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PubMed1999

Contribution of branched-chain amino acids to uteroplacental ammonia production in sheep.

The uteroplacental tissues are a principal site of ammonia production for the conceptus. The goal of this study was to examine the effect of the composition of maternal amino acid (AA) infusate on uteroplacental ammonia production. Seven pregnant ewes (126 +/- 1. 4 days gestation) were infused through the maternal femoral vein (duration 3.5 h, rate 240 ml per hour) with three solutions of AAs. The first infusate was comparable to commercial parenteral nutrition preparations, the second infusate contained the same solution without branched-chain AAs (BCAAs), and the third infusate contained only BCAAs. Blood samples were simultaneously collected from the maternal artery, uterine vein, fetal artery, and umbilical vein to determine plasma AA concentrations and whole blood ammonia concentrations, before (control) and 2 h after (experimental) the start of infusion. Uterine and umbilical blood flows were measured using the ethanol steady-state diffusion method. Results showed that fetal arterial and venous ammonia concentrations increased significantly after infusions with all AAs or only BCAAs, but not without BCAAs. Uteroplacental ammonia production increased in response to each of the three infusates. However, this increase was much greater when the BCAAs were present in infusates. We conclude that there is a significant contribution of BCAAs to the uteroplacental ammonia production. Maternal AA infusions containing BCAAs can result in increased fetal blood ammonia concentrations.

Amino Acids, Branched-Chain↗
PubMed1988

Effects of 16,16-dimethyl-prostaglandin E2 on ammonia- and ethanol-induced mucosal lesions in the rat.

The effect of necrotizing agents, such as ammonia and ethanol, on the gastric mucosa was compared. Intragastric administration of ammonia (0.6-1.0%) and ethanol (60-100%) produced hemorrhagic necrosis of gastric mucosa in a concentration-dependent manner. In the anesthetized rat, the macroscopic lesions induced by ethanol were significantly inhibited by pretreatment with 3 or 10 micrograms/kg of 16,16-dmPGE2, but the lesions induced by ammonia were not inhibited by either 3 or 10 micrograms/kg of 16,16-dmPGE2 in the anesthetized rat. The decrease of gastric transmucosal potential difference and mucosal blood flow produced by ethanol (100%) were significantly attenuated by 16,16-dmPGE2; however, those produced by ammonia (1%) were not inhibited by 16,16-dmPGE2 in the anesthetized rat. In conscious rats, ammonia-induced lesions were not inhibited by pretreatment with 3 micrograms/kg of 16,16-dmPGE2 but they were significantly reduced by the pretreatment of 10 micrograms/kg of 16,16-dmPGE2. These results show that 16,16-dmPGE2 afforded little protection against ammonia-induced gastric lesions in the anesthetized rat and suggest that a different mechanism is involved in the development of gastric mucosal lesions between those induced by ethanol and those induced by ammonia.

16,16-Dimethylprostaglandin E2↗
PubMed1990

Generation of ammonia and mucosal lesion formation following hydrolysis of urea by urease in the rat stomach.

We examined the morphological changes in gastric mucosa and the generation of ammonia after exposure of the rat stomach to urea in the presence of urease, in attempts to investigate a pathophysiological role of urea, urease, and ammonia system in gastric ulcer diseases. Exposure of the stomach for 20 min to 2 ml urea (0.025-0.2%) together with urease (100 IU) induced histological damages in a concentration-related manner. Either urea or urease alone did not induce any histological change in the mucosa. Instillation of urea into the stomach generated ammonia in the presence of urease; the amount of ammonia was increased depending on the concentration of urea, and was closely associated with the severity of histological damage. The exposure of the stomach to ammonia (NH4OH: 0.01-0.1%) also produced histological damages in the gastric mucosa in a concentration-related manner. The characteristics of injury induced by 0.5-1.0% ammonia were stasis of microcirculation, disruption of the surface epithelial cells, and necrosis of the mucosa. These results demonstrated that ammonia generated from the hydrolysis of urea by urease in the stomach causes damages in the gastric mucosa.

Ammonia↗
PubMed2003

Hazardous ammonia releases: public health consequences and risk factors for evacuation and injury, United States, 1993-1998.

