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PubMed1999

[Experimental study about intra-ocular penetration of ammonia].

PURPOSE: The seriousness of ocular alkali burn depends on low quick the alkali to enter the eye. We report the results of an experimental study on intra-ocular penetration of ammonia. MATERIALS AND METHODS: This study included 23 eyes of New Zealand albino rabbits, burned for 1 minute by 100 microl of a solution titrating 15.3% ammonia. An pH meter probe inserted into the anterior chamber measured pH every 5 seconds. Experiment were carried out within 1, 3, 5, 10 and 30 minutes. An anterior chamber puncture was performed at the end of experiments, after of 1, 3, 5, and 10 minutes, for measuring the ammonia concentration in the anterior chamber. RESULTS: PH increased 1 to 3 minutes after applying of ammonia on the cornea, until a maxima 10, 5 to 6 minutes later, followed by an exponential decrease. After 30 minutes, pH was still higher than physiological pH, and the ammonia concentration was low. The penetration-ratio of ammonia through cornea was about 11%. Measured pH differed from pH calculated from the concentration of ammonia. CONCLUSIONS: The difference between measured and calculated pH evidences chemical reactions. The two pH increases interspersed with a plateau prove the existence of 2 successive acido-basic chemical reactions between ammonia and 2 sorts of acid. Also, the density of protein uptake can be calculated from ammonia. This suggests an interesting avenue of research as protein density can be related in the eye with the pK of the base, and thus foresee the potential danger of a base to biological tissues.

Ammonia↗
PubMed2000

Changes in serum ammonia concentration in cirrhotic patients with Helicobacter pylori infection.

OBJECTIVE: To study whether liver cirrhosis associated with Helicobacter pylori (H. pylori) infection will induce increased serum ammonia and whether the peripheral serum ammonia reflects the level of portal vein serum ammonia. METHODS: Blood was taken from the portal vein and the cubital vein in cirrhotic patients with and without H. pylori infection and non-cirrhotic patients (splenic rupture) with and without H. pylori infection, and the serum ammonia was measured. RESULTS: The mean levels of serum ammonia in the group of cirrhotic patients with H. pylori infection were 167.82 +/- 8.97 mumol/L (portal vein) and 142.2 +/- 13.35 mumol/L (cubital vein). They were increased significantly as compared with cirrhotic patients without H. pylori infection (47.68 +/- 12.03 mumol/L portal vein and 37.23 +/- 7.04 mumol/L cubital vein), and also compared with the groups of splenic rupture patients with and without H. pylori infection (P < 0.01). There was no significant difference between the serum ammonia level of the cubital vein and portal vein (P > 0.05). CONCLUSIONS: H. pylori infection can induce an increase in serum ammonia in patients with liver dysfunction, and the peripheral serum ammonia measurement may replace the portal vein serum ammonia as a monitoring method. Eradication of H. pylori in cirrhotic patients may prevent hepatic encephalopathy (HE).

Ammonia↗
PubMed2002

[Consequence calculation of a leak for liquid ammonia storage tank].

OBJECTIVE: To calculate the consequence of acute ammonia poisoning accident which was caused by the leak of liquefied ammonia storage tank, so as to provide theoretical basis for working out the counterplan of accidents. METHOD: The amount of liquefied ammonia to be reserved, the pressure and temperature inside the tank were inputted; based on the physical chemistry principle, the evaporating amount was calculated; and using the proper diffusion model, the size of ammonia cloud, percentages of death and depth range of the poisonous gas etc was calculated. RESULTS: Assuming the leaky tank had liquefied ammonia 50 t, the pressure and the temperature were 2.5 MPa and 30 degrees C respectively, the evaporating amount and the size of ammonia cloud were calculated. The radiuses, of the ammonia released cloud of severe, moderate and mild hazard were 108 m, 216 m, 370 m respectively; if the exposured time was 30 min, the percentage of death would be 50%; if the exposured time was 5 min, the percentage would be 10%; if the exposured time was 2 min, the percentage would be 2.5%. When the stable degree of circumstance was C, the wind speed was 2.3 m/s and the outside concentration of the cloud was 4000 mg/m3, dimension of cloud in X axis was 782 m and in Y axis was 88 m. CONCLUSION: The leaky consequence of liquefied ammonia was very serious. It is necessary to take preventive measures during production, storage, transportation and using of liquefied ammonia.

