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PubMed2003

Community structure of ammonia-oxidizing bacteria within anoxic marine sediments.

The potential for oxidation of ammonia in anoxic marine sediments exists through anaerobic oxidation by Nitrosomonas-like organisms, utilizing nitrogen dioxide, coupling of nitrification, manganese reduction, and anaerobic oxidation of ammonium by planctomycetes (the Anammox process). Here we describe the presence of microbial communities with the potential to carry out these processes in a natural marine sediment system (Loch Duich, Scotland). Natural microbial communities of Planctomycetales-Verrucomicrobia and beta- and gamma-proteobacterial ammonia-oxidizing bacteria were characterized by analysis of 16S rRNA genes amplified using group-specific primers by PCR- and reverse transcription-PCR amplification of 16S rDNA and RNA, respectively. Amplification products were analyzed by sequencing of clones and by denaturant gradient gel electrophoresis (DGGE). Amplification of primers specific for Planctomycetales-Verrucomicrobia and beta-proteobacterial ammonia-oxidizing bacteria generated products at all sampling sites and depths, but no product was generated using primers specific for gamma-proteobacterial ammonia-oxidizing bacteria. 16S rDNA DGGE banding patterns indicated complex communities of beta-proteobacterial ammonia-oxidizing bacteria in anoxic marine sediments. Phylogenetic analysis of sequences from clones and those excised from DGGE gels suggests dominance of Nitrosospira cluster 1-like organisms and of strains belonging to a novel cluster represented in dominant bands in 16S rRNA DGGE banding patterns. Their presence indicates a group of organisms closely related to recognized beta-proteobacterial ammonia-oxidizing bacteria that may be selected in anoxic environments and may be capable of anoxic ammonia oxidation. Sequence analysis of planctomycete clone libraries and sequences excised from DGGE gels also demonstrated a diverse microbial community and suggested the presence of new subdivisions, but no sequence related to recognized Anammox organisms was detected.

Ammonia↗
PubMed2004

Denaturing gradient gel electrophoretic analysis of ammonia-oxidizing bacterial community structure in the lower Seine River: impact of Paris wastewater effluents.

The Seine River is strongly affected by the effluents from the Acheres wastewater treatment plant (WWTP) downstream of the city of Paris. We have shown that the effluents introduce large amounts of ammonia and inoculate the receiving medium with nitrifying bacteria. The aim of the present study was to investigate the diversity of the ammonia-oxidizing bacterial population by identifying autochthonous bacteria from upstream and/or allochthonous ammonia-oxidizing bacteria from the WWTP effluents. Measurements of potential nitrifying activity, competitive PCR, and denaturing gradient gel electrophoresis (DGGE) of 16S ribosomal DNA fragments specific to ammonia-oxidizing bacteria (AOB) were used to explore the succession and shifts of the ammonia-oxidizing community in the lower Seine River and to analyze the temporal and spatial functioning of the system at several different sampling dates. A major revelation was the stability of the patterns. The CTO primers used in this study (G. A. Kowalchuk, J. R. Stephen, W. D. Boer, J. I. Prosser, T. M. Embley, and J. W. Woldendorp, Appl. Environ. Microbiol. 63:1489-1497, 1997) were shown not to be completely specific to AOB of the beta subclass of Proteobacteria. We further demonstrated that when DGGE patterns are interpreted, all the different bands must be sequenced, as one major DGGE band proved to be affiliated with a group of non-AOB in the beta subclass of Proteobacteria. The majority of AOB (75 to 90%) present in the lower Seine river downstream of the effluent output belong to lineage 6a, represented by Nitrosomonas oligotropha- and Nitrosomonas ureae-like bacteria. This dominant lineage was represented by three bands on the DGGE gel. The major lineage-6a AOB species, introduced by the WWTP effluents, survived and might have grown in the receiving medium far downstream, in the estuary; it represented about 40% of the whole AOB population. The other two species belonging to lineage 6a seem to be autochthonous bacteria. One of them developed a few kilometers downstream of the WWTP effluent input in an ammonia-enriched environment, and the other appeared in the freshwater part of the estuary and was apparently more adapted to estuarine conditions, i.e., an increase in the amount of suspended matter, a low ammonia concentration, and high turnover of organic matter. The rest of the AOB population was represented in equal proportions by Nitrosospira- and Nitrosococcus mobilis-like species.