Unplanned releases of ammonia lead more often to evacuation and injury than releases of other chemicals, but few studies have systematically investigated ammonia releases. We analyzed Hazardous Substances Emergency Events Surveillance system data for 1993-1998. Evacuation of a total of at least 40,680 persons resulted from 537 ammonia releases, and 248 ammonia releases led to injury of 1434 persons. Equipment failure and operator error were cited as factors contributing to ammonia releases 90% of the time. Eighty-seven percent of releases occurred at fixed facilities. Risk factors for evacuation and injury differed between the food-manufacturing industry and other industries. Indoor release was a consistent risk factor, whereas quantity of ammonia released was not always a risk factor. Preventive maintenance and worker training may be effective tools to reduce the burdens of hazardous ammonia releases.

Accidents, Occupational↗
PubMed2004

Production of ammonia by Tritrichomonas foetus and Trichomonas vaginalis.

Production of ammonia is difficult to find among the various studies of amino acid metabolism in protozoa. Several studies suggest that catabolism of arginine to ammonium is important for the growth of trichomonads. Trichomonads are amitochondriate zooflagellates that thrive under microaerophilic and anaerobic conditions. The authors were able to detect accumulation of ammonium ions and ammonia in cultures of Tritrichomonas foetus and Trichomonas vaginalis, including those resistant to metronidazole. Ammonium ions and ammonia were detected using the indophenol colorimetric method. Cells incubated overnight under an ambient oxygen gas phase had 0.9 mM soluble ammonium (NH(4)(+) and NH(3)) or a 20 % greater concentration of ammonium relative to sterile growth medium that had been incubated similarly. Production of ammonia itself was confirmed by analysis of a wick that was moistened with sulfuric acid (20 mM) and placed above the liquid in sealed cultures of a strain of Trichomonas vaginalis. The wicks from these cultures captured the equivalent of 0.048 mM volatile ammonia (NH(3)) from the liquid as compared to 0.021 mM volatile ammonia from sterile medium after overnight incubation. Intact trichomonads, 0.7 x 10(6) cells ml(-1) equivalent to 0.7 mg protein ml(-1), incubated in Doran's buffer with or without (1 mM) L-arginine produced significant amounts of soluble ammonium (0.07 mM and 0.04 mM, respectively) during 60 min. The results indicate that ammonium ions and the more irritating ammonia are significant metabolites of trichomonads. In addition, based upon end-product amounts, it appears that the rate of arginine metabolism is of the same order of magnitude as that for carbohydrate metabolism by trichomonads.

Ammonia↗
PubMed1984

Influence of pathological concentrations of ammonia on metabolic fate of 14C-labeled glutamate in astrocytes in primary cultures.

Rates of glutamine formation and of carbon dioxide production (as an indication of oxidative deamination of glutamate) were determined in primary cultures of astrocytes exposed to 50 microM labeled glutamate in the absence or presence of added ammonia (0.1-3 mM). Glutamine formation (1.7 nmol/min/mg protein) was unaffected by all concentrations of added ammonia. This probably reflects the presence of a low content of ammonia (0.1-0.2 mM), originating from degradation of glutamine, in the cells even in the absence of added ammonia, and it shows that pathophysiological concentrations of ammonia do not increase the formation of glutamine from exogenous glutamate. The carbon dioxide production rate was 5.9 nmol/min/mg protein, i.e., three to four times higher than the rate of glutamine formation. It was significantly reduced (to 3.5 nmol/min/mg protein) in the presence of 1 mM or more of ammonia. This is in keeping with suggestions by others that toxic levels of ammonia affect oxidative metabolism.

Ammonia↗
PubMed1992

Physiological levels of ammonia regulate glutamine synthesis from extracellular glutamate in astrocyte cultures.

The effect of ammonia on glutamate accumulation and metabolism was examined in astrocyte cultures prepared from neonatal rat cortices. Intact astrocytes were incubated with 70 microM L-[14C(U)]glutamate and varying amounts of ammonium chloride. The media and cells were analyzed separately by HPLC for amino acids and labelled metabolites. Extracellular glutamate was reduced to 8 microM by 60 min. Removal of glutamate from the extracellular space was not altered by addition of ammonia. The rate of glutamine synthesis was increased from 3.6 to 9.3 nmol/mg of protein/min by addition of 100 microM ammonia, and intracellular glutamate was reduced from 262 to 86 nmol/mg of protein after 30 min. The metabolism of accumulated glutamate was matched nearly perfectly by the synthesis of glutamine, and both processes were proportional to the amount of added ammonia. The transamination and deamination products of glutamate were minor metabolites that either decreased or remained unchanged with increasing ammonia. Thus, ammonia addition stimulates the conversion of glutamate to glutamine in intact astrocyte cultures. At physiological concentrations of ammonia, glutamine synthesis appears to be limited by the rate of glutamate accumulation and the activity of competing reactions and not by the activity of glutamine synthetase.

