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PubMed1994

Muscle ammonia and glutamine exchange during chronic liver insufficiency in the rat.

The aim of this study was to investigate the role of skeletal muscle in ammonia and glutamine metabolism during chronic hyperammonemia induced by liver insufficiency. The hindquarter ammonia and amino acid fluxes and muscle tissue concentrations were studied in two rat models of chronic liver insufficiency, portacaval shunting and portacaval shunting plus bile-duct ligation, as well as in sham-operated animals, 7 and 14 days after surgery, and in normal, unoperated rats. To reduce nutritional influences, portacaval-shunted rats and sham-operated rats were pair-fed to portacaval shunt biliary obstruction rats. Arterial ammonia levels were elevated in both liver insufficiency groups. In the portacaval shunting plus bile-duct ligation group, arterial glutamine levels were elevated compared with sham-operated controls. No net hind-quarter ammonia uptake was observed in any of the groups, despite hyperammonemia in the chronic liver insufficiency groups. Hindquarter glutamine release was always increased in the liver insufficiency groups compared with sham-operated controls, despite similar muscle glutamine levels in the sham-operated and hyperammonemic groups, suggesting enhanced muscle glutamine synthesis in the latter groups. Muscle ammonia levels were always increased and muscle glutamate decreased in the hyperammonemic groups, probably indicating glutamate consumption by enhanced glutamine synthesis. The increased phenylalanine tissue concentrations and efflux in portacaval shunt/biliary obstruction rats suggest that enhanced net muscle protein breakdown, amino acid catabolism and transamination, rather than ammonia uptake from the blood furnish amino acids and ammonia for enhanced glutamine synthesis. These experiments suggest that nutritional factors are important in explaining altered muscle metabolism during chronic liver insufficiency.

Amino Acids↗
PubMed1988

Porcine intestinal ammonia liberation. Influence of food intake, lactulose and neomycin treatment.

Lactulose and neomycin have, besides influencing ammonia production of the intestinal flora, been proposed to reduce glutamine-dependent ammonia formation. To test this hypothesis we determined the effects of lactulose and neomycin on the release or uptake of ammonia, urea, and amino acids across the intestine of freely moving healthy pigs. Blood was sampled from catheterized piglets (20 +/- 0.8 kg; n = 6) before and 1, 2, 3, and 6 h after a standard pig meal (750 g, 12% protein). After a week of lactulose (Legendal; 2 x 60 g/day) or neomycin (8 g/day) treatment this procedure was repeated. Electromagnetic portal and small bowel flow measurements were carried out in separate groups of pigs. Flow measurements were independent of the kind of food ingested. No significant alterations in flow could be detected during the 6 h study period. Portal and porto-arterial ammonia differences were significantly decreased after lactulose (-20%) and neomycin (-35%) treatment. alpha-Amino-nitrogen absorption decreased in both groups as compared to controls, but this decrease did not reach significance. Systemic and portal glutamine levels as well as intestinal glutamine utilization were significantly lower in the treatment groups. Citrulline and glutamate levels and intestinal production decreased after treatment. In this in vivo model, ammonia liberation after protein meals decreased in animals pretreated with lactulose or neomycin. The decreased systemic and consequently intestinal glutamine utilization may contribute to a reduction of endogenous ammonia formation in the gut wall. Diminished absorption from the gut of alpha-amino-nitrogen may, however, also contribute to a decrease in ammonia production.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine↗
PubMedDate not supplied

Delayed induction of apoptosis by ammonia in C6 glioma cells.

Ammonia is a neurotoxin whose administration in large doses causes coma and death of the exposed animals, but whether and in what degree these whole body effects are related to the death of CNS cells is not known. Since the downstream effects of ammonia in cultured CNS cells appear to be partly mediated by overactivation of several putative signalling mechanisms characteristic for the apoptotic program, we speculated that ammonia neurotoxicity may be apoptogenic. In this study, C6 glioma cells grown in 2% serum were exposed to 5 mM or 10 mM NH(4)Cl (ammonia) for 96 h and tested for the appearance of apoptosis by (a) Hoechst staining, (b) TUNEL reaction and (c) DNA ladder, at different times of exposure. In cultures exposed to either 5 mM or 10 mM ammonia, about 10% of the cells were found to enter apoptosis at 48 h of exposure, and the number of apoptotic cells rose to 30% at 72 h, and to 50% at 96 h of exposure, respectively. The first transduction signal purportedly involved in apoptosis, activation of PKCalphabeta, was transient and appeared already after 3-6 h of treatment. Coincident with pronounced manifestation of apoptosis (at 72 h and even more at 96 h of exposure) was an increased transfer of the transcription factor NFkappaB from cytoplasmto nucleus as revealed by EMSA assay. The number of cells affected by ammonia-induced apoptosis was markedly reduced by incubation with a NOS inhibitor, L-NAME at 100 microM concentration. The results indicate that ammonia-induced apoptosis is a result of a complex interplay of at least three signalling molecules: NO, PKC and the transcription factor NFkappaB, with NFkappaB being possibly involved in the induction of iNOS and generation of toxic levels of NO in the cells.