Ammonia↗
PubMed2005

Autotrophic ammonia-oxidizing bacteria contribute minimally to nitrification in a nitrogen-impacted forested ecosystem.

Deposition rates of atmospheric nitrogenous pollutants to forests in the San Bernardino Mountains range east of Los Angeles, California, are the highest reported in North America. Acidic soils from the west end of the range are N-saturated and have elevated rates of N-mineralization, nitrification, and nitrate leaching. We assessed the impact of this heavy nitrogen load on autotrophic ammonia-oxidizing communities by investigating their composition, abundance, and activity. Analysis of 177 cloned beta-Proteobacteria ammonia oxidizer 16S rRNA genes from highly to moderately N-impacted soils revealed similar levels of species composition; all of the soils supported the previously characterized Nitrosospira clusters 2, 3, and 4. Ammonia oxidizer abundance measured by quantitative PCR was also similar among the soils. However, rates of potential nitrification activity were greater for N-saturated soils than for soils collected from a less impacted site, but autotrophic (i.e., acetylene-sensitive) activity was low in all soils examined. N-saturated soils incubated for 30 days with ammonium accumulated additional soluble ammonium, whereas less-N-impacted soils had a net loss of ammonium. Lastly, nitrite production by cultivated Nitrosospira multiformis, an autotrophic ammonia-oxidizing bacterium adapted to relatively high ammonium concentrations, was significantly inhibited in pH-controlled slurries of sterilized soils amended with ammonium despite the maintenance of optimal ammonia-oxidizing conditions. Together, these results showed that factors other than autotrophic ammonia oxidizers contributed to high nitrification rates in these N-impacted forest soils and, unlike many other environments, differences in nitrogen content and soil pH did not favor particular autotrophic ammonia oxidizer groups.

Ammonia↗
PubMed1989

Role of metabolism in the chemotactic response of Rhodobacter sphaeroides to ammonia.

Rhodobacter sphaeroides only showed chemotaxis towards ammonia if grown under nitrogen-limited conditions. This chemotactic response was completely inhibited by the addition of methionine sulfoximine. There was no effect of methionine sulfoximine treatment on motility or taxis towards propionate, demonstrating that the effect is specific to ammonia taxis. It is known that methionine sulfoximine inhibits glutamine synthetase and hence blocks ammonia assimilation. Methionine sulfoximine does not inhibit ammonia transport in R. sphaeroides; therefore, these results suggest that limited metabolism via a specific pathway is required subsequent to transport to elicit a chemotactic response to ammonia. Bacteria grown on high ammonia show transport but no chemotactic response to ammonia, suggesting that the pathway of assimilation is important in eliciting a chemotactic response.

Ammonia↗
PubMed1995

Roles of bovine serum albumin and copper in the assay and stability of ammonia monooxygenase activity in vitro.

We investigated the effects of bovine serum albumin (BSA) on both the assay and the stability of ammonia-oxidizing activity in cell extracts of Nitrosomonas europaea. Ammonia-dependent O2 uptake activity of freshly prepared extracts did not require BSA. However, a dependence on BSA developed in extracts within a short time. The role of BSA in the assay of ammonia-oxidizing activity apparently is to absorb endogenous free fatty acids which are present in the extracts, because (i) only proteins which bind fatty acids, e.g., BSA or beta-lactoglobulin, supported ammonia-oxidizing activity; (ii) exogenous palmitoleic acid completely inhibited ammonia-dependent O2 uptake activity; (iii) the inhibition caused by palmitoleic acid was reversed only by proteins which bind fatty acids; and (iv) the concentration of endogenous free palmitoleic acid increased during aging of cell extracts. Additionally, the presence of BSA (10 mg/ml) or CuCl2 (500 microM) stabilized ammonia-dependent O2 uptake activity for 2 to 3 days at 4 degrees C. The stabilizing effect of BSA or CuCl2 was apparently due to an inhibition of lipolysis, because both additives inhibited the increase in concentrations of free palmitoleic acid in aging extracts. Other additives which are known to modify lipase activity were also found to stabilize ammonia-oxidizing activity. These additives included HgCl2, lecithin, and phenylmethylsulfonyl fluoride.

