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PubMed1993

Renal ammonia and glutamine metabolism during liver insufficiency-induced hyperammonemia in the rat.

Renal glutamine uptake and subsequent urinary ammonia excretion could be an important alternative pathway of ammonia disposal from the body during liver failure (diminished urea synthesis), but this pathway has received little attention. Therefore, we investigated renal glutamine and ammonia metabolism in midly hyperammonemic, portacaval shunted rats and severely hyperammonemic rats with acute liver ischemia compared to their respective controls, to investigate whether renal ammonia disposal from the body is enhanced during hyperammonemia and to explore the limits of the pathway. Renal fluxes, urinary excretion, and renal tissue concentrations of amino acids and ammonia were measured 24 h after portacaval shunting, and 2, 4, and 6 h after liver ischemia induction and in the appropriate controls. Arterial ammonia increased to 247 +/- 22 microM after portacaval shunting compared to controls (51 +/- 8 microM) (P < 0.001) and increased to 934 +/- 54 microM during liver ischemia (P < 0.001). Arterial glutamine increased to 697 +/- 93 microM after portacaval shunting compared to controls (513 +/- 40 microM) (P < 0.01) and further increased to 3781 +/- 248 microM during liver ischemia (P < 0.001). In contrast to controls, in portacaval shunted rats the kidney net disposed ammonia from the body by diminishing renal venous ammonia release (from 267 +/- 33 to -49 +/- 59 nmol/100 g body wt per min) and enhancing urinary ammonia excretion from 113 +/- 24 to 305 +/- 52 nmol/100 g body wt per min (both P < 0.01). Renal glutamine uptake diminished in portacaval shunted rats compared to controls (-107 +/- 33 vs. -322 +/- 41 nmol/100 g body wt per min) (P < 0.01). However, during liver ischemia, net renal ammonia disposal from the body did not further increase (294 +/- 88 vs. 144 +/- 101 nmol/100 g body wt per min during portacaval shunting versus liver ischemia). Renal glutamine uptake was comparable in both hyperammonemic models. These results indicate that the rat kidney plays an important role in ammonia disposal during mild hyperammonemia. However, during severe liver insufficiency induced-hyperammonemia, ammonia disposal capacity appears to be exceeded.

Ammonia↗

PubMed2001

Effects of sublethal ammonia exposure on swimming performance in rainbow trout (Oncorhynchus mykiss).

Adult trout Oncorhynchus mykiss fitted with a dorsal aortic catheter were exposed to 288+/-15 micromol l(-1) (mean +/- S.E.M.) total ammonia for 24h in water at a pH of 8.39+/-0.02, while swimming at a speed equivalent to 0.75 bodylengths s(-1) (BLs(-1)) in a Brett-type tunnel respirometer. The fish were then exposed to stepwise increments in swimming speed (0.25 BLs(-1) every 30 min) until exhaustion. Measurements of oxygen uptake (M(O2)) and plasma total ammonia levels and pH were made at each speed. Control trout were treated identically but without exposure to ammonia. Ammonia exposure caused an increase in plasma total ammonia level to 436+/-34 micromol l(-1), compared to 183+/-30 micromol l(-1)in control animals (N=6). A significant reduction in total plasma ammonia level was found in both groups during exercise, despite a large negative concentration gradient in those exposed to an elevated concentration of ammonia in water, which may indicate an active excretory process. The overall increase in plasma ammonia levels in exposed trout was associated with a significant reduction in critical swimming speed (U(crit)) to 1.61+/-0.17BL s(-1) from 2.23+/-0.15BL s(-1) in control animals. Ammonia-exposed trout had a significantly higher maintenance metabolic rate (MMR) than control fish, when estimated as the y-intercept of the relationship between swimming speed and M(O2). Active metabolic rate (AMR, maximum M(O2) as measured at U(crit)) was significantly lower in ammonia-exposed animals, leading to a profound reduction in factorial aerobic scope (AMR/MMR). Reduced U(crit) was also linked to a reduction in maximum tailbeat frequency. Calculation of membrane potentials (E(M)) in the white muscle of fish swum to U(crit) revealed a significant partial depolarisation of white muscle in ammonia-exposed fish. This may have prevented white muscle recruitment and contributed to the reduced maximum tailbeat frequency and overall impairment of swimming performance in the ammonia-exposed fish.

