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PubMedDate not supplied

Air breathing and ammonia excretion in the giant mudskipper, Periophthalmodon schlosseri.

The giant mudskipper, Periophthalmodon schlosseri, is an amphibious, obligate, air-breathing teleost fish. It uses its buccal cavity for air breathing and for taking and holding large gulps of air. These fish live in mud burrows at the top of the intertidal zone of mangrove mudflats; the burrow water may be hypoxic and hypercapnic and have high ammonia levels. The buccal epithelium is highly vascularized, with small diffusion distances between air and blood. The gill epithelium is densely packed with mitochondria-rich cells. Periophthalmodon schlosseri can maintain tissue ammonia levels in the face of high ammonia concentrations in the water. This is probably achieved by active ammonium ion transport across the mitochondria-rich cells via an apical Na/H+(NH4+) exchanger and a basolateral Na/K+(NH4+) ATPase. When exposed to air, the animal reduces ammonia production, but there is some increase in tissue ammonia levels after 24 h. There is no detoxification by increased production of glutamine or urea, but there is partial amino acid catabolism, leading to the accumulation of alanine. CO2 production and proton excretion cause acidification of the burrow water to reduce ammonia toxicity. The skin has high levels of cholesterol and saturated fatty acids decreasing membrane fluidity and gas, and therefore ammonia, permeability. Exposure to elevated environmental ammonia further decreases membrane permeability. Acidification of the environment and having a skin with a low NH3 permeability reduces ammonia influx, so that the fish can maintain tissue ammonia levels by active ammonium ion excretion, even in water containing high levels of ammonia.

Adaptation, Physiological↗
PubMed1986

Ammonia production and its contribution to urinary nitrogenous compounds in chickens fed low or high protein diet.

The rates of total ammonia production and of ammonia retention and contribution of endogenous ammonia to urinary nitrogenous compounds were assessed using a constant intravenous infusion method with [15N]ammonia for 6 h in adult cockerels fed 7.00 or 1.75 g of protein per kilogram body weight per day for 5 d. At the 7.00-g protein intake level the mean total body ammonia production rate was 47.1 mumol/kg per min, with total excretion and retention rates being 10.1 mumol/kg per min and 37.0 mumol/kg per min, respectively. In birds with 1.75 g protein intake the mean total body ammonia production rate was 27.9 mumol/kg per min, with total excretion and retention rates being 3.1 mumol/kg per min and 24.8 mumol/kg per min, respectively. These values were significantly different between the two dietary groups (P less than 0.05-0.01). Ammonia N produced at low and high levels of dietary protein intake, contributed 33% and 84% of urinary uric acid N and 27% and 58% of urinary total N, respectively. With the above protein intake levels, 88% of urinary ammonia N and 6-9% of urinary nitrogenous compounds other than ammonia and uric acid were donated by ammonia N produced in the body. It is concluded that ammonia N produced in the body is the main source of uric acid N, which entirely explains the increase in urinary total N caused by feeding a high protein diet.

Ammonia↗
PubMedDate not supplied

Helicobacter pylori, gastric juice, and arterial ammonia levels in patients with cirrhosis.

Helicobacter pylori urease activity is a potential source of ammonia in the stomach of patients with cirrhosis. However, the possible role of H. pylori in the pathogenesis of hepatic encephalopathy deserves further investigations. The current study evaluates the relationship among H. pylori infection, gastric juice ammonia concentrations, and arterial ammonia levels in patients with cirrhosis. Overall, 14 patients with cirrhosis with overt hepatic encephalopathy, 19 with subclinical hepatic encephalopathy, and 13 without encephalopathy were enrolled. All patients underwent upper endoscopy, and gastric biopsy specimens were taken for H. pylori assessment (rapid urease test, histology, and culture). A gastric juice sample and an arterial blood sample were obtained for ammonia level assessment. Patients with overt encephalopathy had both higher arterial ammonia levels and a more severe hepatic impairment than the remaining patients, whereas gastric juice ammonia concentrations did not differ among the three groups. H. pylori prevalence was similar among groups. Patients with H. pylori infection had significantly higher gastric juice ammonia concentrations than those without infection (2.3 +/- 1.3 vs. 0.9 +/- 0.6 mmol/L, respectively; p = 0.003); however, no difference in arterial ammonia levels emerged between the two groups (37.7 +/- 18.6 vs. 37.6 +/- 18.8 micromol/L, respectively). No significant correlation was found between gastric juice ammonia concentrations and arterial ammonia levels. The data suggest that liver impairment remains crucial in ammonia disposal in patients with cirrhosis, whereas H. pylori infection does not seem to play a major role in the pathogenesis of hyperammonemia in these patients.