Adsorption↗
PubMed1986

Modified ammonia electrode method to investigate D-asparagine breakdown by Campylobacter strains.

An ammonia electrode method has been developed for investigating the deamination of amino acids by bacteria. It consists of incubating a standard inoculum of organisms in an amino acid solution and then measuring the amount of ammonia evolved by the electrode. Two hundred and twelve Campylobacter strains (118 C. jejuni and 94 C. coli) were tested for their ability to break down D-asparagine by this method. Organism control (bacterial suspension in buffer alone) values ranged from 0.44 to 2.0 (mean 0.93 +/- 0.24) ammonia concentration (AC) units (one AC unit is equal to 10(-5) mol of ammonia per liter), whereas test values ranged from 0.60 to 46.0 units. Test ACs of less than 2 units (97 strains) were considered negative, whereas ACs of greater than or equal to 10 (77 strains) were considered positive for D-asparaginase; 38 (18%) strains with ACs between 2 and 10 units were provisionally assigned an intermediate status. The amount of ammonia produced by strains with ACs of greater than or equal to 10 increased greatly when the inoculum size was increased, whereas this was not a feature of strains with ACs of less than 2 units. The presence or absence of an inoculum effect was instrumental in classifying strains with intermediate ACs and allowed a breakpoint to be defined. When the ammonia electrode method was repeated, 97.6% of the 212 strains gave the same positive or negative reaction that they did on the first occasion. Thus the test was highly reproducible. Five strains (all porcine C. coli from Germany) were unclassifiable because they repeatedly gave either a weak-positive or negative reaction. Overall, 12.7% of C. jejuni strains and 86.2% of C. coli strains were positive for D-asparaginase. The ammonia electrode method was found to be simple and reliable for separating strains on the basis of D-asparaginase activity.

Ammonia↗
PubMed1996

Synergistic role of gaseous ammonia in etiology of Pasteurella multocida-induced atrophic rhinitis in swine.

One-week-old Large White piglets were weaned and allocated to 14 experimental groups, each composed of five animals. Each group was housed in a separate Rochester exposure chamber and exposed continuously to gaseous ammonia at either 0, 5, 10, 15, 25, 35, or 50 ppm (two groups per exposure level). One week after ammonia exposure commenced, the pigs from one group at each exposure level were inoculated intranasally with 9 x 10(7) CFU of Pasteurella multocida type D. After a further 4 weeks of exposure, all the pigs were euthanized and the extent of turbinate degeneration was assessed by using a morphometric index (J.T. Done, D. H. Upcott, D. C. Frewin, and C. N. Hebert, Vet. Rec. 114:33-35, 1984) and a subjective scoring system (Ministry of Agriculture, Fisheries and Food, Atrophic Rhinitis: a System of Snout Grading, 1978). Exposure to ammonia at a concentration of 5 ppm or greater resulted in a significant increase in the severity of turbinate atrophy induced by P. multocida compared with that occurring in pigs kept in 0 ppm of ammonia. This effect was maximal at 10 ppm but decreased progressively at concentrations above 25 ppm. Regression analysis revealed a significant relationship between the severity of turbinate degeneration and the number of P. multocida organisms isolated from the nasal epithelium at the end of the experiment (R2 = 0.86). These findings suggest that exposure to ammonia facilitates the growth and/or survival of P. multocida within the upper respiratory tract of the pig, thereby contributing to the severity of the clinical disease atrophic rhinitis. Furthermore, exposure of pigs to ammonia at 10 ppm or greater, in the absence of either P. multocida or Bordetella bronchiseptica, induced a mild but statistically significant degree of turbinate atrophy. The findings of this study demonstrate that exposure to ammonia, at concentrations within the range encountered commonly in commercial piggeries, contributes to the severity of clinical lesions associated with atrophic rhinitis.

Ammonia↗
PubMed2005

Modulation of electroneutral Na transport in sheep rumen epithelium by luminal ammonia.