Ammonia↗

PubMed1978

Effects of ammonia on monoamine oxidase and enzymes of GABA metabolism in mouse brain.

Acute and chronic ammonia toxicity was produced in the mice by intraperitoneal injection of ammonium chloride (200 mg/kg) and by exposure of mice to ammonia vapours (5% v/v) continuously for 2 days and 5 days respectively. The ammonia content was elevated in the cerebellum, cerebral cortex and brain stem and in liver. In acute ammonia intoxication there was a decrease in the monoamine oxidase (MAO) activity in all the three regions of brain. In chronic ammonia toxicity (2 days of exposure) a significant increase in the activity of MAO was observed in the cerebral cortex while in cerebellum and brain stem there was a significant decrease. In cerebral cortex and cerebellum there was a rise in the activity of MAO as a result of exposure to ammonia vapours for 5 days. A significant decrease was observed in the activity of glutamate decarboxylase (GAD) in all the three regions of the brain both in acute and chronic ammonia toxicity (2 days). There was a decrease in the activity of this enzyme only in the cerebral cortex in the animals exposed to ammonia for 5 days. The activity of GABA-aminotransferase (GABA-T) showed a significant rise in cerebellum and a fall in the brain stem in acute ammonia toxicity. In chronic ammonia toxicity GABA-T showed a rise in all the three regions of brain. Chronic ammonia toxicity produced a significant decrease in the content of glutamate in all the three regions without a significant change in the content of aspartate. GABA and glutamine. The content of alanine increased in all the three regions of brain under these experimental conditions. The ratio of glutamate + aspartate/GABA and glutamate/glutamine showed a decrease in all the three regions as a result of ammonia toxicity.

4-Aminobutyrate Transaminase↗

PubMed2005

Metabolic fates of ammonia-N in ruminal epithelial and duodenal mucosal cells isolated from growing sheep.

The objective of this experiment was to determine the capability of ruminant gut tissues to detoxify ammonia-N using short-term incubations of isolated cells in vitro. Ruminal epithelial cells (REC) and duodenal mucosal cells (DMC) were isolated from growing Texel-Polypay ram lambs (n = 4) fed a pelleted forage:concentrate-based diet. Immediately after isolation, primary cells were incubated for 60 min with glucose (1mM), glutamate (1mM), [15N]ammonium chloride (5, 10, 20, or 40 mM), and 1 of 4 combinations of substrates (1 mM each) that could support urea synthesis [control, N-carbamoylglutamate (NCG); NCG + ornithine (ONCG); and ONCG + aspartate (AONCG)]. Treatments were arranged in a 4 x 4 factorial design. Incorporation of ammonia-15N into alanine, citrulline, arginine, and urea was determined by gas chromatography-mass spectrometry. For both cell types, ammonia-N transfer to alanine was lower when incubation medium contained NCG compared with control, whereas use of ammonia-N for net alanine synthesis increased quadratically with ammonia concentration regardless of substrate treatment. For REC, ammonia-N was not incorporated into citrulline, arginine, or urea, nor into arginine or urea by DMC. Ammonia-N use for net citrulline synthesis exhibited an inverse relationship with ammonia concentration, decreasing linearly as media ammonia concentration increased. Thus, ala-nine synthesis may be a significant metabolic pathway for ruminant gut tissues to detoxify ammonia-N when it is presented luminally at high concentrations as compared with detoxification by the ornithine-urea cycle. Furthermore, DMC do exhibit a metabolic capability to incorporate ammonia-N into citrulline, but low or absent activity of downstream enzymes of the ornithine-urea cycle appears to limit ammonia-N transfers to urea.

Alanine↗

PubMed1983

Ammonia metabolism in exercise and fatigue: a review.