Ammonia↗
PubMed2001

Autotrophic ammonia oxidation at low pH through urea hydrolysis.

Ammonia oxidation in laboratory liquid batch cultures of autotrophic ammonia oxidizers rarely occurs at pH values less than 7, due to ionization of ammonia and the requirement for ammonium transport rather than diffusion of ammonia. Nevertheless, there is strong evidence for autotrophic nitrification in acid soils, which may be carried out by ammonia oxidizers capable of using urea as a source of ammonia. To determine the mechanism of urea-linked ammonia oxidation, a ureolytic autotrophic ammonia oxidizer, Nitrosospira sp. strain NPAV, was grown in liquid batch culture at a range of pH values with either ammonium or urea as the sole nitrogen source. Growth and nitrite production from ammonium did not occur at pH values below 7. Growth on urea occurred at pH values in the range 4 to 7.5 but ceased when urea hydrolysis was complete, even though ammonia, released during urea hydrolysis, remained in the medium. The results support a mechanism whereby urea enters the cells by diffusion and intracellular urea hydrolysis and ammonia oxidation occur independently of extracellular pH in the range 4 to 7.5. A proportion of the ammonia produced during this process diffuses from the cell and is not subsequently available for growth if the extracellular pH is less than 7. Ureolysis therefore provides a mechanism for nitrification in acid soils, but a proportion of the ammonium produced is likely to be released from the cell and may be used by other soil organisms.

Ammonia↗
PubMed2006

Evidence from knockout mice against physiologically significant aquaporin 8-facilitated ammonia transport.

Aquaporin (AQP)8-facilitated transport of NH(3) has been suggested recently by increased NH(3) permeability in Xenopus oocytes and yeast expressing human or rat AQP8. We tested the proposed roles of AQP8-facilitated NH(3) transport in mammalian physiology by comparative phenotype studies in wild-type vs. AQP8-null mice. AQP8-facilitated NH(3) transport was confirmed in mammalian cell cultures expressing rat or mouse AQP8, in which the fluorescence of a pH-sensing yellow fluorescent protein was measured in response to ammonia (NH(3)/NH(4)(+)) gradients. Relative AQP8 single-channel NH(3)-to-water permeability was approximately 0.03. AQP8-facilitated NH(3) and water permeability in a native tissue was confirmed in membrane vesicles isolated from testes of wild-type vs. AQP8-null mice, in which BCECF was used as an intravesicular pH indicator. A series of in vivo studies were done in mice, including 1) serum ammonia measurements before and after ammonia infusion, 2) renal ammonia clearance, 3) colonic ammonia absorption, and 4) liver ammonia accumulation and renal ammonia excretion after acute and chronic ammonia loading. Except for a small reduction in hepatic ammonia accumulation and increase in ammonia excretion in AQP8-null mice loaded with large amounts of ammonia, there were no significant differences in wild-type vs. AQP8-null mice. Our results support the conclusion that AQP8 can facilitate NH(3) transport but provide evidence against physiologically significant AQP8-facilitated NH(3) transport in mice.

Ammonia↗
PubMed1984

Mechanism of ammonia secretion by cortical collecting ducts of rabbits.