Ammonia is an abundant fermentation product in the forestomachs of ruminants and the intestine of other species. Uptake as NH3 or NH4+ should modulate cytosolic pH and sodium-proton exchange via Na+/H+ exchanger (NHE). Transport rates of Na+, NH4+, and NH3 across the isolated rumen epithelium were studied at various luminal ammonia concentrations and pH values using the Ussing chamber method. The patch-clamp technique was used to identify an uptake route for NH4+. The data show that luminal ammonia inhibits electroneutral Na transport at pH 7.4 and abolishes it at 30 mM (P < 0.05). In contrast, at pH 6.4, ammonia stimulates Na transport (P < 0.05). Flux data reveal that at pH 6.4, approximately 70% of ammonia is absorbed in the form of NH4+, whereas at pH 7.4, uptake of NH3 exceeds that of NH4+ by a factor of approximately four. The patch-clamp data show a quinidine-sensitive permeability for NH4+ and K+ but not Na+. Conductance was 135 +/- 12 pS in symmetrical NH(4)Cl solution (130 mM). Permeability was modulated by the concentration of permeant ions, with P(K) > P(NH4) at high and P(NH4) > P(K) at lower external concentrations. Joint application of both ions led to anomalous mole fraction effects. In conclusion, the luminal pH determines the predominant form of ammonia absorption from the rumen and the effect of ammonia on electroneutral Na transport. Protons that enter the cytosol through potassium channels in the form of NH4+ stimulate and nonionic diffusion of NH3 blocks NHE, thus contributing to sodium transport and regulation of pH.

Adsorption↗
PubMed1982

Stimulation of ammonia production from glutamine by intraluminal glucose in small intestine of dogs.

Previous studies have shown that the quantity of ammonia derived from the small intestinal metabolism of arterial glutamine was equal to ammonia released by the colon. Little is known, however, about processes that may alter small intestinal glutamine metabolism. The purpose of this study was to evaluate the effect of intraluminal, nonnitrogenous compounds on ammonia release into mesenteric venous blood and glutamine uptake from arterial blood by in situ intestinal segments in anesthetized, fasted dogs. In paired luminal perfusion studies, either 50 mM glucose, 3-O-methylglucose, or 3-hydroxybutyric acid was compared with a control perfusate containing 50 mM mannitol. In the jejunum, glucose perfusion significantly increased ammonia release into mesenteric venous blood by 21 +/- 5 nmol.min-1.g intestine-1 or 32 +/- 7% and glutamine uptake from arterial blood by 21 +/- 3 nmol.min-1.g intestine-1. Perfusion of ileum with glucose also significantly increased ammonia release by 8 +/- 1 nmol.min-1.g intestine-1 or 12 +/- 2% and glutamine uptake by 11 +/- 4 nmol.min-1.g intestine-1, although the increments were less than in the jejunum. Perfusion of the jejunum with 3-hydroxybutyric acid or nonmetabolizable 3-O-methylglucose caused no increase in ammonia release, even though glucose, 3-hydroxybutyric acid, and 3-O-methylglucose were absorbed at similar rates and there were similar increments in water absorption. The results indicated that glucose absorbed from the lumen of both the jejunum and ileum stimulated glutamine uptake from arterial blood and ammonia release into mesenteric venous blood. These effects were quantitatively greater in the jejunum. Stimulation of intestinal glutamine metabolism was probably related to cellular metabolism of glucose and could not be attributed to a stimulation of solute or water absorption.

Absorption↗
PubMed1988

Ammonia production from intraluminal amino acids in canine jejunum.

Dietary protein increases the blood ammonia concentration when hepatic metabolic function is impaired, but the site of ammonia production and its specific precursors have not been clearly defined. The purpose of this study is to determine if individual luminal amino acids are metabolized to ammonia by the jejunum during the process of absorption. In anesthetized, fasted dogs, a cannula was inserted into the mesenteric vein draining a segment of the jejunum weighing approximately 18 g, and the ends of the segment were ligated to isolate its blood flow. Ammonia and amino acids were determined in luminal fluid as well as arterial and mesenteric venous blood. One of six amino acids (10 mM) was luminally perfused for a 15-min equilibration period and two 15-min collection periods, and the results were compared with control periods that preceded and followed the amino acid perfusion. Alanine, leucine, and glutamine significantly (P less than 0.01) increased ammonia release into mesenteric venous blood by 37, 42, and 106%, respectively, whereas threonine, serine, and glycine had no effect. Net jejunal uptake of glutamine from arterial blood, which accounts for ammonia release by the jejunum in the basal state, was not altered by perfusions other than with glutamine. Luminal glycine perfusion also caused an increased release of serine into mesenteric venous blood and alanine perfusion increased the release of glutamate. Glutamine perfusion caused increased release of glutamate, alanine, proline, and citrulline. These results indicate that some, but not all, luminal amino acids are partially metabolized to ammonia during the process of absorption in the small intestine.