Accidents, Occupational↗
PubMed2004

[The changes of ammonia and epidermal growth factor concentration in gastric juice before and after the Helicobacter pylori eradication].

BACKGROUND/AIMS: Helicobacter pylori (H. pylori) infection is the cause of peptic ulcer diseases, and gastric cancer. Hydrolysis of urea generating ammonia may cause cytotoxic effects on the gastric epithelium. The ammonia may induce the synthesis of epidermal growth factor (EGF) in gastric epithelium as an adaptive cytoprotective mechanism. The first aim was to examine the concentration of ammonia and EGF in gastric juice before and after H. pylori eradication in functional dyspepsia patients. The second aim was to examine the correlation among ammonia concentration, EGF concentration, and inflammatory score of gastritis. METHODS: The concentration of ammonia and EGF were measured by ELISA. The grade and severity of gastritis were measured according to the updated Sydney system. RESULTS: The concentration of ammonia in gastric juice was much higher in the H. pylori positive subjects (10,787 +/- 6,584 micro mol/L) than in the negative subjects (2,339 +/- 1,158 micro mol/L, p<0.0001). The concentrations of EGF in gastric juice was much higher in the positive subjects (1,462 +/- 393 pg/mL) than in the negative subjects (1,088 +/- 499 pg/mL, p<0.005). The concentration of ammonia and EGF in gastric juice showed significant correlation (r=0.63, p<0.0001). The concentrations of ammonia and histologic severities showed significant correlation (r=0.41, p<0.0001). Moreover, the level of EGF in gastric juice and histologic severities showed positive correlation (r=0.20, p<0.005). CONCLUSIONS: As the concentration of ammonia in gastric juices increased, the concentration of EGF was also increased in functional dyspepsia with H. pylori infection. The concentration of EGF in gastric juice may play a role in the adaptive cytoprotection in H. pylori- induced gastritis.

Adult↗
PubMed2004

Biological removal of air loaded with a hydrogen sulfide and ammonia mixture.

The nuisance impact of air pollutant emissions from wastewater pumping stations is a major issue of concern to China. Hydrogen sulfide and ammonia are commonly the primary odor and are important targets for removal. An alternative control technology, biofiltration, was studied. The aim of this study is to investigate the potential of unit systems packed with compost in terms of ammonia and hydrogen sulfide emissions treatment, and to establish optimal operating conditions for a full-scale conceptual design. The laboratory scale biofilter packed with compost was continuously supplied with hydrogen sulfide and ammonia gas mixtures. A volumetric load of less than 150 gH2S/(m3 x d) and 230 gNH3/(m3 x d) was applied for about fifteen weeks. Hydrogen sulfide and ammonia elimination occurred in the biofilter simultaneously. The removal efficiency, removal capacity and removal kinetics in the biofilter were studied. The hydrogen sulfide removal efficiency reached was very high above 99%, and ammonia removal efficiency was about 80%. Hydrogen sulfide was oxidized into sulphate. The ammonia oxidation products were nitrite and nitrate. Ammonia in the biofilter was mainly removed by adsorption onto the carrier material and by absorption into the water fraction of the carrier material. High percentages of hydrogen sulfide or ammonia were oxidized in the first section of the column. Through kinetics analysis, the presence of ammonia did not hinder the hydrogen sulfide removal. According to the relationship between pressure drop and gas velocity for the biofilter and Reynolds number, non-Darcy flow can be assumed to represent the flow in the medium.

Air Pollutants↗
PubMed2005

Anhydrous ammonia thefts and releases associated with illicit methamphetamine production--16 states, January 2000-June 2004.

Anhydrous ammonia, a colorless gas with a pungent, suffocating fumes, is used primarily as an agricultural fertilizer and industrial refrigerant. Anhydrous ammonia is also a key ingredient for illicit methamphetamine (meth) production in makeshift laboratories. Exposure to anhydrous ammonia can be immediately dangerous to life or health. Anhydrous ammonia generally is not available for sale to the public; states require a license for purchase. Because of this, many illicit meth producers (i.e., "cookers") resort to stealing anhydrous ammonia. If released into the environment, anhydrous ammonia can cause acute injuries to emergency responders, the public, and the cookers themselves. In addition, when handled improperly, anhydrous ammonia can be explosive and deadly. This report describes examples of anhydrous ammonia thefts associated with illicit meth production, summarizes ammonia theft events reported to the Agency for Toxic Substances and Disease Registry (ATSDR), and suggests injury prevention recommendations, such as installing valve locks or fencing on unattended tanks and donning appropriate personal protective equipment (PPE) when responding to releases.