The collecting duct system is a major site of ammonia addition to the tubule fluid. To study the mechanisms involved, we measured total ammonia and total CO2 transport in isolated, perfused cortical collecting ducts (CCD) from deoxycorticosterone-(DOC) treated rabbits. Perfusate and bath solutions contained 25 meq/liter HCO3 and 4 mM total ammonia. Net fluid transport was not significantly different from zero. Net secretion of total CO2 occurred in all tubules (mean collected concentration, 44.2 mM). Despite bicarbonate secretion, there was net secretion of total ammonia (mean collected concentration, 6.4 mM). There was no detectable ammonia addition to the collected fluid when ammonia was excluded from the perfusate and bath, ruling out a major contribution from synthesis. Ouabain did not significantly affect net transport of total ammonia or total CO2. To test the hypothesis that an acid pH disequilibrium may lower the luminal pH enough to drive ammonia secretion by nonionic diffusion, we perfused CCD from DOC-treated rabbits with carbonic anhydrase (CA) (0.1 mg/ml). Without CA, there was net total ammonia secretion (-2.2 pmol X min-1 X mm-1) and net total CO2 secretion (-16.6 pmol X min-1 X mm-1). Luminal CA converted the net total ammonia secretion to net absorption (1.0 pmol X min-1 X mm-1) while the bicarbonate secretion persisted (-11.2 pmol X min X mm-1). We conclude that total ammonia secretion in these tubules occurs primarily by diffusion of NH3 and is dependent on a luminal acid pH disequilibrium.

Ammonia↗
PubMed1999

Emergency planning and the acute toxic potency of inhaled ammonia.

Ammonia is present in agriculture and commerce in many if not most communities. This report evaluates the toxic potency of ammonia, based on three types of data: anecdotal data, in some cases predating World War 1, reconstructions of contemporary industrial accidents, and animal bioassays. Standards and guidelines for human exposure have been driven largely by the anecdotal data, suggesting that ammonia at 5,000-10,000 parts per million, volume/volume (ppm-v), might be lethal within 5-10 min. However, contemporary accident reconstructions suggest that ammonia lethality requires higher concentrations. For example, 33,737 ppm-v was a 5-min zero-mortality value in a major ammonia release in 1973 in South Africa. Comparisons of secondary reports of ammonia lethality with original sources revealed discrepancies in contemporary sources, apparently resulting from failure to examine old documents or accurately translate foreign documents. The present investigation revealed that contemporary accident reconstructions yield ammonia lethality levels comparable to those in dozens of reports of animal bioassays, after adjustment of concentrations to human equivalent concentrations via U.S. Environmental Protection Agency (EPA) procedures. Ammonia levels potentially causing irreversible injury or impairing the ability of exposed people to escape from further exposure or from coincident perils similarly have been biased downwardly in contemporary sources. The EPA has identified ammonia as one of 366 extremely hazardous substances subject to community right-to-know provisions of the Superfund Act and emergency planning provisions of the Clean Air Act. The Clean Air Act defines emergency planning zones (EPZs) around industrial facilities exceeding a threshold quantity of ammonia on-site. This study suggests that EPZ areas around ammonia facilities can be reduced, thereby also reducing emergency planning costs, which will vary roughly with the EPZ radius squared.

Air Pollution↗
PubMed1999

Blood ammonia response during incremental and steady-state exercise in military staff.

BACKGROUND: Although in the last few years it has been possible to determine blood ammonia, its application in coaching practice has not yet been fully established. This study was designed to evaluate the blood ammonia response to a laboratory incremental exercise test and three steady-state field tests. METHODS: There were 26 military personnel who performed a submaximal and maximal exercise test on a treadmill, and a field test which included three different constant velocity stages. Gas exchange parameters were monitored throughout the maximal test. Capillary blood samples were obtained from fingertips during the submaximal and field tests for the determination of ammonia and lactate. RESULTS: The ammonia threshold was detected in 23 subjects (88.5%) during the submaximal test. No significant differences were found between the ammonia and lactate thresholds which were shown to be significantly correlated. Blood ammonia levels showed a progressive increase during the last two stages of the field test while lactate levels remained stable at less than 4 mmol x L(-1). CONCLUSIONS: The steady increase in blood ammonia concentration recorded in the field test suggests the possibility of using blood ammonia levels to monitor the duration of exercise although further investigation is required to explore this possibility. Moreover, the assessment of blood ammonia levels during incremental exercise protocols confirms the existence of an ammonia threshold, defined as the intensity of exercise at which ammonia shows a progressive increase.

Adult↗
PubMed2004

Biological treatment of ammonia gas at high loading.