Ammonia↗
PubMed1993

Cerebral cortex ammonia and glutamine metabolism in two rat models of chronic liver insufficiency-induced hyperammonemia: influence of pair-feeding.

Enhanced cerebral cortex ammonia uptake, subsequent glutamine synthesis, and glutamine release into the bloodstream have been hypothesized to deplete cerebral cortex glutamate pools. We investigated this hypothesis in rats with chronic liver insufficiency-induced hyperammonemia and in pair-fed controls to rule out effects of differences in food intake. Cerebral cortex plasma flow and venous-arterial concentration differences of ammonia and amino acids, as well as cerebral cortex tissue concentrations, were studied 7 and 14 days after surgery in portacaval-shunted/bile duct-ligated, portacaval-shunted, and sham-operated rats, while the latter two were pair-fed to the first group, and in normal unoperated ad libitum-fed control rats. At both time points, arterial ammonia was elevated in the chronic liver insufficiency groups and arterial glutamine was elevated in portacaval shunt/biliary obstruction rats compared to the other groups. In the chronic liver insufficiency groups net cerebral cortex ammonia uptake was observed at both time points and was accompanied by net glutamine release. Also in these groups, cerebral cortex tissue glutamine, many other amino acid, and ammonia levels were elevated. Tissue glutamate levels were decreased to a similar level in all operated groups compared with normal unoperated rats, irrespective of plasma and tissue ammonia and glutamine levels. These results demonstrate that during chronic liver insufficiency-induced hyperammonemia, the rat cerebral cortex enhances net ammonia uptake and glutamine release. However, the decrease in tissue glutamate concentrations in these chronic liver insufficiency models seems to be related primarily to nutritional status and/or surgical trauma.

Amino Acids↗
PubMed2001

Effects of high-volume plasmapheresis on ammonia, urea, and amino acids in patients with acute liver failure.

OBJECTIVE: In acute liver failure (ALF), urea production is severely impaired, and detoxification of ammonia by glutamine synthesis plays an important protective role. The aim of this study was to examine the effects of therapeutic high-volume plasmapheresis (HVP) on arterial concentrations and splanchnic exchange rates of ammonia, urea, and amino acids-in particular, glutamine. METHODS: A quantity of 8 L of plasma was exchanged over the course of 7 h in 11 patients with ALF after development of hepatic encephalopathy grade III-IV. Splanchnic exchange rates of ammonia, urea, and amino acids were measured by use of liver vein catheterization. RESULTS: HVP removed ammonia and glutamine at a rate of 1 micromol/min and 27 micromol/min, respectively. Arterial ammonia decreased from 160 +/- 65 to 114 +/- 50 micromol/L (p < 0.001). In contrast, arterial glutamine was only minimally changed from 1791 +/- 1655 to 1764 +/- 1875 micromol/L (NS). This implied that the rate of systemic glutamine synthesis was increased by 27 micromol/min. Splanchnic exchange rates (before vs after HVP) were as follows: for ammonia, -93 +/- 101 versus -70 +/- 80 micromol/min (NS); urea-nitrogen, 0.08 +/- 1.64 versus -0.31 +/- 0.45 mmol/min (NS); alanine, -73 +/- 151 versus 12 +/- 83 micromol/min (p < 0.05); and glutamine: 132 +/- 246 versus 186 +/- 285 micromol/min (NS), with negative values denoting release. CONCLUSIONS: Arterial ammonia decreased during HVP in patients with ALF. The data suggest that this effect of HVP could be explained by increased hepatic urea synthesis and possibly by increased glutamine synthesis in muscle tissue.

Adult↗
PubMed2006

The influence of synthetic sheep urine on ammonia oxidizing bacterial communities in grassland soil.