Accidents↗
PubMed1990

Role of ammonia in tubulointerstitial injury.

Accelerated rates of ammonia production by the renal proximal tubule constitute an important adaptation to chronic renal injury. Although serving to maintain net acid excretion, this augmented production of ammonia per nephron results in increased renal cortical levels of ammonia and contributes to progressive renal injury. Ammonia fosters progressive injury via its ability to modify the third component of complement and initiate alternative complement pathway activity. This interaction of ammonia with complement incites inflammation in models of nonimmune chronic renal disease in the rat and may contribute to tissue injury in pyelonephritis involving urease-positive organisms. The long recognized in vivo association between increased renal ammoniagenesis, renal growth, and progressive injury in several models of renal disease has been advanced by the recent demonstration of ammonia as a direct stimulus to growth of renal tubular epithelium in culture. Additionally, evidence from studies of acute ischemic renal injury suggests a contributory role for ammonia in mediating tissue injury in this model. Elevated renal levels of ammonia, therefore, contribute to tubulointerstitial injury primarily through the proinflammatory and growth-promoting properties of ammonia.

Acute Disease↗
PubMed1993

Growth and reproductive performance, during exposure to ammonia, of gilts afflicted with pneumonia and atrophic rhinitis.

From 2 to 4.5 months of age, 80 crossbred gilts were reared in a conventional grower unit where they were naturally exposed to mycoplasmal and bacterial pathogens that cause pneumonia and atrophic rhinitis. At 4.5 months of age, gilts were moved to environmentally regulated rooms (4.9 x 7.3 m) and assigned at random to 1 of 2 treatment groups: low aerial concentration of ammonia (4 to 12 ppm; mean, 7 ppm) or moderate aerial concentration of ammonia (26 to 45 ppm, mean, 35 ppm). Low concentration of ammonia was obtained by flushing of manure pits weekly, whereas moderate concentration of ammonia was maintained by adding anhydrous ammonia to manure pits that were not flushed. Gilts were weighed biweekly. Mean daily gain (MDG) was less (P < 0.01) for gilts exposed to moderate concentration of ammonia than for gilts exposed to low concentration of ammonia after 2 weeks in their respective environments. By 4 and 6 weeks, however, MDG was similar between the 2 treatment groups. After 6 weeks in these environments, 20 gilts from each treatment group were slaughtered, and prevalence and severity of lung lesions and snout grades were determined. At slaughter, body weight was greater (P < 0.01) in gilts exposed to low, rather than moderate, ammonia concentration (94.5 vs 86.8 kg; SEM, 3.3 kg). Percentage of lung tissue containing lesions (18 vs 12) and snout grade (2.8 vs 3.1) were similar between gilts exposed to low or moderate concentration of ammonia. The remaining 20 gilts in each treatment group were maintained in their respective environments, exposed daily to mature boars and bred at first estrus.(ABSTRACT TRUNCATED AT 250 WORDS)

Ammonia↗
PubMed1997

Ammonia determination as an early indicator in experimental superior mesenteric artery occlusion.

Superior mesenteric artery occlusion (SMAO) is often fatal. An indicator which enables the early diagnosis of SMAO is needed. As we think putrefaction products must appear and increase in the blood and ascites in SMAO, changes in the concentrations of ammonia, one of the putrefaction products, were measured in this study. Thirteen adult mongrel dogs were used for the in vitro experiment. The jejunum, ileum, and ascending colon were resected and incubated in saline. Changes in ammonia concentrations in the saline were examined at various incubation times. In the in vivo experiment, 11 mongrel dogs comprised the SMAO group and another 10 mongrel dogs comprised the control group. Changes in ammonia concentrations in the blood and ascites were examined in both groups. In the in vitro experiment, ammonia concentrations in the saline bath increased in all samples. It was highest in the sample from around the ascending colon, and lowest from around the jejunum. However, at the end of experiment, this difference became insignificant. In the in vivo experiment, ammonia concentrations in samples of the blood increased early and significantly in the SMAO group, compared with the control group. Ammonia concentrations in samples of the ascites also increased significantly. The in vitro experiment showed that ammonia leaked from the ischemic intestines, and secondarily, a large amount of ammonia was produced from intestinal putrefaction. The in vivo experiment revealed that the ammonia level in the blood could be used as a good early indicator of acute mesenteric ischemia.