The exhaust gas from compost processing plants contains a large amount of ammonia. To treat ammonia gas at high loads, bench-scale experiments were carried out. First, nitrifying bacteria were enriched from soil and immobilized on porous ceramics. The ceramics were packed in an acrylic cylinder (diameter, 100 mm; packed height, 190 mm) and ammonia gas was introduced to the top of the cylinder. The concentration and flow rate of ammonia gas were gradually increased and finally 85 ppm was introduced at a space velocity of 800 h(-1) (empty bed residence time (EBRT), 4.5 sec). The ammonia load was 1.0 kg N/m3 day(-1). The exhaust contained 1.5-2 ppm of ammonia. Then the packed ceramics were transferred to another acrylic cylinder (diameter, 50 mm; packed height, 800 mm). A high concentration of ammonia gas (1,000 ppm) was introduced at a space velocity of 96 h(-1) (ammonia loading, 1.44 kg N/m3 day(-1); EBRT, 37.5 sec). The exhaust contained 2 ppm of ammonia (removal rate, 99.8%). The packed bed was washed with water intermittently or continuously, and the wastewater from the cylinder contained a large amount of ammonium and nitrate ions of at a 1:1 ratio. Stoichiometric analysis showed that half of the introduced ammonia was oxidized to nitrate, and the rest was converted to ammonium ion. Thus, ammonia gas was effectively treated at a high load by biofiltration with nitrifying bacteria.

Ammonia↗
PubMed1990

Ammonia transport in the proximal tubule.

The transport of ammonia in the proximal tubule is a complex interaction of a number of processes. Ammonia transport in the proximal tubule is clearly bidirectional; ammonia is secreted into the early proximal tubule lumen, but later in the proximal tubule, efflux out of the lumen may result in net ammonia reabsorption. Two mechanisms of ammonia transport have clearly been established: NH3 diffusion and NH4+ transport on the Na(+)-H+ exchanger. The relative contribution of these pathways to ammonia transport is still unsettled. Other pathways for ammonia transport, particularly NH4+ efflux out of the lumen, may be important as well. A variety of factors may modulate ammonia transport: plasma, cell and luminal pH, luminal flow rate, luminal potassium, and angiotensin II. Each of these factors also alters ammonia production rates and in most circumstances, ammonia transport appears to follow ammonia production rates.

Ammonia↗
PubMed1987

Relationship of K and ammonia transport by the turtle bladder.

The relationship between K and ammonia transport was investigated in the turtle bladder. At serosal pH 6.4, ammonia transport is preferentially from serosa to mucosa and is, at least in part, mediated by NH4+ transport. Since K and NH4+ share similar features such as permeability and stimulation of Na-K-ATPase, we studied the interaction of transport of these ions by the turtle bladder. Removal of K from the mucosal solution inhibited partially ammonia transport from serosa to mucosa and the inhibition was reversible by restoration of K. In contrast, removal of serosal K failed to inhibit ammonia transport. Since NH4+ can replace K in the activation of Na-K-ATPase in turtle bladder plasma membrane fraction with similar K, we examined the effect of ouabain on ammonia transport. Ouabain added to the serosal solution failed to inhibit ammonia transport thus, suggesting that the Na-K-ATPase is not required for ammonia entry into the cell. Methylammonium (a competitive inhibitor of NH4+ transport in other systems) decreased both ammonia transport and the observed increase in short circuit current elicited by NH4Cl addition to the serosal solution. This finding suggests that NH4+ and methylammonium are transported through a common pathway in the serosal side. Since the permeability of the serosal side to K and NH4+ is similar, we evaluated the effect of serosal depolarization and the effect of barium, an inhibitor of K channels, on ammonia transport. Serosal depolarization inhibited ammonia transport but barium did not affect ammonia flux.(ABSTRACT TRUNCATED AT 250 WORDS)

Ammonia↗
PubMed1978

Contents and implications of ammonia human and canine bile.

The quantification and physiological significance of ammonia in human and canine bile has not been clearly documented or analyzed previously. Bile from the gallbladder, common hepatic duct, and from T-tubes obtained from patients undergoing cholecystectomy and choledochotomy. Similar samples were obtained in 6 dogs by cannulation of their hepatic duct and various blood vessels. Simultaneous blood and bile samples were obtained at 15-min intervals before during, and after an exogenous load of ammonia, given intravenously. Ammonia levels were measured in all samples. Ammonia was measurable by conventional methods in human and canine bile. In both species the gallbladder bile contained at least twice as much ammonia as bile from the common hepatic duct. After an exogenous ammonia load, the levels of ammonia in canine bile increased in similar patterns, but in lesser magnitude than the ammonia levels measured at several sites in the circulation. The findings document that the bile contains ammonia in different quantities and suggest that bile could be an additional pathway for the removal of ammonia by the liver, in addition to the urea cycle. The loss of the biliary pathway for ammonia excretion could contribute to the pathophysiology of the signs and symptoms attributed to hyperammoniemia occurring in human beings and dogs with decreased hepatic function.