Amino Acids↗
PubMed1983

Renal ammonia excretion and production in goldfish, Carassius auratus, at low environmental pH.

Renal ammonia excretion and production were investigated in normal and acidotic goldfish (Carassius auratus). Goldfish were made acidotic by exposure to a low pH environment (pH 4.0), which caused a lowering of blood pH from 7.88 to 7.61. Environmental acidification resulted in an increase in total renal ammonia excretion (from 0.43 to 1.00 mueq X 100 g-1 X h-1) and urinary concentration (from 0.58 to 0.76 mM), as well as a rise in renal titratable acid output (from -0.57 to +0.62 mueq X 100 g-1 X h-1). The acidotic fish showed a rise in urine flow that was due to an increased glomerular filtration rate. In vitro studies demonstrated the capacity for renal ammonia formation from aspartate, alanine, glutamine, glutamate, and glycine. The relatively high level of glutamate in the renal tissue suggested that the generation of ammonia from these amino acids occurs via the formation of glutamate, either by deamidation of glutamine or transdeamination of aspartate and alanine. Both ammonia production by isolated renal tubules and individual enzyme assays in kidney homogenates indicated that aspartate has the greatest potential as a renal ammonia precursor in vitro. The purine nucleotide cycle, investigated with the use of the inhibitor coformycin, does not appear to contribute to ammonia production in the kidney of this species.

Acidosis↗
PubMed1987

Transepithelial ammonia concentration gradients in inner medulla of the rat.

Transport of NH3 from loops of Henle to medullary collecting ducts has been proposed to play an important role in renal ammonia excretion. To determine whether transepithelial ammonia concentration gradients capable of driving this transport are present in the inner medulla, micropuncture experiments were performed in control rats and in rats with chronic metabolic acidosis. In situ pH and total ammonia concentrations were measured to calculate NH3 concentrations ([NH3]) for base and tip collecting duct, loop of Henle, and vasa recta. In control and acidotic rats, [NH3] in the loop of Henle was significantly greater than [NH3] in the collecting ducts. [NH3] did not differ in loop of Henle and adjacent vasa recta in either group of rats, indicating that NH3 concentration gradients between loop and collecting duct represent NH3 gradients that are present between medullary interstitium and collecting duct. During acidosis, an increase in collecting duct ammonia secretion was associated with an increase in the NH3 concentration difference between loop of Henle and collecting duct but occurred in the absence of a fall in collecting duct pH. The NH3 concentration gradient favoring diffusion of NH3 into the collecting ducts increased during acidosis because [NH3] in the loop of Henle and medullary interstitium increased more than [NH3] in the collecting duct. These findings indicate that transport processes involved in medullary ammonia accumulation play an important role in regulating ammonia secretion into the inner medullary collecting duct in vivo and that a fall in inner medullary collecting duct pH is not necessarily required for ammonia secretion by this segment to increase during chronic metabolic acidosis.

Acidosis↗
PubMed1994

Ammonia transport in a mathematical model of rat proximal tubule.