Ammonia↗
PubMed2000

Study on the free amino acid levels in the hemolymph, gill, hepatopancreas and muscle of Penaeus monodon exposed to elevated ambient ammonia.

Tiger shrimp Penaeus monodon following 24 h exposure to 0.002 (control), 0.072 and 0.718 mM ammonia were examined for the free amino acid (FAA), ammonia and urea levels in the hemolymph, gill, hepatopancreas and muscle. Control shrimps contained total FAA in hemolymph (1.19 µmol ml(-1)), gill (21.81 µmol g(-1)), hepatopancreas (100.81 µmol g(-1)) and muscle (239.54 µmol g(-1)). Glycine and arginine were the major contributors to the total FAA pool, and made up of 90% of the total FAA in the muscle of P. monodon. The total FAA level in the hemolymph increased directly with ambient ammonia, whereas the total FAA level in the hepatopancreas was inversely related to ambient ammonia. No significant difference of total FAA was observed in the gill and muscle among the shrimps in three treatments. Ammonia level increased by 160% in hemolymph, 105% in gill, 236% in hepatopancreas and 68% in muscle for the shrimps exposed to 0.718 mM ammonia. Urea and ornithine in the hepatopancreas increased by 107 and 1446%, whereas arginine level in the hepatopancreas decreased by 50% for the 0.718 mM ammonia-exposed shrimps. Decreases of arginine and other FAA with a concomitant increase of ornithine and urea level in the hepatopancreas indicated catabolism of FAA and ureogenesis. Increases of ammonia, urea, taurine, glutamine, proline, alanine, glycine and asparagine in the hemolymph revealed a intracellular osmoregulation for P. monodon under the stress of ambient ammonia at 0.718 mM.

Journal Article↗
PubMed2000

High ammonia tolerance in fishes of the family Batrachoididae (Toadfish and Midshipmen).

Three fish species of the family Batrachoididae, the gulf toadfish (Opsanus beta), the oyster toadfish (Opsanus tau), and the plainfin midshipman (Porichthys notatus) demonstrated exceptionally high tolerances to elevated water ammonia with 96-h LC50 values of 9.75, 19.72 and 6 mM total ammonia, respectively. Using pH values we calculated the corresponding unionized ammonia (NH(3)) values to be 519, 691 and 101 µM, respectively. These values are well above typical values for most teleost fishes, but close to those of ureotelic fish examined to date. Following sublethal high ammonia exposure (HAE) blood and tissue (brain, liver and muscle) sampling confirmed that internal ammonia levels rose substantially in all three species, suggesting that they were not simply avoiding toxicity by impermeance to ammonia. The three species of batrachoidids can be characterized in the following manner with respect to the inabilities to synthesize and excrete urea, based on these studies and prior research: O. beta (fully ureotelic)>O. tau (moderately ureotelic)>P. notatus (ammoniotelic). While some of the high ammonia tolerance for O. beta and O. tau can be explained by their ability to detoxify it to urea, other mechanisms must be at play for P. notatus. Further experiments determined that all three species possess rather high activities of glutamine synthetase (GSase) in brain especially (60-180 U g(-1)), that glutamine accumulates in many tissues, and that LC50 values are correlated positively with brain GSase activity. Taken together, our results suggest that alternative/additional mechanisms for ammonia detoxification via urea synthesis must be considered to explain the exceptionally high ammonia tolerance of this group.

Journal Article↗
PubMed1997

Control of ammonia toxicity to Hyalella azteca by sodium, potassium and pH.

