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Ammonia and urea transport by the excluded human colon.

1. Ammonia and urea transport across the colonic mucosa was studied by a perfusion technique in four subjects with colonic exclusion for chronic hepatic encephalopathy. 2. Reduction of luminal pH inhibited net and unidirectional transport of ammonia from lumen to plasma, but net absorption from high luminal concentrations persisted at low pH. 3. Neither addition of urea to the perfusate nor intravenous infusion of urea produced a consistent increase in the colonic excretion of ammonia when ammonia-free solutions were perfused. 4. In one subject intravenous infusion of (15N)-ammonium chloride produced rapid labelling of colonic effluent ammonia and within 60 min the specific enrichments of ammonia in effluent and in arterial plasma were approximately equal. 5. During perfusion of nitrogen-free solutions, only small amounts of urea appeared in the effluent, suggesing limited permeability of the colonic mucosa to urea. 6. These results are discussed in relation to the equilibration of ammonia across the colonic mucosa by both ionic and non-ionic diffusion. The lack of evidence of 'juxtamucosal' (as opposed to luminal) ureolysis is in contrast to other observations on the intact colon. The possible reasons for and implications of this discrepancy are discussed.

Ammonia↗

Ammonia response to constant exercise: differences to the lactate response.

1. We evaluated the plasma ammonia response to constant exercise at different intensities. Ten healthy male volunteers were asked to perform constant exercise for 15 min at five different intensities: 80, 90, 100, 110 and 120% of their ventilatory threshold (VT). Blood concentrations of lactate, ammonia and hypoxanthine were measured during and after exercise. 2. The concentration of lactate increased continuously during exercise intensities equivalent to 100, 110 and 120% VT. Plasma ammonia began to increase at 6 min exercise and continued increasing during exercise at all five exercise intensities. Plasma hypoxanthine levels also increased continuously during exercise at all exercise intensities; however, they peaked at 5-10 min after exercise. The response of plasma ammonia and hypoxanthine increased with increasing intensities of exercise. 3. While the extent of the increase in lactate levels during exercise at 100, 110 and 120% VT was significantly higher than that at 80% VT, only the increase in ammonia and hypoxanthine levels at 120% VT were significantly higher than those at 80% VT. 4. In conclusion, the plasma ammonia response to constant exercise differed to the lactate and ammonia responses to short-term exhaustive exercise.

Adult↗

High concentrations of ammonia, but not volatile amines, in gastric juice of subjects with Helicobacter pylori infection.

BACKGROUND: Helicobacter pylori (H. pylori) produces large amounts of ammonia. Based on higher readings obtained with an ammonia-sensitive electrode when compared to a specific enzymatic assay, it has been claimed that H. pylori also produces potentially toxic volatile amines. METHOD: We measured ammonia concentrations (NH3) in gastric aspirates from 11 H. pylori positive subjects (22-40 y, 6 M), using an ammonia electrode sensitive to ammonia and amines, and an enzymatic assay specific for ammonia. Continuous aspiration was performed overnight and 220 aspirates were analyzed before and 6 weeks after cure of H. pylori. Gastric samples were diluted 1:3 (before cure) and 1:1 (after cure) according to dilution curves constructed prior to the assays. RESULTS: Median (95% CI) NH3 detected by the electrode/enzymatic assay were 4.34 mM[4.12-4.61]/4.50 mM [4.28-4.68] (p > .05) before cure and 0.54 mM[0.42-0.60]/0.73 mM[0.71-0.81] after cure (p > .05). Intra-class correlation coefficient between the two methods was 0.91 before cure and 0.90 after cure (p < .001). Without dilution, the enzymatic assay was linear for NH3 from 0.01 to 1 mM and saturated at 2.5 mM; the electrode was linear for NH3 from 0.01 to 20 mM. When appropriate dilutions were performed, the enzymatic assay was accurate for NH3 greater than 2.5 mM. CONCLUSION: In subjects with H. pylori infection there is a high NH3 in gastric juice; production of volatile amines appears to be negligible in vivo. An ammonia-sensitive electrode and a specific enzymatic assay are both suitable methods for determining NH3 in the gastric juice of subjects with H. pylori infection.