Although fatigue is a well-known phenomenon and the phrase "exercised until exhaustion" is commonly understood, there is no unequivocal agreement on the fundamental nature of the fatigue process. Ammonia was linked to the development of fatigue as early as 1922, when ammonia production was observed from stimulated nerve and the question whether there could be a relationship between ammonia production and the muscle activity was raised. The immediate source of ammonia from muscle appears to be a result of the deamination of AMP and is more apparent in fast-twitch than in slow-twitch fibers. More recently, increases in blood ammonia levels have been reported in rats after swimming and in humans after arm work, maximal cycle ergometry, and treadmill exercise. Elevated blood ammonia has also been linked to a surprising variety of functional and metabolic neurological disturbances other than exercise and fatigue, including the development of hepatic coma, convulsions from ammonia toxicity precipitated by high-pressure oxygen breathing, epileptic seizures, and decreased neuronal excitability. In addition, a number of genetic disorders (inborn errors in metabolism, or IEMs) are characterized by elevated blood ammonia concentrations. Symptoms of neural disability in all of the above conditions have been related to the concentration of ammonia in blood. Although these studies do not relate to exercise or fatigue directly, it is conceivable that our understanding of the effect of high concentrations of blood ammonia in these clinical conditions may provide valuable insight into the effect of ammonia during exercise. This paper reviews the effect of ammonia production during exercise and other conditions upon purposeful activity and the development of fatigued states.

AMP Deaminase↗

PubMed1998

Ammonium Limitation Results in the Loss of Ammonia-Oxidizing Activity in Nitrosomonas europaea.

The effects of limiting concentrations of ammonium on the metabolic activity of Nitrosomonas europaea, an obligate ammonia-oxidizing soil bacterium, were investigated. Cells were harvested during late logarithmic growth and were incubated for 24 h in growth medium containing 0, 15, or 50 mM ammonium. The changes in nitrite production and the rates of ammonia- and hydroxylamine-dependent oxygen consumption were monitored. In incubations without ammonium, there was little change in the ammonia oxidation activity after 24 h. With 15 mM ammonium, an amount that was completely consumed, there was an 85% loss of the ammonia oxidation activity after 24 h. In contrast, there was only a 35% loss of the ammonia oxidation activity after 24 h in the presence of 50 mM ammonium, an amount that was not consumed to completion. There was little effect on the hydroxylamine oxidation activity in any of the incubations. The loss of ammonia oxidation activity was not due to differences in steady-state levels of ammonia monooxygenase (AMO) mRNA (amoA) or to degradation of the active site-containing subunit of AMO protein. The incubations were also conducted at a range of pH values to determine whether the loss of ammonia oxidation activity was correlated to the residual ammonium concentration. The loss of ammonia oxidation activity after 24 h was less at lower pH values (where the unoxidized ammonium concentration was higher). When added in conjunction with limiting ammonium, short-chain alkanes, which are alternative substrates for AMO, prevented the loss of ammonia oxidation activity at levels corresponding to their binding affinity for AMO. These results suggest that substrates of AMO can preserve the ammonia-oxidizing activity of N. europaea in batch incubations by protecting either AMO itself or other molecules associated with ammonia oxidation.

Journal Article↗

PubMed1994

AMMONIA EXCRETION IN FRESHWATER RAINBOW TROUT (ONCORHYNCHUS MYKISS) AND THE IMPORTANCE OF GILL BOUNDARY LAYER ACIDIFICATION: LACK OF EVIDENCE FOR Na+/NH4+ EXCHANGE

Net ammonia fluxes (JAmm) were measured in adult freshwater rainbow trout in vivo under a variety of conditions designed to inhibit unidirectional sodium uptake (JinNa; low external [NaCl], 10(-4) mol l-1 amiloride), alter transbranchial PNH3 and NH4+ gradients [24 h continuous (NH4)2SO4 infusion, or exposure to 1 mmol l-1 external total ammonia at pH 8] and prevent gill boundary layer acidification (5 mmol l-1 Hepes buffer). Inhibition of JinNa with amiloride or low external [NaCl] under normal conditions reduced JAmm by about 20 %, but did not prevent the net excretion of ammonia during exposure to high concentrations of external ammonia. Increasing the buffer capacity of the ventilatory water with Hepes buffer (pH 8) reduced JAmm by 36 % and abolished the effect of amiloride on ammonia excretion. No evidence could be found to support a directly coupled apical Na+/NH4+ exchange. We suggest that any dependence of ammonia excretion on sodium uptake is caused by alteration of transbranchial PNH3 gradients within the gill microenvironment secondary to changes in net H+ excretion. Under normal conditions (pH 8, low external ammonia) gill boundary layer acidification facilitates over one-third of the total ammonia excretion. During exposure to high concentrations of external ammonia in poorly buffered water, estimates of transbranchial PNH3 gradients from measurements of bulk water pH and total ammonia concentration (TAmm) may be grossly in error because of boundary layer acidification. Prevention of boundary layer acidification with Hepes buffer during exposure to high cocncentrations of external ammonia revealed that the local transbranchial PNH3 gradient at the gill may in fact be positive (blood to water), negating the need for an active NH4+ transport mechanism. In freshwater trout, NH3 diffusion may account for all ammonia excretion under all experimental conditions used in the present study.