The toxicity of ammonia to Hyalella azteca at constant pH in artificial media was controlled by sodium and potassium, and not by calcium, magnesium, or anions. Small increases in the LC50 for total ammonia (from 0.15 to 0.5 mM) occurred as sodium was increased from 0.1 to 1 mM and above, but major increases in the LC50 (to over 10 mM total ammonia) required the addition of potassium. Potassium was, however, more effective at reducing ammonia toxicity at high (1 mM) sodium than at low (0.1 mM) sodium. Ammonia toxicity was independent of pH at low sodium and potassium concentrations, when ammonia toxicity appeared to be associated primarily with aqueous ammonium ion concentrations. At high sodium and potassium concentrations, the toxicity of ammonia was reduced to the point where un-ionized ammonia concentrations also affected toxicity, and the LC50 became pH dependent. A mathematical model was produced for predicting ammonia toxicity from sodium and potassium concentrations and pH.

Journal Article↗
PubMed1997

Can nitrogen-13 ammonia kinetic modeling define myocardial viability independent of fluorine-18 fluorodeoxyglucose?

OBJECTIVES: The hypothesis of this study was that evaluation of myocardial flow and metabolism using nitrogen-13 (N-13) ammonia kinetic modeling with dynamic positron emission tomographic (PET) imaging could identify regions of myocardial scar and viable myocardium as defined by fluorine-18 fluorodeoxyglucose (F-18 FDG) PET. BACKGROUND: Uptake of most perfusion tracers depends on both perfusion and metabolic retention in tissue. This characteristic has limited their ability to differentiate myocardial scar from viable tissue. The kinetic modeling of N-13 ammonia permits quantification of blood flow and separation of the metabolic component of its uptake, which may permit differentiation of scar from viable tissue. METHODS: Sixteen patients, > 3 months after myocardial infarction, underwent dynamic N-13 ammonia and F-18 FDG PET imaging. Regions of reduced and normal perfusion were defined on static N-13 ammonia images. Patients were classified into two groups (group I [ischemic viable], n = 6; group II [scar], n = 10) on the basis of percent of maximal F-18 FDG uptake in hypoperfused segments. Nitrogen-13 ammonia kinetic modeling was applied to dynamic PET data, and rate constants were determined. Flow was defined by K1; volume of distribution (VD = K1/k2) of N-13 ammonia was used as an indirect indication of metabolic retention. RESULTS: Fluorine-18 FDG uptake was reduced in patients with scar compared with normal patients with ischemic viable zones (ischemic viable 93 +/- 27% [mean +/- SD]; scar 37 +/- 16%, p < or = 0.01). Using N-13 ammonia kinetic modeling, flow and VD were reduced in the hypoperfused regions of patients with scar (ischemic viable flow: 0.65 +/- 0.20 ml/min per g, scar: 0.36 +/- 0.16 ml/min per g, p < or = 0.01; VD: 3.9 +/- 1.3 and 2.0 +/- 1.07 ml/g, respectively, p < or = 0.01). For detection of viable myocardium in these patients, the sensitivity and specificity were 100% and 80% for N-13 ammonia PET flow > 0.45 ml/min per g; 100% and 70% for VD > 2.0 ml/g; and 100% and 90% for both flow > 0.45 ml/min per g and VD > 2.0 ml/g, respectively. The positive and negative predictive values for the latter approach were 86% and 100%, respectively. CONCLUSIONS: In this cohort, patients having regions with flow < or = 0.45 ml/min per g or VD < or = 2.0 ml/g had scar. Viable myocardium had both flow > 0.45 ml/min per g and VD > 2.0 ml/g. Nitrogen-13 ammonia kinetic modeling permits determination of blood flow and metabolic integrity in patients with previous myocardial infarction and can help differentiate between scar and ischemic but viable myocardium.

Aged↗
PubMed1986

Increased Arginine Biosynthesis during Phosphorus Deficiency : A Response to the Increased Ammonia Content of Leaves.