Adult↗

Arteriovenous difference of blood ammonia in uremic patients under hemodialysis.

In this study the ammonia concentration was determined in arterial and venous blood samples pre- and posthemodialysis (HD) in 18 uremic patients and in 18 health subjects (controls). The mean values (+/- SD) of ammonia in the arterial blood of uremic patients pre-HD were 98.32 +/- 26.55; post-HD, 63.18 +/- 17.09; and in control group patients, 72.37 +/- 10.09 micrograms/dl. In venous blood they were pre-HD, 71.70 +/- 20.68; post-HD, 58.05 +/- 16.73; and in control patients, 74.46 +/- 12.0 micrograms/dl. According to our findings, the ammonia concentration in the arterial blood of uremic patients pre-HD exceeds the normal limits and is significantly higher (p < 0.001) than that post-HD and that of control patients. The ammonia contents of venous blood pre- and post-HD ranges were within normal values, but the post-HD range was significantly lower than the pre-HD range (p < 0.05) and the control range (p < 0.01). Comparison between ammonia levels from arterial and venous blood showed significant and positive arteriovenous differences pre-HD (p < 0.001), which disappeared post-HD and were not observed in the control patients. In conclusion, uremic patients under HD present pre-HD high levels of ammonia in arterial blood with a significantly positive arteriovenous difference. In contrast, the post-HD ammonia levels in arterial and venous blood are decreased, and the arteriovenous difference is not significant.

Ammonia↗

Ammonia accumulation during highly intensive long-lasting cycling: individual observations.

In a number of individual cycling tests lasting 2.5-5 h with alternating exercise intensities of 50%-85% of maximal working capacity, it was observed that plasma ammonia levels may rise above 250 mumol/l when reaching exhaustion, while lactate levels remain relatively low. Acute quantitative ammonia production during intensive endurance exercise may be enhanced by a reduced glycogen availability in muscle. However, adequate amounts of glycogen itself do not prevent ammonia production when exercise is at high intensity and long-lasting. The continuous ammonia accumulation in blood during endurance exercise in trained individuals may be the result of a relatively low blood flow to the liver and thereby low clearance in contrast to lactate which may not accumulate due to a high clearance rate in both active and nonactive oxidative muscle fibers. In a number of subjects it was observed that exhaustion, when performing endurance exercise at high exercise intensities, occurred when plasma ammonia levels were high. Muscle cramps occurred in subjects who reached their highest individual ammonia values and seemed not to be related to serum potassium, plasma lactate, or muscle glycogen. These individual observations give rise to the hypothesis that high intramuscular ammonia levels may be related to the etiology of muscle exhaustion and muscle cramping during highly intensive endurance exercise.

Ammonia↗

Increased neonatal urinary ammonia: a marker for in utero caloric deprivation?

The decline in the urinary urea to ammonia ratio represents a simple measure of nutritional status in the adult. We examined the relationship of this ratio to nutrient-related fetal growth retardation. Levels of ammonia and urea nitrogen were measured in the first voided urine and cord blood from 15 term infants exhibiting a wide range of growth. Analysis by multiple regression with neonatal ponderal index as the primary dependent variable revealed a significant correlation between lowered ponderal index and decreased urinary urea and ammonia. The correlation was primarily a function of increasing ammonia levels, with no relationship between fetal leanness and urinary urea. Comparable cord artery and vein ammonia suggest that placental ammoniagenesis was not a major determinant of observed elevations in urinary ammonia. Confirmation of the striking correlation between increased urinary ammonia and lowered neonatal ponderal index may afford a simple test for the identification of nutrient-related growth retardation.

Adult↗

A review of the literature on the application of blood ammonia measurement in sports science.