Journal Article↗

PubMed1996

Excretion and distribution of ammonia and the influence of boundary layer acidification in embryonic rainbow trout (Oncorhynchus mykiss)

This study examined ammonia excretion by embryos of the rainbow trout (Oncorhynchus mykiss). The distribution of ammonia in relation to the H+ distribution and electrical potential was determined. The influence of the pH of the unstirred layer (USL) of water next to the external surface of the embryo was also assessed. Eyed-up embryos (3540 days post-fertilization) were exposed to various external water conditions [pH 6.0, pH 10.0, 1.6 mmol l-1 NaCl, 0.0 mmol l-1 NaCl, 0.2 mmol l-1 NH4Cl, 2.5 mmol l-1 borax buffer (Na2B4O7.10H2O), 2.5 mmol l-1 Hepes, 0.1 mmol l-1 amiloride] for 30 min and ammonia excretion rates, ammonia concentration in the perivitelline fluid (PVF) and yolk, and the pH of the PVF, yolk and USL were measured. The rate of ammonia excretion was dependent, in part, on the partial pressure gradient of NH3 ( PNH3) from the PVF to the USL. Exposure to water of pH 6 increased, whereas NH4Cl or pH 10 exposure decreased, ammonia excretion rates. Elevated external Na+ levels also influenced the rate of ammonia excretion, but neither Na+-free water nor amiloride had any effect. The distribution of ammonia between the PVF and USL was dependent on the H+ distribution, but ammonia was distributed according to the electrical potential between the PVF and yolk. The USL was 0.32 pH units more acidic than the bulk water. Addition of buffer to the external water eliminated the acid USL and decreased ammonia excretion rates. We conclude that rainbow trout embryos excrete ammonia primarily as NH3, but when external Na+ levels are elevated, ammonia excretion may be independent of the PNH3 gradient. The acidic USL next to the chorion probably facilitates NH3 diffusion by maintaining the PNH3 through the conversion of NH3 to NH4+ upon entry into the USL.

Journal Article↗

PubMed2004

Effects of peritoneal injection of NH4HCO3 on nitrogen excretion and metabolism in the swamp eel Monopterus albus-- increased ammonia excretion with an induction of glutamine synthetase activity.

Monopterus albus has to deal with high environmental ammonia concentrations during dry seasons and agricultural fertilization in rice fields. In this study, NH4HCO3 (10 micromol per g fish) was injected into the peritoneal cavity of M. albus, raising the level of ammonia in the body, in order to elucidate the strategies involved in defense against the toxicity of exogenous ammonia. During the subsequent 24 h after NH4HCO3 injection, there was a significant increase in the ammonia excretion rate, which indicates that the main strategy adopted by M. albus was to remove the majority of the exogenous ammonia through enhanced ammonia excretion. Exogenous ammonia was not detoxified into urea for excretion or accumulation. Six hours post-injection of NH4HCO3, ammonia content in the tissues built up significantly, especially in the brain, which suggests that M. albus had high tolerance of ammonia toxicity at the cellular and sub-cellular levels. By hour 12 post-injection, there were significant increases in the activities of glutamine synthetase in the muscle, liver, and gut, accompanied by significant increases in glutamine contents in the muscle and the liver. There was also a significant increase in the glutamine content in the brain at hour 6 post-injection of NH4HCO3. These results confirm the capability of M. albus to detoxify ammonia through glutamine synthesis. Overall, injection of NH4HCO3 had only minor effects on the contents of FAAs, other than glutamine, in tissues of M. albus because the majority (70%) of the injected ammonia was excreted within the 24-h period.

Ammonia↗

PubMed2003

A comparison of the effects of environmental ammonia exposure on the Asian freshwater stingray Himantura signifer and the Amazonian freshwater stingray Potamotrygon motoro.