In grazed, grassland soils, sheep urine generates heterogeneity in ammonia concentrations, with potential impact on ammonia oxidizer community structure and soil N cycling. The influence of different levels of synthetic sheep urine on ammonia oxidizers was studied in grassland soil microcosms. 'Total' and active ammonia oxidizers were distinguished by comparing denaturing gradient gel electrophoresis (DGGE) profiles following PCR and RT-PCR amplification of 16S rRNA gene fragments, targeting DNA and RNA, respectively. The RNA-based approach indicated earlier, more reproducible and finer scale qualitative shifts in ammonia oxidizing communities than DNA-based analysis, but led to amplification of a small number of nonammonia oxidizer sequences. Qualitative changes in RNA-derived DGGE profiles were related to changes in nitrate accumulation. Sequence analysis of excised DGGE bands revealed that ammonia oxidizing communities in synthetic sheep urine-treated soils consisted mainly of Nitrosospira clusters 2, 3 and 4. Nitrosospira cluster 2 increased in relative abundance in microcosms treated with all levels of synthetic sheep urine. Low levels additionally led to increased relative abundance of Nitrosospira cluster 4 and medium and high levels increased relative abundance of cluster 3. Synthetic sheep urine is therefore likely to influence the spatial distribution and composition of ammonia oxidizer communities, with consequent effects on nitrate accumulation.

Ammonia↗
PubMed1992

Influence of short-chain fatty acids on ammonia absorption across the rumen wall in sheep.

The effects of short-chain fatty acids (SCFA) on ammonia net absorption from the sheep rumen in vivo and on ammonia transport across rumen wall mucosa in vitro were studied. Ammonia net absorption was directly, though in a non-linear manner, correlated with the SCFA concentration in the artificial rumen fluid. Almost 70% of total ammonia absorption was dependent upon the presence of SCFA when 12 mmol l-1 ammonia and 67.5 mmol l-1 SCFA were present. Lactic acid was ineffective. Incubation experiments showed that mucosal disappearance and serosal appearance of ammonia were reduced by 38% and 32%, respectively, when SCFA (63 mmol l-1) were replaced by lactic acid. The SCFA effect was independent of the type of SCFA used. In part of the experiments up to 54% of the ammonia taken up by the tissue was not recovered in the serosal incubation solution and must have been metabolized in the mucosa.

Absorption↗
PubMed1976

Lithium protection against oxygen toxicity in rats: ammonia and amino acid metabolism.

1. The use of Li pre-treatment in rats before high pressure oxygen exposure has been reported effective in controlling convulsions. This is an effect which is better demonstrated if exposure to oxygen follows shortly after Li injection than exposure following several hours later. 2. This study has investigated the hypothesis that the protective action of Li may be exerted, in the short term, by its removing ammonia from the blood and alleviating the latter's known toxic action. 3. A normal Li distribution time profile in unstressed rat brain and blood following intraperitoneal injection has been established. Brain and blood ammonia, amino acids and Li concentrations were also measured in Li-treated animals exposed and convulsed by oxygen. These measurements were made both shortly (15 min) and also several hours after (24 hr) Li treatment. Ammonia and amino acid values in Li-protected groups were compared to normal unstressed animal values and also to values in animals convulsed by oxygen unprotected by Li pre-treatment. 4. In rat brain abd blood significant (P less than 0-001) elevation of ammonia and glutamine and depression of gamma-amino butyric acid (brain only) and glutamate was noted following oxygen treatment in unprotected animals. Prior injection of Li 15 min before high pressure oxygen exposure delayed convulsions twice as long. Additionally if these animals were only exposed to oxygen for a period of time equal to that which would normally produce convulsions in unprotected animals, brain and blood ammonia and amino acids were maintained near to unstressed animal levels. Concomitantly, blood Li concentrations were considerably depressed below the values one would expect from the previously determined Li distribution time profile. 5. In rats exposed to high pressure oxygen 24 hr after Li treatment there was no protective action against high pressure oxygen convulsion, rather a potentiating effect for convulsion was seen. 6. These data present compelling evidence for the controlling effect of Li in rats, on rising blood ammonia concentration which occurs in high pressure oxygen exposure. The effect might well be due to the known chelating properties of Li with ammonia.

Amino Acids↗
PubMed1993

[Cytotoxic effect of ammonia produced by Helicobacter pylori urease on the cultural cells].