The accumulation of arginine in leaves of four citrus rootstock cultivars during P deficiency has been demonstrated to be due to increased de novo synthesis rather than decreased catabolism or increased protein degradation (E Rabe, CJ Lovatt, 1984, Plant Physiol 76: 747-752). In this report, we provide evidence (a) that the increased activity of the arginine biosynthetic pathway observed for citrus rootstocks grown under P-deficient conditions for 7 months is due to an increase in the concentration of ammonia in leaves of P-deficient plants and (b) that ammonia accumulation and removal through arginine systhesis are early responses to phosphorus deficiency for both a woody perennial, rough lemon (Citrus limon), and an herbaceous annual, summer squash (Cucurbita pepo). Transferring 5-day-old squash plants to a phosphorus-deficient nutrient solution for only 10 days resulted in a 2-fold increase in the concentration of nitrate in the youngest fully expanded leaves (YFE). Concomitantly, the specific activity of nitrate reductase doubled and the ammonia content of P-deficient YFE leaves increased to a concentration significantly greater that of leaves from healthy control plants (P < 0.05). Consistent with increased availability of ammonia, the incorporation of NaH(14)CO(3) into arginine plus urea doubled during phosphorus deficiency and arginine accumulated. Despite the accumulation of nitrate and ammonia in YFE leaves during phosphorus deficiency, the total nitrogen content of these leaves was less than that of the healthy control plants. Similar results were obtained for rough lemon. Nitrate content of the YFE leaves increased 1.5- and 3.0-fold in plants deprived of phosphorus for 6 and 12 weeks, respectively. Ammonia content of the leaves increased as P deficiency progressed to 1.4 +/- 0.08 mg (+/- se, n = 4) per gram dry weight, a level 1.8-fold greater than that of the P-sufficient control plants. During P deficiency de novo arginine biosynthesis in rough lemon increased 10-fold. Immersing the petiole of YFE leaves from P-sufficient squash and rough lemon plants in 50 millimolar NH(4) (+) for 3 hours resulted in the accumulation of ammonia in the leaves, and a 4-fold increase in the incorporation of NaH(14)CO(3) into arginine plus urea. Taken together, these results provide strong evidence that the accumulation of nitrate and ammonia in leaves is an early response of both woody and herbaceous plants to P deprivation. The data are consistent with the hypothesis that increased de novo arginine biosynthesis in leaves during P deficiency is in response to ammonia content of the leaves.

Journal Article↗
PubMed1991

Factors Limiting Aliphatic Chlorocarbon Degradation by Nitrosomonas europaea: Cometabolic Inactivation of Ammonia Monooxygenase and Substrate Specificity.

The soil nitrifying bacterium Nitrosomonas europaea is capable of degrading trichloroethylene (TCE) and other halogenated hydrocarbons. TCE cometabolism by N. europaea resulted in an irreversible loss of TCE biodegradative capacity, ammonia-oxidizing activity, and ammonia-dependent O(2) uptake by the cells. Inactivation was not observed in the presence of allylthiourea, a specific inhibitor of the enzyme ammonia monooxygenase, or under anaerobic conditions, indicating that the TCE-mediated inactivation required ammonia monooxygenase activity. When N. europaea cells were incubated with [C]TCE under conditions which allowed turnover of ammonia monooxygenase, a number of cellular proteins were covalently labeled with C. Treatment of cells with allylthiourea or acetylene prior to incubation with [C]TCE prevented incorporation of C into proteins. The ammonia-oxidizing activity of cells inactivated in the presence of TCE could be recovered through a process requiring de novo protein synthesis. In addition to TCE, a series of chlorinated methanes, ethanes, and other ethylenes were screened as substrates for ammonia monooxygenase and for their ability to inactivate the ammonia-oxidizing system of N. europaea. The chlorocarbons could be divided into three classes depending on their biodegradability and inactivating potential: (i) compounds which were not biodegradable by N. europaea and which had no toxic effect on the cells; (ii) compounds which were cooxidized by N. europaea and had little or no toxic effect on the cells; and (iii) compounds which were cooxidized and produced a turnover-dependent inactivation of ammonia oxidation by N. europaea.

Journal Article↗
PubMed1996

Influence of pH on Ammonia Accumulation and Toxicity in Halophilic, Methylotrophic Methanogens.