The white-edge whip tail ray Himantura signifer inhabits a freshwater environment but has retained the capability to synthesize urea de novo through the arginine-ornithine-urea cycle (OUC). The present study aimed to elucidate whether the capacity of urea synthesis in H. signifer could be upregulated in response to environmental ammonia exposure. When H. signifer was exposed to environmental ammonia, fairly high concentrations of ammonia were accumulated in the plasma and other tissues. This would subsequently reduce the net influx of exogenous ammonia by reducing the NH(3) partial pressure gradient across the branchial and body surfaces. There was also an increase in the OUC capacity in the liver. Since the ammonia produced endogenously could not be excreted effectively in the presence of environmental ammonia, it was detoxified into urea through the OUC. In comparison, the South American freshwater stingray Potamotrygon motoro, which has lost the capability to synthesize urea de novo, was unable to detoxify ammonia to urea during ammonia loading. No increase in glutamine was observed in the various tissues of H. signifer exposed to environmental ammonia despite a significant increase in the hepatic glutamine synthetase activity. These results indicate that the excess glutamine formed was channelled completely into urea formation through carbamoyl phosphate synthetase III. It has been reported elsewhere that both urea synthesis and urea retention were upregulated in H. signifer exposed to 20 per thousand water for osmoregulatory purposes. By contrast, for H. signifer exposed to environmental ammonia in freshwater, the excess urea formed was excreted to the external medium instead. This suggests that the effectiveness of urea synthesis de novo as a strategy to detoxify ammonia is determined not simply by an increase in the capacity of urea synthesis but, more importantly, by the ability of the animal to control the direction (i.e. absorption or excretion) and rate of urea transport. Our results suggest that such a strategy began to develop in those elasmobranchs, e.g. H. signifer, that migrate into a freshwater environment from the sea but not in those permanently adapted to a freshwater environment.

Amino Acids↗

PubMed2006

Transient receptor potential vanilloid receptor-1 does not contribute to slowly adapting airway receptor activation by inhaled ammonia.

Inhalation of ammonia influences the activity of slowly adapting airway receptors (SARs), but the mechanism(s) is uncertain. Release of inflammatory mediators by transient receptor potential vanilloid receptor-1 (TRPV1) containing nerve endings could affect SAR response to ammonia. We examined how sensitization and subsequent desensitization of the TRPV1 by resiniferatoxin (RTX), affected the responses of SARs to inhaled ammonia. In pentobarbital-anesthetized, paralyzed and artificially ventilated rats, the left cervical vagus nerve was exposed, sectioned rostrally, and desheathed. Single fibers of SARs were identified and recorded. Two milliliters of ammonia vapor (from a 30% NH(4)OH solution) was inhaled over 20 s and responses to ammonia were measured. RTX was injected intravenously at 2 microg/Kg. Twenty minutes later, ammonia inhalation was repeated. Isoproterenol (ISO, 100 microg/kg, i.v.) was used in another set of experiments to block possible ammonia-induced bronchoconstriction. Ammonia increased tonic activity of SARs (n=10, P<0.0001), with complex changes in ventilator-related activity. SAR firing rate began to increase 2.3+/-0.2 min after RTX and returned to control levels at 13.6+/-1.4 min (n=10). By 20 min after RTX cardiovascular responses to ammonia were abolished, but effects on SAR activity were essentially unchanged. ISO did not modify the response of SARs to ammonia (n=8). These data suggest that responses of SARs to ammonia in rats do not depend on release of mediators by nerve endings containing TRPV1 and are not secondary to bronchoconstriction. However, when TRPV1 containing nerve endings were initially activated by RTX, the release of mediators may have affected SAR discharges.

Action Potentials↗

PubMed2006

Ammonia as a respiratory gas in water and air-breathing fishes.

Ammonia is produced in the liver and excreted as NH(3) by diffusion across the gills. Elevated ammonia results in an increase in gill ventilation, perhaps via stimulation of gill oxygen chemo-receptors. Acidification of the water around the fish by carbon dioxide and acid excretion enhances ammonia excretion and constitutes "environmental ammonia detoxification". Fish have difficulties in excreting ammonia in alkaline water or high concentrations of environmental ammonia, or when out of water. The mudskipper, Periphthalmodon schlosseri, is capable of active NH(4)(+) transport, maintaining low internal levels of ammonia. To prevent a back flux of NH(3), these air-breathing fish can increase gill acid excretion and reduce the membrane NH(3) permeability by modifying the phospholipid and cholesterol compositions of their skin. Several air-breathing fish species can excrete ammonia into air through NH(3) volatilization. Some fish detoxify ammonia to glutamine or urea. The brains of some fish can tolerate much higher levels of ammonia than other animals. Studies of these fish may offer insights into the nature of ammonia toxicity in general.