Pathways for ammonia transport have been incorporated within a model of rat proximal tubule [A. M. Weinstein. Am. J. Physiol. 263 (Renal Fluid Electrolyte Physiol. 32): F784-F798, 1992]. The luminal membrane includes a Na+/NH4+ exchanger, while at the peritubular membrane there is uptake of NH4+ on the Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase); both luminal and peritubular cell membranes contain conductive pathways for NH4+. The model equations have been expanded to include cellular ammoniagenesis. The principal focus of this study is the interplay of forces that can raise proximal tubule fluid total ammonia concentration 10-fold higher than in arterial plasma. Analysis of a cellular model reveals that luminal membrane Na+/NH4+ exchange, cellular production of ammonia, and peritubular membrane NH4+ uptake (via Na(+)-K(+)-ATPase or via K+ channel) all act in parallel to drive ammonia secretion. This derives from the cellular interconversion of NH4+ and NH3 and the free permeation of NH3 across cell membranes. It implies that inhibition of the luminal membrane transporter does not block the contribution of peritubular uptake to the overall active transport of ammonia. Conversely, when inhibition of the luminal membrane Na+/NH4+ entry (i.e., Na+/H+ inhibition) depresses transcellular Na+ flux, then the decrease of NH4+ flux through the peritubular Na+ pump enhances the apparent importance of the luminal membrane pathway. This analysis is confirmed in the numerical calculations and is a departure from the Ussing paradigm of series membrane Na+ transport. Although active secretion of ammonia by this tubule is substantial, the relative contribution of luminal Na+/NH4+ exchange and of peritubular uptake via the Na+ pump remains uncertain. The determination of peritubular capillary NH4+ concentration will be crucial to resolving this uncertainty, with lower concentration (i.e., closer to systemic arterial ammonia) obligating greater luminal membrane Na+/NH4+ exchange.

Ammonia↗
PubMed1995

Effect of luminal angiotensin II on ammonia production and secretion by mouse proximal tubules.

Angiotensin II is an important regulator of acid-base and ammonia metabolism in the proximal tubule. Because angiotensin II receptors exist on the apical membrane and because luminal fluid angiotensin II concentrations may be substantial, the effects of luminal angiotensin II on ammonia production rates and net luminal total ammonia (tNH3) secretion rates were examined in dissected mouse S2 proximal tubule segments. Ammonia production rates reflected the total release of ammonia via the basolateral and luminal aspects of the tubule, whereas net luminal secretion rates reflected the rates at which ammonia left the tubule via the luminal fluid leaving the distal end of the perfused segment. The results demonstrated that 1) luminal angiotensin II affected tNH3 production in a concentration-dependent fashion, 2) luminal angiotensin II at concentrations that stimulated tNH3 production could counteract the effect of inhibitory basolateral concentrations of angiotensin II, 3) the stimulation of tNH3 production and the rise in intracellular calcium concentration induced by 10(-10) M luminal angiotensin II were blocked by the addition of an angiotensin II receptor inhibitor, saralasin, or the calcium channel blocker nifedipine to the luminal perfusion solution, and 4) in contrast to basolateral angiotensin II, which inhibited net luminal tNH3 secretion, luminal angiotensin II stimulated amiloride-sensitive net luminal tNH3 secretion in parallel with stimulation of luminal fluid acidification. Thus luminal angiotensin II at physiological and superphysiological concentrations has important effects on ammonia production and transport in the proximal tubule that in some ways differ from the effects of basolateral angiotensin II.

Acids↗
PubMed1987

Altitude acclimatization attenuates plasma ammonia accumulation during submaximal exercise.

This study examined the effects of acclimatization to 4,300 m altitude on changes in plasma ammonia concentrations with 30 min of submaximal [75% maximal O2 uptake (VO2max)] cycle exercise. Human test subjects were divided into a sedentary (n = 6) and active group (n = 5). Maximal uptake (VO2max) was determined at sea level and at high altitude (HA; 4,300 m) after acute (t less than 24 h) and chronic (t = 13 days) exposure. The VO2max of both groups decreased 32% with acute HA when compared with sea level. In the sedentary group, VO2max decreased an additional 16% after 13 days of continuous residence at 4,300 m, whereas VO2max in the active group showed no further change. In both sedentary and active subjects, plasma ammonia concentrations were increased (P less than 0.05) over resting levels immediately after submaximal exercise at sea level as well as during acute HA exposure. With chronic HA exposure, the active group showed no increase in plasma ammonia immediately after submaximal exercise, whereas the postexercise ammonia in the sedentary group was elevated but to a lesser extent than at sea level or with acute HA exposure. Thus postexercise plasma ammonia concentration was decreased with altitude acclimatization when compared with ammonia concentrations following exercise performed at the same relative intensity at sea level or acute HA. This decrease in ammonia accumulation may contribute to enhanced endurance performance and altered substrate utilization with exercise following acclimatization to altitude.