We studied the effects of pH and ammonia concentration on the growth of three methanogens. These three halophilic, methylotrophic methanogens, Methanolobus bombayensis, Methanolobus taylorii, and Methanohalophilus zhilinaeae, grew at environmental pH ranges that overlapped with each other and spanned the pH range from 7.0 to 9.5. During growth they had reversed membrane pH gradients ((Delta)pH) at all pH values tested. The (Delta)pH was in the range of -0.4 to -0.9 pH units, with the cytosol being more acidic than the environmental pH. Methanohalophilus zhilinaeae had the most negative (Delta)pH (-0.9 pH units). These negative pH gradients resulted in the accumulation of ammonium (NH(inf4)(sup+)), and when grown at the highest external ammonia concentrations that allowed good growth, cells had cytosolic NH(inf4)(sup+) concentrations as high as 180 mM. The high concentrations of cytosolic NH(inf4)(sup+) were accompanied by greater (Delta)pH and lower concentrations of the major cytosolic cation K(sup+) (compared with cells grown in medium with only 5 mM ammonia). Methanolobus bombayensis and Methanolobus taylorii were more sensitive to total external ammonia at higher external pH values, but the inhibitory concentration of un-ionized ammonia that resulted in a 50% reduction of the growth rate was about 2 to 5 mM, regardless of the pH. This is consistent with growth inhibition by ammonia in other bacteria. However, Methanohalophilus zhilinaeae was more resistant to un-ionized ammonia than any other known organism. It had a 50% inhibitory concentration for un-ionized ammonia of 13 mM at pH 8.5 and 45 mM at pH 9.5. We examined the effects of pH on three ammonia-assimilating activities (glutamine synthetase, glutamate dehydrogenase, and alanine dehydrogenase) in cell lysates and found that the pH ranges were consistent with the observed ranges of intracellular pH.

Journal Article↗
PubMed1998

Inactivation of Cryptosporidium parvum Oocysts by Ammonia.

The survival of Cryptosporidium parvum oocysts in soil and water microhabitats may be affected by the environmental production and release of free ammonia. The objective of this study was to determine the effects of increasing free ammonia concentrations and times of exposure on oocyst viability. Wild-type oocysts were obtained from naturally infected calf feces by chemical (continuous-flow) centrifugation and sucrose gradients. Ammonia (NH(3)) from a commercial solution was applied in concentrations ranging from 0.007 to 0.148 M. Exposure times ranged from 10 min to 24 h at a constant temperature of 24 +/- 1 degrees C. Viability of oocysts was determined with a dye permeability assay and an in vitro excystation assay (M. B. Jenkins, L. J. Anguish, D. D. Bowman, M. J. Walker, and W. C. Ghiorse, Appl. Environ. Microbiol. 63:3844-3850, 1997). Even the lowest concentration of ammonia decreased significantly the viability of oocysts after 24 h of exposure. Increasing concentrations of ammonia increased inactivation rates, which ranged from 0.014 to 0.066 h. At the highest concentration of ammonia, a small fraction of viable oocysts still remained. Exposure to pH levels corresponding to those associated with the ammonia concentrations showed minimal effects of alkaline pH alone on oocyst viability. This study shows that environmentally relevant concentrations of free ammonia may significantly increase the inactivation of oocysts in ammonia-containing environments.

Journal Article↗
PubMed1996

Severity of hyperammonemic encephalopathy correlates with brain ammonia level and saturation of glutamine synthetase in vivo.

Correlation among in vivo glutamine synthetase (GS) activity, brain ammonia and glutamine concentrations, and severity of encephalopathy was examined in hyperammonemic rats to obtain quantitative information on the capacity of GS to control these metabolites implicated in the etiology of hepatic encephalopathy. Awake rats were observed for neurobehavioral impairments after ammonium acetate infusion to attain a steady-state blood ammonia concentration of 0.9 (group A) or 1.3 mumol/g (group B). As encephalopathy progressed from grade III to IV, brain ammonia concentration increased from 1.9 to 3.3 mumol/g and then decreased to 1.3 mumol/g on recovery to grade III. In contrast, brain glutamine concentration was 26, 23, and 21 mumol/g, respectively. NH(4+)-infused rats pretreated with L-methionine DL-sulfoximine reached grade IV when brain ammonia and glutamine concentrations were 3.0 and 5.5 mumol/g, respectively; severity of encephalopathy correlates with brain ammonia, but not glutamine. In vivo GS activity, measured by NMR, was 6.8 +/- 0.7 mumol/h/g for group A and 6.2 +/- 0.6 mumol/h/g for group B. Hence, the in vivo activity, shown previously to increase with blood ammonia over a range of 0.4-0.64 mumol/g, approaches saturation at blood ammonia > 0.9 mumol/g. This is likely to be the major cause of the observed accumulation of brain ammonia and the onset of grade IV encephalopathy.

Ammonia↗