This article summarizes previous studies on blood ammonia levels in relation to exercise. The dynamics of blood ammonia were reviewed with consideration to its production, removal, and distribution in various tissue compartments. During intense exercise, the primary source of ammonia is adenosine monophosphate deamination. Catabolism of branched-chain amino acids becomes important during submaximal exercise. Ammonia response to various types of exercise was also compared to lactate response. A comprehensive summary on factors affecting blood ammonia levels is provided. These reveal the possibility of applying blood ammonia measurement in monitoring and prescribing exercise, indirect measurement of muscle fiber composition, and muscle glycogen levels. However, more studies need to be conducted to evaluate these possibilities before blood ammonia measurement can be widely used.

Ammonia↗

Relationship between tumor necrosis factor-alpha and ammonia in patients with hepatic encephalopathy due to chronic liver failure.

BACKGROUND: We have recently demonstrated that in humans, circulating levels of tumor necrosis factor-alpha (TNF) correlate positively with severity of hepatic encephalopathy (HE) due to chronic liver failure.AIM. The main aim of this larger population study is to determine the relationship between TNF and ammonia in patients with HE and chronic liver failure due to liver cirrhosis. METHODS: Circulating levels of TNF and ammonia were measured in 108 patients with liver cirrhosis due to various etiologies in various clinical grades of HE (grades 0-4). TNF concentrations were measured in venous serum using commercially available solid-phase high sensitivity enzyme-linked immunosorbent assay. Ammonia levels were determined in venous plasma by the enzymatic method, using the glutamate dehydrogenase reaction. RESULTS: The mean+/-SEM values of circulating levels of TNF and ammonia at presentation in patients with grade 0 of HE (n = 30) were 3.89+/-0.2 pg/mL and 49.8+/-2.8 microg/mL respectively, in patients with grade 1 of HE (n = 26) were 8.56+/-0.34 pg/mL and 101.6+/-6.5 microg/mL respectively, in patients with grade 2 of HE (n = 22) were 11.59+/-0.48 pg/mL and 160.3+/-10.7 microg/mL respectively, in patients with grade 3 of HE (n = 20) were 19.98+/-0.94 pg/mL and 228.8+/-16.1 microg/mL respectively, and in patients with grade 4 of HE (n = 10) were 51.53+/-8.59 pg/mL and 284.2+/-20.3 microg/mL respectively. A significant positive correlation was found between circulating levels of TNF and those of ammonia (r = 0.62, P< 0.0001), and also between circulating levels of both substances and severity of HE in these patients (r = 0.95, P<0.0001, and r = 0.9, P<0.0001 respectively). TNF and ammonia were both significant independent predictors of severity of HE (P<0.0001 for both variables). CONCLUSION: The results of this study demonstrate a significant relationship between TNF and ammonia in patients with chronic liver failure and HE, and so strengthen the suggestion that TNF could be strongly involved in the pathogenesis of HE in these patients. Hence, we suggest a new theory in the pathogenesis of HE, the "TNF theory".

Aged↗

Remediation of ammonia-rich minewater in constructed wetlands.

A three-year study of ammonia removal from minewater was carried out employing constructed wetland systems (surface flow wetland and subsurface flow wetland cells) at the former Woodey Mine in West Yorkshire, UK. The 1.4 Ha surface flow wetland (constructed in 1995) reduced the ammonia concentration from 3.5 - 45 mg l(-1) to < 2.3 mg l(-1) during the first half of the study and to essentially zero in the last year (2000 - 2001). About 25% of contained ammonia was converted to nitrate, about 10% was consumed by the plants and up to 30% was converted to nitrogen gas. This maturation effect was attributed to increased depth of sludge from sedimentation of ochre, providing increased surface area for immobilisation of ammonia oxidising bacteria. The surface flow wetland finally removed 2.3 g m(-2) day(-1) ammonia in comparison with 3.8 g m(-2) day(-1) for the subsurface flow (pea gravel) wetland cells, constructed for the present work and dosed with ammonium salts. Removal of ammonia by both systems was consistent with well-established mechanisms of nitrification and denitrification. It was also consistent with ammonia removal in wastewater wetland systems, although the greater aeration in the minewater systems obviated the need for special aeration cycles. The general role of wetland plants in such aerated conditions was attributed to maintaining hydraulic conditions (such as hydraulic efficiency and hydraulic resistance of substratum in subsurface flow systems) in the wetlands and providing a suspended solids filter for minewater.