Ammonia↗
PubMed1994

Influence of ammonia solution on gastric mucosa and acetic acid induced ulcer in rats.

Aqueous ammonia in concentrations of 0.02 or 0.1% was continuously administered to rats to study its effect on the gastric mucosa histologically and cell kinetically. Furthermore, acetic acid ulcer, which is a model of chronic gastric ulcer, was experimentally induced in the stomachs of rats to assess the influence of 0.02% ammonia on the course of this ulcer. Male Donryu rats were divided into three groups given 0.02% ammonia, 0.1% ammonia or tap water. On several occasions (1, 3 and 5 days and 1, 4, 8, 12 and 24 weeks from the beginning of the experiment), the gastric mucosa in the fundic gland region and the antrum was examined histologically, and from the viewpoint of cell kinetics. The assessment in the 8th and 24th weeks employed the double labeling technique with bromodeoxyuridine and 3H-thymidine. The assessment on the other occasions used the flash labeling technique with bromodeoxyuridine. Both the 0.02% and 0.1% ammonia treatment groups showed a decrease in PAS-positive mucus and an enhanced cell cycling in the early stage of the experiment. After long periods of treatment, these groups showed a reduction in the gland height, a recovery in PAS-positive mucus and a suppression of cell cycle, suggesting direct toxicity of ammonia on the gastric mucosa. Although glandular atrophy was observed in these animals, infiltration of inflammatory cells was not observed. Thus, the relationship between ammonia and gastritis remained obscure. No ulcer developed in any group. Subsequently, we experimentally induced Ul-IV or Ul-V acetic acid ulcers in the stomachs of rats, according to the method of Okabe et al. (1971, 1972). These rats were divided into two groups given 0.02% ammonia or tap water. In the 4th and 8th weeks of the experiment, the stomachs of these rats were examined histologically and from the viewpoint of cell kinetics. The 0.02% ammonia treatment group showed a significant increase in the ulcer index (long diameter x short diameter; mm2) in the 4th and 8th weeks. This group also showed suppressed cell cycling of the regenerative epithelium and fibroblasts in the ulcer margin, suggesting direct toxicity of ammonia. Thus, healing of peptic ulcer was delayed by continuous administration of 0.02% ammonia.

Acetates↗
PubMed1996

Ammonia in ruminal and abomasal contents of cows with abomasal displacement.

Ruminal and abomasal ammonia concentrations were determined in cows with left displaced abomasum (LDA), right displaced abomasum (RDA), or abomasal volvulus (AV) before the abomasum was corrected, as well as one and three days later, and compared with those from healthy control cows fed hay or hay and concentrates. In LDA, RDA, and AV, ruminal and abomasal ammonia concentrations before correction of the position of the abomasum significantly exceeded ammonia concentrations in control cows during hay diet. In LDA, ruminal and abomasal ammonia concentration before correction did not differ from control cows during hay/concentrate diet, whereas in RDA and AV, ruminal and abomasal ammonia significantly exceeded control cows during hay/concentrate diet. Ammonia concentrations significantly differed between forms of displacement before correction and one day after correction, with LDA showing lowest, RDA intermediate and AV highest ruminal ammonia values, and LDA and RDA showing lower abomasal ammonia values than AV. However, three days after correction, ruminal and abomasal ammonia concentrations did not differ between LDA, RDA and AV. Up to the third day after correction, ruminal and abomasal ammonia concentrations significantly decreased in LDA, RDA and AV. On the third day after correction, ruminal and abomasal ammonia concentrations in LDA, RDA and AV did not differ from control cows during hay diet, and were significantly lower than in control cows during hay/concentrate diet. These findings suggest disturbances in the protein metabolism of cows with abomasal displacement.

