMed2005

Ammonia emissions from the composting of different organic wastes. Dependency on process temperature.

Ammonia emissions were quantified for the laboratory-scale composting of three typical organic wastes with medium nitrogen content: organic fraction of municipal solid wastes, raw sludge and anaerobically digested sludge; and the composting of two wastes with high nitrogen content: animal by-products from slaughterhouses and partially hydrolysed hair from the leather industry. All the wastes were mixed with the proper amount of bulking agent. Ammonia emitted in the composting of the five wastes investigated revealed a strong dependence on temperature, with a distinct pattern found in ammonia emissions for each waste in the thermophilic first stage of composting (exponential increase of ammonia emitted when increasing temperature) than that of the mesophilic final stage (linear increase of ammonia emissions when increasing temperature). As composting needs high temperatures to ensure the sanitisation of compost and ammonia emissions are one of the main environmental impacts associated to composting and responsible for obtaining compost with a low agronomical quality, it is proposed that sanitisation is conducted after the first stage in large-scale composting facilities by a proper temperature control. CAPSULE: Ammonia emission pattern and correlation with process temperature are presented for the composting process of different organic wastes.

Air Pollutants↗
PubMed2004

Fate of ammonia in the atmosphere--a review for applicability to hazardous releases.

The physical and chemical mechanisms responsible for the removal of ammonia from the atmosphere have been reviewed. Capture by atmospheric moisture (clouds, rain, fog), surface water (rivers, lakes, seas), and deposition on vegetation and soil constitute the main pathways for ammonia removal from the troposphere. Ammonia catalyzes the atmospheric oxidation of sulfur dioxide to sulfur trioxide and reacts rapidly with acidic components of the atmosphere (sulfuric, nitric, and hydrochloric acids). The ammonium salts formed are the main components of smog aerosols and thus affect the opacity of the atmosphere and the earth radiation budget. Slow oxidation of ammonia in the atmosphere plays only a minor role in its removal. The data obtained for ammonia reactions under normal atmospheric conditions are generally applicable to model chemical reactions occurring during massive release of ammonia in the atmosphere, provided the impact of high ammonia concentration on the mass transfer processes that control some of these reactions, are taken into account.

Ammonia↗
PubMed2006

Pretreatment of anaerobic digestion effluent with ammonia stripping and biogas purification.

In this study, ammonia stripping was optimized for pretreating anaerobic digestion effluent from an anaerobic digestion plant, and the possibility of using CO(2) stripping and biogas injection for adjusting the pH of the effluent before and after the ammonia stripping process was also investigated. For ammonia stripping, the results showed that an overdose of calcium hydroxide, i.e., 27.5g/L wastewater, achieved higher ammonia, phosphorus, chemical oxygen demand, suspended solids, and turbidity removal efficiency. An air flow rate of 5L/min for 1L of wastewater was thought as suitable for engineering application. The pH of the anaerobic digestion effluent can be increased from about 7 to about 9 by CO(2) stripping, however which is insufficient for ammonia stripping. For 1L of wastewater treated after ammonia stripping, the pH can be neutralized to about 7 from greater than 11 through biogas injection at 1L/min for less than 30min, and continuous injection does not decrease the pH. It was roughly estimated that 43m(3) of biogas (CH(4):CO(2) approximately 60%:40%) produced daily could be purified to CH(4):CO(2) approximately 74%:26% by neutralizing the pH of the 5m(3) anaerobic digestion effluent pretreated by ammonia stripping.

Ammonia↗
PubMed2005

Ammonia effects on pyruvate/lactate production in astrocytes--interaction with glutamate.

Ammonia exerts a multitude of metabolic and non-metabolic effects on brain tissue. In the present communication we have investigated its effect on lactate production rates, pyruvate production rates and pyruvate/lactate ratios in mouse cerebrocortical astrocytes and neurons in primary cultures. No effects were found in neurons. All three parameters were affected by ammonia in astrocytes, but less potently and to a smaller degree in cells that had been treated with dibutyryl cyclic AMP (morphologically differentiated cells) than in untreated cells (morphologically undifferentiated cells). In the differentiated cells ammonia had virtually no effect up to a concentration of 1.0 mM, but at 3.0 mM it increased lactate production and decreased pyruvate/lactate ratio significantly. In the undifferentiated cells ammonia greatly increased lactate accumulation (by 80% at 3.0 mM) and it inhibited pyruvate accumulation (by 40% at 3.0 mM). It thereby reduced the pyruvate/lactate ratio progressively within the entire range 0.1-3.0 mM ammonia. In support of the hypothesis that the ammonia-induced reduction of pyruvate/lactate ratio is secondary to depletion of cellular glutamate by formation of glutamine (and glutathione) and a resulting interruption of the malate-aspartate shuttle (MAS), the addition of glutamate to the incubation medium significantly diminished the ammonia-induced reduction of pyruvate/lactate ratio, whereas it had no effect on the increased lactate production. It is discussed that MAS interruption may have additional consequences in astrocytes.

Ammonia↗
PubMed2006

Inhibition of biohydrogen production by ammonia.