Acclimatization↗
PubMed1987

Muscle and blood ammonia and lactate responses to prolonged exercise with hyperoxia.

Investigations using nonsteady-state and fatiguing exercise protocols have demonstrated a strong relationship between ammonia and lactate metabolism and have suggested a cause and effect relationship between these two variables. We investigated the lactate-ammonia response using prolonged exercise and inspiration of hyperoxic gas (60% O2-40% N2). The exercise consisted of either 70-75% maximal O2 uptake (VO2 max) for 40 min (series 1, n = 6) or 75-80% VO2max for 30 min (series 2, n = 6) with the subjects inspiring room air on one occasion and hyperoxia in the other test. In both series blood ammonia rose continuously throughout the exercise regardless of the inspired gas treatment; in contrast blood lactate did not increase after 10 min with room air, and with hyperoxia blood lactate was reduced. Muscle lactate and ammonia (series 2; vastus lateralis) had responses similar to the blood data. The data demonstrated no apparent lactate-ammonia relationship with prolonged exercise or in response to hyperoxia, suggesting that ammonia production can be independent of lactate metabolism. The data also suggest that type I fibers can be a major source of ammonia in humans.

Adult↗
PubMed2006

Role of ammonia and nitric oxide in the decrease in plasma prolactin levels in prehepatic portal hypertensive male rats.

OBJECTIVES: Since very little is known about neuroendocrine changes that occur in portal-systemic hepatic encephalopathy, we studied plasma prolactin (PRL) levels and the involvement of hyperammonemia, nitric oxide (NO) and dopaminergic and adrenergic systems in the control of this hormone secretion in a male rat model of prehepatic portal hypertension (PH). METHODS: We conducted in vivo studies to determine plasma ammonia and PRL levels. Dopamine (DA), dihydroxyphenylacetic acid (DOPAC), epinephrine and norepinephrine content in medial basal hypothalamus (MBH) and anterior pituitary (AP) were measured. In addition, NO synthase (NOS) activity and protein expression were evaluated in APs. In in vitro studies, the APs from intact rats were incubated with different doses of ammonia and PRL secretion was determined. In ex vivo studies, the APs from normal and PH rats were incubated in the presence of ammonia and/or a NOS inhibitor, NG-nitro-L-arginine-methyl ester (L-NAME) and PRL secretion was determined. RESULTS: PH rats had a significant increase in plasma ammonia levels (p < 0.001) and a decrease in plasma PRL levels (p < 0.05). Neither DA nor DOPAC content or DOPAC/DA ratios were modified in both MBH and APs; however, we observed a significant increase in norepinephrine content in both MBH and AP (p < 0.001 and p < 0.05, respectively) and a significant increase in epinephrine in APs (p < 0.001). Moreover, PH produced an increase in NOS activity (p < 0.01) and NOS protein expression (p < 0.0001) in APs. The ammonia (100 microM) significantly reduced PRL secretion from APs in vitro (p < 0.05). The presence of L-NAME, an inhibitor of NOS, abrogated the inhibitory effect of ammonia on PRL secretion from APs from control and PH rats. CONCLUSIONS: We found that plasma PRL levels were decreased in PH rats probably due to the high ammonia levels. The central noradrenergic system could also mediate this decrease. Also, the increase in NOS activity and/or content in AP induced NO production that directly inhibited PRL secretion from the AP, without the participation of the dopaminergic system.

Ammonia↗
PubMed1976

Respiratory failure: correlation between encephalopathy, blood gases and blood ammonia.

In 59 patients with respiratory insufficiency due to chronic obstructive pulmonary disease (COPD) the relationship between the state of consciousness, the blood gases and blood ammonia were studied. Interindividually, a significant correlation was found between the encephalopathy and SaO2, PaCO2 or ammonia, and also between the blood gases and ammonia. On the other hand, an intraindividual study, performed on patients with minor cerebral dysfunction, showed that only PaCO2 was significantly correlated with the stage of consciousness. Ammonia did not appear to have a neurotoxic influence. The ammonia level seemed to be influenced primarily by other factors than the blood gases, although there was a borderline influence of SaO2 on aterial ammonia and a significant influence of PaCO2-HCO3 and pH on venous ammonia.

Adult↗