Abomasum↗
PubMed2000

Effects of ammonia and lactate on growth, metabolism, and productivity of BHK cells.

The aim of the present work was to study the effect of ammonia and lactate on growth, metabolism, and productivity of BHK cells producing a recombinant fusion protein. Results show that cell growth was reduced with the increase in ammonia or lactate: k(1/2) of 1.1 mM and 3.5 mM for stirred and stationary cultures, respectively, for ammonia and of 28 mM for both stationary and stirred cultures for lactate, were obtained. The cell-specific consumption rates of both glucose (q(Glc)) and glutamine (q(Gln)) increased, whereas that of oxygen (q(O2)) decreased, with the increase in ammonia or lactate concentrations. The cell-specific production rates of lactate (q(Lac)) increased with an increase in ammonia concentration; similarly for the cell-specific production rates of ammonia (q(Amm)), which also increased with an increase in lactate concentration; on the other hand, both q(Lac) and q(Amm) markedly decreased when lactate or ammonia concentrations were increased, respectively; lactate was consumed at lactate concentrations above 30 mM and ammonia was consumed at ammonia concentrations above 5 mM. In vivo (31)P NMR experiments showed that ammonia and lactate affect the intracellular pH, leading to intracellular acidification, and decrease the content in phosphomonoesters, whereas the cell energy state was maintained. The effect of lactate on cell growth and q(Gln) is partially due to osmolarity, on q(Glc) and q(Amm) is entirely due to osmolarity, but on q(Lac) is mainly due to lactate effect per se. An increase in ammonia from 0 to 20 mM induced a 50% reduction in specific productivity, whereas an increase in lactate from 0 to 60 mM induced a 40% decrease.

Journal Article↗
PubMed1982

Influence of Nitrate and Ammonia on Photosynthetic Characteristics and Leaf Anatomy of Moricandia arvensis.

The leaf anatomy and certain photosynthetic properties of nitrate- and ammonia-grown plants of Moricandia arvensis (L.) DC., a species previously reported to be a C(3)-C(4) intermediate, were investigated. Nitrate-grown plants had a high level of malate in the leaves while ammonia-grown plants had low levels of malate. In young leaves of nitrate-grown plants, there was a diurnal fluctuation of malate content, increasing during the day and decreasing during the night. Titratable acidity remained low in leaves of both nitrate- and ammonia-grown plants.In nitrate-grown plants, the activity of phosphoenolpyruvate (PEP) carboxylase was about 2-fold higher than in ammonia-grown plants, the latter having activity typical of C(3) species. Also, in nitrate-grown plants, the ratio of activities of ribulose 1,5-bisphosphate (RuBP) carboxylase/PEP carboxylase was lower than in ammonia-grown plants. Nitrate reductase activities were higher in nitrate- than in ammonia-grown plants and the greatest activity was found in younger leaves.With nitrate-grown plants, during a pulse-chase experiment the label in malate, as a percentage of the total labeled products, increased from about 7% after a 10-second pulse with (14)CO(2) up to 17% during a 5-minute chase with (12)CO(2). The pattern of (14)C labeling in various metabolites suggests the primary carboxylation is through RuBP carboxylase with a secondary carboxylation through PEP carboxylase. In similar experiments, with ammonia-grown plants, the percentage label in malate was only 0% to 4% with no increase in malate labeling during the chase period. The CO(2) compensation point was lower in nitrate-grown than ammonia-grown plants.There was no evidence of Kranz-like anatomy in either the nitrate or ammonia-grown plants. Mitochondria of bundle-sheath cells were strikingly positioned along the inner tangential wall. This might allow the chloroplasts of these cells to fix the mitochondrial photorespired CO(2) more effectively and contribute to the low CO(2) compensation point in the species. Chloroplasts of bundle-sheath cells and contiguous mesophyll cells were similar in size and structure in plants grown on different media, although chloroplast thylakoids and stromata of the ammonia-grown plants stained more intensely than those of nitrate-grown plants. In addition, irregular clusters of phytoferritin particles occurred in the chloroplasts of the ammonia-grown plants.The results indicate that the substantial activity of PEP carboxylase, incorporation of CO(2) into malate, the high malate content, and in part the relatively low CO(2) compensation point in Moricandia arvensis may be accounted for by metabolism of nitrate rather than by a state of C(3)-C(4) intermediacy.