We investigated the action of the ammonia produced by Helicobacter pylori urease on the cultured cells. The urease was purified from supernatant fluid of sonicated cell of H. pylori cultured on blood agar for 2 days at 37 degrees C under microaerophilic condition. Purification was carried out by DEAE-Sepharose chromatography, Phenyl-Sepharose chromatography, Sephacryl S-200 SF chromatography and fast protein liquid chromatography on Mono-Q. Vero, HeLa and Intestin 407 cells with or without the addition of 30 mM urea were exposed to the purified urease. Those cells showed cytotoxic effects within 80 minutes after addition of purified urease in the presence of urea. The ammonia production was observed on tissue culture medium within 10 minutes, and the ammonia concentration ranged from 5.56 mg/ml to 7.3 mg/ml and pH in the medium was over pH 9.0. No such effect was observed on the cells exposed to urease without urea. Ammonia water added to Vero cells showed the same cytotoxic effect within 70 minutes on the production of ammonia and raised the pH. However, when the cells were exposed to the ammonia water pre-neutralized to a given pH 7-8 using 1 N HCl cytotoxic effect was not observed. It was concluded that the cytotoxic effect of H. pylori urease was dependent on ammonia generated by hydrolysis of urea.

Ammonia↗
PubMed1976

Toxicity of ammonia to algae in sewage oxidation ponds.

Ammonia, at concentrations over 2.0 mM and at pH values over 8.0, inhibits photosynthesis and growth of Scenedesmus obliquus, a dominant species in high-rate sewage oxidation ponds. Photosynthesis of Chlorella pyrenoidosa, Anacystis nidulans, and Plectonema boryanum is also susceptible to ammonia inhibition. Dark respiration and cell morphology were unaffected by any combination of pH and ammonia concentrations tested, thus limiting the apparent effect to inhibition of the normal function of the chloroplasts. Methylamine had the same effect as ammonia, and its penetration into the cells was found to be pH dependent. Therefore, the dependence of toxicity of amines to algae on pH apparently results from the inability to penetrate the cell membrane in the ionized form. When operated at 120-h detention time of raw wastewater, the high-rate oxidation pond maintained a steady state with respect to algal growth and oxygen concentration, and the concentration of ammonia did not exceed 1.0 mM. Shifting the pond to 48-h detention time caused an increase in ammonia concentration in the pond water to 2.5 mM, and the pond gradually turned anaerobic. Photosynthesis, which usually elevates the pH of the pond water to 9.0 to 10.0, could not proceed beyond pH 7.9 because of the high concentration of ammonia, and the algal population was washed out and reduced to a concentration that could maintain a doubling time of 48 h without photosynthesis bringing the pH to inhibitory levels. Under these conditions, the pH of the bond becomes a factor that limits the operational efficiency of the oxidation pond.

Ammonia↗
PubMed1988

Enrichment and isolation of a ruminal bacterium with a very high specific activity of ammonia production.

When mixed ruminal bacteria were inoculated into semicontinuous cultures (25% transfer every other day) containing lactate, dulcitol, pectin, or xylose and Trypticase (1 g/liter) as the sole nitrogen source, the specific activity of ammonia production increased. The greatest enrichment was observed with lactate and xylose, and in these cases the specific rate of ammonia production was eightfold higher than that of the ruminal fluid control (approximately 35 nmol of ammonia per mg of protein per min). Isolates with different morphologies were obtained from each of the enrichments, but in no case did the specific activity of any isolate exceed that of the mixed ruminal bacteria. If Trypticase (15 g/liter) was used as the only energy and nitrogen source, there was an even greater increase in ammonia production, and two monensin-sensitive bacteria, a Peptostreptococcus species and a Clostridium species, were obtained. The Peptostreptococcus species was unable to grow on any of 25 carbohydrate or carbohydrate derivatives tested; but the Clostridium species was able to use glucose, maltose, fructose, cellobiose, trehalose, sorbitol, and salicin as energy sources. Neither organism was able to grow in the absence of an amino acid source, but growth rates on Trypticase were greater than 0.35/h. The specific activities of ammonia production were 346 and 427 nmol/mg of protein per min for strains of Peptostreptococcus and Clostridium, respectively. Megasphaera elsdenii and Bacteroides ruminicola, previously isolated ruminal ammonia producers, had specific activities of only 11 and 19 nmol of ammonia per mg of protein per min, respectively. The most probable number of Clostridium species in ruminal fluid was less than 10(3)/ml, but the Peptostreptococcus species was present at 10(8)/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Ammonia↗
PubMed1993

Effect of monensin on the specific activity of ammonia production by ruminal bacteria and disappearance of amino nitrogen from the rumen.