Ammonia inhibition of biohydrogen production was investigated in batch and continuous flow reactors with glucose as a substrate. In batch tests, biohydrogen production rate was highly dependent on pH and ammonia (defined as the sum of NH3 of NH4+ species) concentrations above 2 g N/L. At pH = 6.2, the maximum production decreased from 56 mL/h at 2 g N/L to 16 mL/h at 10 g N/L. At pH = 5.2, production decreased from 49 mL/h (2g N/L) to 7 mL/h (16 g N/L). Hydrogen yield remained relatively constant in batch tests, varying from 0.96 to 1.17 mol-H2/mol-glucose. In continuous flow tests, both hydrogen production rates and yields were adversely affected by ammonia. When the reactor (2.0 L) was first acclimated under batch conditions to a low nitrogen concentration (<0.8 g N/L), H2 production and yields under continuous flow mode conditions were 170 mL/h and 1.9 mol-H2/mol-glucose, but decreased with increased ammonia concentrations up to 7.8 g N/L to 105 mL/h and 1.1 mol-H2/mol-glucose. There was no hydrogen production under continuous flow conditions if the reactor was initially operated under batch flow conditions at ammonia concentrations above 0.8 g N/L. It is concluded that the hydrogen production is possible at high concentrations (up to 7.8 g N/L) of ammonia in continuous flow systems as long as the reactor is initially acclimated to a lower ammonia concentration (<0.8 g N/L).

Ammonia↗
PubMed2006

Electrochemical conversion characteristics of ammonia to nitrogen.

In order to evaluate the electrolytic decomposition characteristics of ammonia to nitrogen, this work has studied several experimental variables of electrolytic ammonia decomposition. The effects of the pH and the chloride ion in the solution, kinds of anodes such as IrO(2,) RuO(2), and Pt on the electrolytic decomposition of ammonia were compared, and the existence of a membrane equipped in the cell, the changes of the current density, the initial ammonia concentration, and so on were investigated for the decomposition. The performances of the electrode were totally in the order of RuO(2) approximately IrO(2) > Pt in both the acid and alkali conditions. The ammonia decomposition was the highest at a current density of 80 mA/cm(2), over which it decreased, because the adsorption of the ammonia at the electrode surface was hindered by the hydroxyl ions in the solution. The ammonia decomposition yield increased with the concentration of the chloride ion in the solution. However, the increment rate became much lesser over 10 g/l of the chloride ion. The RuO(2) electrode among the tested anodes generated the most OH radicals which could oxidize the ammonium ion at pH 7.

Ammonia↗
PubMed2003

Assessment of ammonia toxicity in tests with the microalga, Nephroselmis pyriformis, Chlorophyta.

Previous studies of an industrial effluent have indicated toxic effects by the ammonium/water system in tests with the unicellular green alga, Nephroselmis pyriformis. This investigation was undertaken to determine the toxicity of ammonia to this alga, and to identify the dominant toxicant in an industrial process effluent. The algal standard test was modified to improve the pH control, i.e. by testing at shorter exposure time and in the presence of a buffering agent, 3 mM HEPES. Ammonia was found to be the predominant toxic form in the dissociating ammonium/water system and the specific toxicity of ammonia (EC50, 24 h exposure) was 2.34 microM (32.8 microg ammonia nitrogen/L). Due to the dissociation, the toxicity is strongly pH dependent. Joint toxicity with additive effects of ammonia and ammonium ions was indicated, but the toxicity of ammonium ions was almost a factor 100 less (EC50, 24 h exposure, 224 microM or 3140 microg ammonium-nitrogen/L). According to the results the EC50 for effect on growth rate of N. pyriformis in seawater of pH 8.0 is 71 microM total ammonium. Hence, this alga appears to be more sensitive to ammonia than other studied marine plankton algae. Ammonia was found to be the dominant toxicant in the industrial effluent, using N. pyriformis as test organism.

Ammonia↗
PubMed1982

Propranolol increases arterial ammonia in liver cirrhosis.

Propranolol (20 mg 4 times a day) was given to patients with liver cirrhosis or fatty infiltration of the liver. In six patients with cirrhosis and a stable arterial plasma ammonia concentration before treatment, blood ammonia was increased significantly on day 3 of propranolol treatment. Arterial plasma ammonia concentration was still high on day 6 of propranolol. Individual percentage change in arterial ammonia ranged from 8% to 66%. After propranolol had been discontinued ammonia concentration returned to pretreatment concentrations in 3 to 6 days. In 3 patients with fatty livers and normal pretreatment ammonia concentrations no change was detected in arterial plasma ammonia while they were on propranolol.

Adult↗
PubMed1986

Effect of ammonia on glucagon secretion from the perfused pancreas of cirrhotic rats.

Effects of ammonia on glucagon and insulin secretion from the perfused pancreas of cirrhotic rats were investigated to clarify the occurring mechanism of hypersecretion of pancreatic glucagon in liver cirrhotics. The results were as follows: During ammonia loading, insulin secretion was inhibited in a dose-related manner, whereas glucagon secretion was gradually increased at high concentrations of ammonia (2 mM) in control rats; this tendency was augmented in the presence of alpha-ketoglutarate in cirrhotic rats. On cessation of ammonia loading, a transient but definite increase in glucagon and insulin secretion was observed. Basal plasma glucagon and ammonia levels as well as basal glucagon secretion from the perfused pancreas of cirrhotic rats were significantly higher than in control rats. Basal insulin secretion from the perfused pancreas of cirrhotic rats was not different in spite of high levels of plasma insulin. Glucagon secretory response to glucose and arginine from the perfused pancreas of cirrhotic rats was higher than in the control pancreas, whereas insulin secretion was lower. In these cirrhotic rats, an increase in the number of islet cells, particularly A cells, was observed. These data suggested that hypersecretion of pancreatic glucagon which was responsible for hyperglucagonemia in cirrhotic rats might be attributed to high levels of ammonia and alpha-ketoglutarate in blood as well as to the fluctuation of abnormal ammonia concentration in blood and to the hypertrophy of islets, particularly of the A cell group due to hypersecretion.

Ammonia↗