Adaptation, Physiological↗

PubMed2006

The application of high frequency ultrasound waves to remove ammonia from simulated industrial wastewater.

This article aims at applying the ultrasound technique in the field of clean technology to protect environment. The principle of ultrasound was conducted here to remove and recover ammonia from industrial wastewater. Three different concentrations of ammonia namely 5%, 15% and 25% (vol.%) were used to study the efficiency of removing ammonia from water. These concentrations are exactly similar to what may be found in wastewater resulting from strippers at petroleum refinery. High ultrasound frequency device with 2.4 and 1.7 MHz was conducted to study the effect of waves on the removal of ammonia. It was found that the ultrasound has the ability to remove ammonia with 5% concentration to meet the local standard of treated wastewater within less than 2 h for 0.080 L solution. It was also found that as the concentration of the ammonia increases the removing of ammonia within 2 h decreases, still the concentration of the ammonia meets the standard of the treated wastewater. The ability of the ultrasound to remove the ammonia failed to produce any mist when the height of the liquid solution increased, namely when the height reached (0.0337 m). This is equivalent to liquid volume of 0.150 L. It means that the device capacity to remove ammonia has certain limitations based on liquid heights. The best condition for ammonia removal was obtained at 5% concentration and 0.080 L liquid volume (equivalent to 0.0165 m).

Ammonia↗

PubMed2003

Effect of ammonia toxicity on the competition among three species of cladocerans (Crustacea: Cladocera).

Among the natural abiotic variables affecting the species density and composition of cladocerans, ammonia is important. Using population growth data as tool, we studied the competitive outcome of three cladoceran species (Ceriodaphnia dubia, Daphnia pulex, and Moina macrocopa) grown alone and together at three different concentrations (0, 25, and 100 mg L(-1)) of ammonia at one density (1 x 10(6)cells ml(-1)) of the microalga Chlorella vulgaris. Regardless of the presence or absence of competing species, C. dubia showed little population growth at 100 mg L(-1) of ammonia. At 25 mg L(-1) of ammonia, the population density of C. dubia increased but the value was much lower than that in control. D. pulex was able to grow at the ammonia concentration of 25 mg L(-1), comparable to controls. However, at 100 mg L(-1) of ammonia, the population declined and more rapidly when competed with other cladocerans. M. macrocopa showed decreased population density with increasing ammonia concentration in the medium. This trend was accelerated by the presence of competing cladocerans. M. macrocopa was benefited by the presence of D. pulex at 0 and 25 mg L(-1) of ammonia in the medium. The peak population density of C. dubia varied from 0.5 to 9 ind.ml(-1), whereas for D. pulex and M. macrocopa, these values varied from 1 to 3 ind.ml(-1) and 7 to 18 ind.ml(-1), respectively, depending on the ammonia concentration and the presence of competing species. The rates of population increase per day of C. dubia, D. pulex, and M. macrocopa ranged from -0.12+/-0.001 to 0.30+/-0.01, 0.04+/-0.001 to 0.22+/-0.002, and 0.201+/-0.028 to 0.235+/-0.019, respectively, depending on the ammonia concentration and the presence of competitors. Our study showed that while competition within the chosen cladoceran species caused suppression of one or two competing species, the presence of ammonia expedited this process based on the relative sensitivities of the tested zooplankton.

Ammonia↗

PubMed2004

Blood ammonia levels and hepatic encephalopathy.

The importance of measurements of the blood ammonia concentration in the evaluation of patients with known or suspected hepatic encephalopathy (HE) is still disputed in spite of a general acknowledgment that ammonia is important in the pathogenesis of the disorder. Several recent studies have suggested that it is not necessary to utilize arterial blood when measuring ammonia in the blood. Venous blood or a computation of the partial pressure of ammonia gas in blood samples may suffice. The value of blood ammonia measurements is limited by the fact that this is not the variable that is the most important. Ideally, one would like to know how much ammonia enters the brain, not how much is in the blood. The blood-brain barrier (BBB) is the critical and poorly understood element in this relationship. Although both ammonia in the gas and ionic forms cross the BBB, the ease with which this movement occurs is significantly higher in patients with HE. In the absence of simple methods to measure the brain ammonia metabolic rate and to assess the BBB to ammonia in conjunction with measuring the blood ammonia concentration, the variables that would be the most desirable to measure, the use of arterial and/or venous blood measurements needs to be coupled with a complete understanding of the physiology of cerebral ammonia metabolism.