Ammonia↗

Effect of temperature and dissolved oxygen on biological nitrification at high ammonia concentrations.

Effect of temperature and dissolved oxygen concentration on nitrification rate were investigated with enrichment cultures of nitrifying bacteria. Values of specific nitrite oxidation rate in the absence of ammonia were 2.9-12 times higher than maximum specific ammonia oxidation rates at the same temperatures. The presence of high ammonia levels reversed this relationship, causing maximum specific nitrite oxidation rates to fall to 19 to 45% as high as maximum specific ammonia oxidation rates. This result suggests that nitrification at high ammonia levels will invariably result in nitrite accumulation. The K(O2) for nitrite oxidation in the presence of high ammonia levels was higher than the K(O2) for ammonia oxidation when temperature exceeded 18 degrees C, whereas the opposite was true at lower temperatures. These results indicate that low oxygen tensions will exacerbate nitrite accumulation when water temperature is high.

Ammonia↗

Model estimation and measurement of ammonia emission from naturally ventilated dairy cattle buildings with slatted floor designs.

Laboratory experiments were carried out in a wind tunnel with a model of a slurry pit to investigate the characteristics of ammonia emission from dairy cattle buildings with slatted floor designs. Ammonia emission at different temperatures and air velocities over the floor surface above the slurry pit was measured with uniform feces spreading and urine sprinkling on the surface daily. The data were used to improve a model for estimation of ammonia emission from dairy cattle buildings. Estimates from the updated emission model were compared with measured data from five naturally ventilated dairy cattle buildings. The overall measured ammonia emission rates were in the range of 11-88 g per cow per day at air temperatures of 2.3-22.4 degrees C. Ammonia emission rates estimated by the model were in the range of 19-107 g per cow per day for the surveyed buildings. The average ammonia emission estimated by the model was 11% higher than the mean measured value. The results show that predicted emission patterns generally agree with the measured one, but the prediction has less variation. The model performance may be improved if the influence of animal activity and management strategy on ammonia emission could be estimated and more reliable data of air velocities of the buildings could be obtained.

Air Pollutants↗

The African sharptooth catfish Clarias gariepinus can tolerate high levels of ammonia in its tissues and organs during four days of aerial exposure.

The African sharptooth catfish Clarias gariepinus lives in freshwater, is an obligatory air breather, and can survive on land during drought. The objective of this study was to elucidate how C. gariepinus defends against ammonia toxicity when exposed to terrestrial conditions. During 4 d of aerial exposure, there was no accumulation of urea in its tissues, and the rate of urea excretion remained low. Thus, exposure to terrestrial conditions for 4 d did not induce ureogenesis or ureotely in C. gariepinus. Volatilization of NH(3) was not involved in excreting ammonia during aerial exposure. In addition, there were no changes in levels of alanine in the muscle, liver, and plasma of C. gariepinus; nor were there any changes in the glutamine levels in these tissues. However, there were extraordinarily high levels of ammonia in the muscle (14 micromol g(-1)), liver (18 micromol g(-1)), and brain (11 micromol g(-1)) of fish exposed to terrestrial conditions for 4 d. This is the first report on a fish adopting high tolerance of ammonia in cells and tissues as the single major strategy to defend against ammonia toxicity during aerial exposure. At present, it is uncertain how C. gariepinus tolerates such high levels of ammonia, especially in its brain, but it can be concluded that, contrary to previous reports on two air-breathing catfishes (Clarias batrachus and Heteropneustes fossilis) from India, C. gariepinus does not detoxify ammonia to urea or free amino acids on land.