Journal Article↗
PubMedDate not supplied

Effect of Helicobacter pylori eradication on serum ammonia levels in patients with chronic liver disease.

BACKGROUND: Helicobacter pylori infection has been implicated in the development of encephalopathy in chronic liver disease (CLD); this is possibly due to increased production of ammonia by the action of bacterial urease on urea in the gastric lumen. AIM: To evaluate whether H. pylori eradication in patients with CLD affects arterial ammonia levels. METHODS: Forty-six patients with CLD (40 alcoholic, 6 post hepatitis B; Child's class A 7, B 17, C 22) and 36 patients with symptoms of acid-peptic disease (APD) underwent gastrointestinal endoscopy and biopsy; gastric biopsies were evaluated for H. pylori status using rapid urease test and histology. H. pylori-positive subjects received quadruple-drug eradication therapy for 2 weeks. Fasting arterial plasma ammonia levels were estimated before and after eradication of H. pylori. RESULTS: H. pylori infection was present in 21 of 46 (45.7%) patients with CLD and 23 of 36 (63.9%) with APD. At baseline, mean (SD) ammonia levels were higher in the CLD group (97.4 [10.9] versus 81.3 [7.7] mcg/dL in the APD group; p = 0.0001), irrespective of H. pylori status. Amongst patients with liver disease, arterial ammonia levels were similar in the H. pylori-positive and -negative patients (94.1 [9.7] and 100.2 [11.3] mcg/dL, respectively); however, ammonia levels were higher in patients in Child's class C (102.7 [11.4] mcg/dL/dL) than in those in class A (88.4 [1.6] mcg/dL; p < 0.002) or B (94.1 [9.7] mcg/dL; p < 0.002). In patients with APD, ammonia levels were higher in H. pylori-positive patients (85.3 [6.4] versus 74.1 [3.3] mcg/dL; p < 0.001). After eradication of H. pylori infection, ammonia levels decreased to 88.4 (10.0) mcg/dL in CLD and 76.7 (4.8) mcg/dL in APD (p = 0.001 as compared to baseline). There was no difference in post-eradication ammonia levels between Child's classes. CONCLUSION: Levels of arterial blood ammonia are higher in CLD than in APD, and correlate with severity of liver disease. H. pylori eradication was associated with reduction in arterial ammonia levels in patients with CLD.

Analysis of Variance↗
PubMed2001

Ammonia induces the mitochondrial permeability transition in primary cultures of rat astrocytes.

Ammonia is a toxin that has been strongly implicated in the pathogenesis of hepatic encephalopathy (HE), and the astrocyte appears to be the principal target of ammonia toxicity. The specific neurochemical mechanisms underlying HE, however, remain elusive. One of the suggested mechanisms for ammonia toxicity is impaired cellular bioenergetics. Because there is evidence that the mitochondrial permeability transition (MPT) is associated with mitochondrial dysfunction, we determined whether the MPT might be involved in the bioenergetic alterations related to ammonia toxicity. Accordingly, we examined the mitochondrial membrane potential (Deltapsi(m)) in cultured astrocytes and neurons using laser-scanning confocal microscopy after loading the cells with the voltage-sensitive dye JC-1. We found that ammonia induced a dissipation of the Deltapsi(m) in a time- and concentration-dependent manner. These findings were supported by flow cytometry using the voltage-sensitive dye tetramethylrhodamine ethyl ester (TMRE). Cyclosporin A, a specific inhibitor of the MPT, completely blocked the ammonia-induced dissipation of the Deltapsi(m). We also found an increase in the mitochondrial permeability to 2-deoxyglucose in astrocytes that had been exposed to 5 mM NH(4)Cl, further supporting the concept that ammonia induces the MPT in these cells. Pretreatment with methionine sulfoximine, an inhibitor of glutamine synthetase, blocked the ammonia-induced collapse of Deltapsi(m), suggesting a role of glutamine in this process. Over a 24-hr period, ammonia had no effect on the Deltapsi(m) in cultured neurons. Collectively, our data indicate that ammonia induces the MPT in cultured astrocytes, which may be a factor in the mitochondrial dysfunction associated with HE and other hyperammonemic states.

Ammonia↗