When unadapted mixed ruminal bacteria (312 mg of protein per liter) were treated with monensin (5 mM) in vitro, the rates of ammonia production from enzymatic digests of casein, gelatin, and soy protein (0.5 g of N per liter) were decreased from 46 +/- 2 to 24 +/- 1, 20 +/- 1 to 7 +/- 1, and 40 +/- 2 to 18 +/- 2 nmol/mg of protein per min, respectively. Monensin also caused a decrease in ammonia production in vivo. Nonlactating dairy cows which were fed 0.56 kg of timothy hay 12 times per day had a steady-state ruminal ammonia concentration of 2.7 +/- 0.1 mM, and the ammonia concentration decreased to 1.2 +/- 0.2 mM when monensin (350 mg/day) was added to the diet. The decrease in ammonia production was associated with a 10-fold reduction (4.1 x 10(6) versus 4.2 x 10(5)/ml) in the most probable number of ammonia-producing ruminal bacteria that could use protein hydrolysate as an energy source. Monensin had little effect on the most probable number of carbohydrate-utilizing ruminal bacteria (6.5 versus 7.0 x 10(8)/ml). The addition of protein hydrolysates (560 g) to the rumen caused a rapid increase in the ammonia concentration, but this increase was at least 30% lower when the animals were fed monensin.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1999

Phylogenetic differences between particle-associated and planktonic ammonia-oxidizing bacteria of the beta subdivision of the class Proteobacteria in the Northwestern Mediterranean Sea.

The aim of this study was to determine if there were differences between the types of ammonia-oxidizing bacteria of the beta subdivision of the class Proteobacteria associated with particulate material and planktonic samples obtained from the northwestern Mediterranean Sea. A nested PCR procedure performed with ammonia oxidizer-selective primers was used to amplify 16S rRNA genes from extracted DNA. The results of partial and full-length sequence analyses of 16S rRNA genes suggested that different groups of ammonia-oxidizing bacteria were associated with the two sample types. The particle-associated sequences were predominantly related to Nitrosomonas eutropha, while the sequences obtained from the planktonic samples were related to a novel marine Nitrosospira group (cluster 1) for which there is no cultured representative yet. A number of oligonucleotide probes specific for different groups of ammonia oxidizers were used to estimate the relative abundance of sequence types in samples of clone libraries. The planktonic libraries contained lower proportions of ammonia oxidizer clones (0 to 26%) than the particulate material libraries (9 to 83%). Samples of the planktonic and particle-associated libraries showed that there were depth-related differences in the ammonia oxidizer populations, with the highest number of positive clones in the particle-associated sample occurring at a depth of 700 m. The greatest difference between planktonic and particle-associated populations occurred at a depth of 400 m, where only 4% of the clones in the planktonic library were identified as Nitrosomonas clones, while 96% of these clones were identified as clones that were related to the marine Nitrosospira species. Conversely, all ammonia oxidizer-positive clones obtained from the particle-associated library were members of the Nitrosomonas group. This is the first indication that Nitrosomonas species and Nitrosospira species may occupy at least two distinct environmental niches in marine environments. The occurrence of these groups in different niches may result from differences in physiological properties and, coupled with the different environmental conditions associated with these niches, may lead to significant differences in the nature and rates of nitrogen cycling in these environments.

Ammonia↗
PubMed2002

Nitrite as a stimulus for ammonia-starved Nitrosomonas europaea.

Ammonia-starved cells of Nitrosomonas europaea are able to preserve a high level of ammonia-oxidizing activity in the absence of ammonium. However, when the nitrite-oxidizing cells that form part of the natural nitrifying community do not keep pace with the ammonia-oxidizing cells, nitrite accumulates and may subsequently inhibit ammonia oxidation. The maintenance of a high ammonia-oxidizing capacity during starvation is then nullified. In this study we demonstrated that cells of N. europaea starved for ammonia were not sensitive to nitrite, either when they were starved in the presence of nitrite or when nitrite was supplied simultaneously with fresh ammonium. In the latter case, the initial ammonia-oxidizing activity of starved cells was stimulated at least fivefold.

Ammonia↗