Ammonia↗

PubMed2024

Ammonia-oxidizing bacteria and archaea exhibit differential nitrogen source preferences.

Ammonia-oxidizing microorganisms (AOM) contribute to one of the largest nitrogen fluxes in the global nitrogen budget. Four distinct lineages of AOM: ammonia-oxidizing archaea (AOA), beta- and gamma-proteobacterial ammonia-oxidizing bacteria (β-AOB and γ-AOB) and complete ammonia oxidizers (comammox), are thought to compete for ammonia as their primary nitrogen substrate. In addition, many AOM species can utilize urea as an alternative energy and nitrogen source through hydrolysis to ammonia. How the coordination of ammonia and urea metabolism in AOM influences their ecology remains poorly understood. Here we use stable isotope tracing, kinetics and transcriptomics experiments to show that representatives of the AOM lineages employ distinct regulatory strategies for ammonia or urea utilization, thereby minimizing direct substrate competition. The tested AOA and comammox species preferentially used ammonia over urea, while β-AOB favoured urea utilization, repressed ammonia transport in the presence of urea and showed higher affinity for urea than for ammonia. Characterized γ-AOB co-utilized both substrates. These results reveal contrasting niche adaptation and coexistence patterns among the major AOM lineages.

Archaea↗

PubMed2002

Monitoring ammonia to assess halitosis.

OBJECTIVE: This study examined the applicability of ammonia monitoring for assessing halitosis. STUDY DESIGN: The actual degree of halitosis was determined by using an organoleptic test in 61 subjects aged 28 +/- 10 years (mean +/- SD). Levels of volatile sulfur compounds and ammonia were determined by using gas chromatography and ammonia monitoring, respectively. Levels of ammonia and methyl mercaptan produced by bacteria in dental plaque and tongue-coating samples obtained from 25 subjects were quantified. In addition, changes in ammonia levels were measured before and after removing tongue coating or dental plaque. RESULTS: There was no significant correlation between the organoleptic score and the ammonia level measured with ammonia monitoring, whereas there was a significant correlation between ammonia level and the total level of volatile sulfur compounds measured with gas chromatography. Significant correlations were also observed between ammonia level and levels of methyl mercaptan produced by bacteria in dental plaque and tongue coating. Furthermore, the ammonia level decreased after the removal of tongue coating and dental plaque. CONCLUSION: These results indicate that measuring ammonia levels is useful for assessing halitosis, specifically for halitosis arising from a lack of oral hygiene.

Adult↗

PubMed2006

Heterogeneous decomposition of indoor ammonia in a photoreactor with TiO2-finished cotton fabrics.

Addition of urea-based antifreeze admixtures during cement mixing can make it possible to concrete cement in construction of buildings in cold weather. This, however has led to increasing indoor air pollution due to continuous transformation and emission from urea to gaseous ammonia in indoor concrete walls. In order to control ammonia from indoor concrete walls, aqueous dispersion of nano-titanium dioxide (TiO2) was prepared and mixed with silicone additive to establish a treating bath. Cotton fabrics were finished with this treating bath by using pad-dry-cure process and then characterized by X-Ray Diffractometer, Infrared Fourier Transform Spectrometer and Scanning Electron Microscope. The gaseous ammonia was derived from an environmental condition simulated chamber. The heterogeneous decomposition of gaseous ammonia by UV/TiO2 process in an annular photoreactor fixed with the TiO2-coated cotton fabric was studied under various dosages of aqueous nano-TiO2 dispersion, initial ammonia concentration, relative humidity and gas flow rate. A design equation of surface catalytic kinetics was developed for describing the decomposition of ammonia in air streams by UV/TiO2 process at given operating conditions. Experimental results indicated that increasing dosage of aqueous nano-TiO2 dispersion improved the ammonia decomposition of cotton fabric, which was prepared. At a constant temperature of 25 degrees C, ammonia in the air stream was effective removed by decreasing initial ammonia concentration and gas flow rate. For moisture in the range of 15-65%, when the relatively humidity level was increased to 45%, the decomposition of ammonia was remarkably enhanced, and the decomposition of ammonia could be inhibited by excessive moisture.

Air Pollutants↗