Acclimatization↗

Diet and cell growth modulation by ammonia.

Fiber is not digested by endogenous enzymes but is fermented by microbes principally in the large intestine. With fermentable energy available, microbes synthesize protein by using ammonia released by their enzymes from urea and other nitrogenous substances in ingesta and intestinal secretions. Fibber fermentation also yields fatty acids that lower the concentration of free ammonia by lowering pH. Fiber increases bulk and water of intestinal contents, shortens transit time, and decreases the concentration of toxic substances in contact with the intestinal mucosa. These processes decrease duration and intensity of exposure of the intestinal mucosa to free ammonia, the form of nitrogen that is most toxic and most readily absorbed by cells. At concentrations found in the lower bowel on usual Western diets, ammonia destroys cells, alters nucleic acid synthesis, increases intestinal mucosal cell mass, increases virus infections, favors growth of cancerous cells over noncancerous cells in tissue culture, and increases virus infections. Ammonia in the bowel increases as protein intake increases. The attributes of ammonia and the epidemiological evidence comparing populations that maintain low intakes of unrefined carbohydrate with those that consume high intakes of protein, fat, and refined carbohydrates implicate ammonia in carcinogenesis and other disease processes.

Ammonia↗

Mechanism for ammonia-induced promotion of gastric carcinogenesis in rats.

Although an association is suggested between gastric cancer and prior infection with Helicobacter pylori (HP), the role of HP in gastric carcinogenesis remains obscure. HP has potent urease activity and produces ammonia, a factor causing HP-related gastroduodenal mucosal lesions. In this study, rats were examined in an effort to determine effects of ammonia on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). After pretreatment with MNNG (83 mg/l) for 24 weeks, a solution of either 0.01% ammonia or plain tap water was administered to the animals as drinking water for an additional 24 weeks. The administration of the 0.01% ammonia solution significantly increased the incidence and number of cancers in the glandular stomach. The numbers of cases in which these cancers penetrated the muscle layer or deeper and of low-grade differentiated adenocarcinomas were significantly higher in rats receiving the ammonia solution. Continuing administration of ammonia accelerated cell proliferation in the gastric mucosa, but had no effect on the serum gastrin level. Therefore, gastric ammonia, which stimulates mucosal cell proliferation, appears to be an important promoter in carcinogenesis in rats and possibly in the HP-related gastric carcinogenesis in humans.

Ammonia↗

Synergism between ammonia, lactic acid and carboxylic acids as kairomones in the host-seeking behaviour of the malaria mosquito Anopheles gambiae sensu stricto (Diptera: Culicidae).

Host odours play a major role in the orientation and host location of blood-feeding mosquitoes. Anopheles gambiae Giles sensu stricto, which is the most important malaria vector in Africa, is a highly anthropophilic mosquito species, and the host-seeking behaviour of the females of this mosquito is guided by volatiles of human origin. Ammonia, lactic acid and several carboxylic acids are known to be present in the human odour blend. We investigated the effect of these compounds on naive female mosquitoes using a dual-port olfactometer. Ammonia was an attractant on its own, whereas lactic acid was not attractive. Carboxylic acids, offered as a mixture of 12 compounds, were repellent at the concentration tested. The addition of ammonia to the carboxylic acid mixture overruled the repellent effect of the latter. Combining ammonia with either lactic acid or the carboxylic acids did not enhance the attractiveness of ammonia alone. However, a synergistic effect was found when ammonia, lactic acid and the carboxylic acids were applied as a blend. Our findings indicate that An. gambiae s.s. relies on the combination of ammonia, lactic acid and carboxylic acids in its orientation to human hosts. The role of lactic acid in this tripartite synergism differs from that reported for the yellow fever mosquito Aedes aegypti.

Ammonia↗

Independent effects of fiber and protein on colonic luminal ammonia concentration.

The potential interactive effects of protein and fiber on cecal and colonic surface areas, colonic luminal ammonia concentrations, luminal pH and blood indices of nitrogen metabolism were tested using two levels of protein (8% and 24%) and two types of fiber (8% pectin or cellulose). Pectin supplementation resulted in larger cecal surface areas and longer large intestines than those of rats fed fiber-free or cellulose-supplemented diets. All high protein diets resulted in total large bowel luminal ammonia (NH3 + NH4+) concentrations that were twice as high as their low protein counterparts (P less than 0.05). The effect of fiber on ammonia concentration depended on the fiber type. In the distal colon, pectin-fed animals had three times the ammonia concentration of the fiber-free animals, and 4-5 times the ammonia concentration of the cellulose-fed animals (P less than 0.001). Blood urea nitrogen values were higher in the high protein than in the low protein groups (P less than 0.05), and highest in the high protein/pectin animals (P less than 0.01). This study clearly demonstrates that luminal ammonia concentration is dependent upon both protein level and fiber type, and that a fermentable fiber (pectin), rather than decreasing colonic ammonia concentrations, actually increases them several-fold.

Ammonia↗

Stimulation of epithelial cell proliferation of isolated distal colon of rats by continuous colonic infusion of ammonia or short-chain fatty acids is nonadditive.

Dietary fibers accelerate colonic epithelial cell proliferation at least in part by modulating bacterial metabolism in the large intestine. Ammonia and short-chain fatty acids (SCFA) are major metabolites of hindgut bacteria and are believed to affect epithelial cell kinetics of the colon. However, the effect of luminal ammonia itself and the possible interaction of ammonia with SCFA on colonic epithelial cell proliferation have not yet been studied. The colon of rats was surgically isolated and continuously administered infusates with saline, ammonia, SCFA or both into the isolated colon for 7 d in a two-way factorial design. On d 7, vincrystine sulfate was administered intravenously to cause metaphase arrest. The activity of epithelial cell proliferation in the distal colon was estimated by using a stathmokinetic method and by histologic examination. The crypt size was significantly larger in rats given infusates containing SCFA than in rats given infusates without SCFA. Infusion of ammonia or SCFA significantly stimulated colonic epithelial cell proliferation compared with the saline infusion. Infusion of both ammonia and SCFA resulted in accumulated mitoses per crypt that did not differ from the other three infusions although the value tended to be lower than when SCFA alone were infused. Thus, stimulation of epithelial cell proliferation by ammonia and SCFA is not additive, and the interaction between them should be considered when the effects of dietary fibers on gut epithelial proliferation are investigated.

Ammonia↗

Atmospheric ammonia is detrimental to the performance of modern commercial broilers.

Atmospheric ammonia inhibits broiler performance. Quantified effects are based on older genetic stock with a BW of 2000 g at 7 wk. In contrast, modern genetic stock reaches 3200 g at 7 wk of age. To assess the impact on present day broilers, 2 trials were conducted exposing male broilers to graded levels (0, 25, 50, and 75 ppm) of aerial ammonia from 0 to 4 wk of age. Sixty, 1-d-old chicks were placed in environmentally controlled chambers, weighed weekly as a group, and processed with yield determined at 7 wk of age. Final BW was significantly depressed by 6 and 9% for the 50 and 75 ppm concentrations of ammonia as compared with 0 ppm. Also, mortality was significantly greater at the 75 ppm ammonia concentration, 13.9% compared with 5.8% for the 0 ppm treatment. Percentage yield of deboned meat per bird decreased slightly with increasing exposure to ammonia but was not statistically significant. Although current genetic stock reaches growout weights that are approximately 60% greater than those 2 decades ago, the relative quantified effects of ammonia exposure were similar. Additionally, statistical analysis of the results provided a simple equation, presented herein, for predicting the decline in BW of male broilers after exposure to ammonia.

Ammonia↗