Ammonia↗
PubMed2002

Neurobiology of ammonia.

Hyperammonemia resulting from inherited urea cycle enzyme deficiencies or liver failure results in severe central nervous system dysfunction including brain edema, convulsions and coma. Neuropathologic evaluation in these disorders reveals characteristic alterations of astrocyte morphology ranging from cell swelling (acute hyperammonemia) to Alzheimer Type II astrocytosis (chronic hyperammonemia). Having no effective urea cycle, brain relies on glutamine synthesis for the removal of excess ammonia and the enzyme responsible, glutamine synthetase, has a predominantly astrocytic localization. Accumulation of ammonia in brain results in a redistribution of cerebral blood flow and metabolism from cortical to sub-cortical structures. In addition to changes in astrocyte morphology, increased brain ammonia concentrations result in alterations in expression of key astrocyte proteins including glial fibrillary acidic protein, glutamate and glycine transporters and "peripheral-type" (mitochondrial) benzodiazepine receptors. Such changes result in alterations of astrocytic volume and increased extracellular concentrations of excitatory and inhibitory substances. In addition, the ammonium ion has direct effects on excitatory-inhibitory transmission via distinct mechanisms involving cellular chloride extrusion and postsynaptic receptor function. Acute ammonia exposure leads to activation of NMDA receptors and their signal transduction pathways. Chronic hyperammonemia also results in increased concentrations of neuroactive L-tryptophan metabolites including serotonin and quinolinic acid. Therapy in hyperammonemic syndromes continues to rely on ammonia-lowering strategies via peripheral mechanisms (reduction of ammonia production in the gastrointestinal tract, increased ammonia removal by muscle).

Ammonia↗
PubMed2001

Ammonia concentration in human preovulatory ovarian follicles.

OBJECTIVES: To determine ammonia concentrations in both the direct environment of the oocyte, ovarian follicular fluid, and peripheral blood. STUDY DESIGN: Samples of preovulatory follicular fluid and antecubital venous blood were obtained from 23 randomly selected women attending an in vitro fertilization program in an academic department. Ammonia concentrations were measured using the indophenol method. RESULTS: In every patient examined, the ratio of ammonia concentration in follicular fluid to that in blood exceeded 1.0. Mean ammonia concentration in follicular fluid (38.01+/-2.61 microM) was significantly higher than that in blood (22.70+/-1.35 microM; P<0.001 paired Student's t test). CONCLUSIONS: There is an ammonia gradient from follicular fluid to blood. The human preovulatory oocyte grows in an environment of a moderately increased ammonia concentration. This study suggests that the preovulatory follicle is a source of ammonia production.

Adult↗
PubMed2000

Comparison of organic and inorganic packing materials in the removal of ammonia gas in biofilters.

Two organic and two inorganic packing materials were compared with regard to the removal of ammonia gas in a biofilter inoculated with night-soil sludge. By gradually increasing the inlet load of ammonia, the complete removal capacity, which was defined as the inlet load of ammonia that was completely removed, and the maximum removal capacity of ammonia, which was the value when the removal capacity leveled off for each packing material, were estimated. Both values which were based on a unit volume of packing material, were higher for organic packing materials than inorganic ones. By using kinetic analysis, the maximum removal rate of ammonia, V(m), and the saturation constant, K(s), were determined for all packing materials and the values of V(m) for organic packing materials were found to be larger. By using the kinetic parameters, the removal rates for ammonia were compared among the four packing materials, and the organic packing materials showed superior performance for the removal of ammonia in the concentration range of 0-300 ppm as compared to inorganic packing materials.

Aluminum Silicates↗
PubMedDate not supplied

The role of nitrogen 13 ammonia positron emission tomography in predicting functional outcome after coronary revascularization.

BACKGROUND: We sought to evaluate the predictive value of positron emission tomography (PET) by using blood flow imaging with semiquantitative data analysis techniques for predicting recovery of regional function after revascularization. Positron emission tomography in combination with fluorodeoxyglucose (FDG) has been shown to predict tissue recovery after revascularization. Previous studies have suggested a quantitative threshold for perfusion as evaluated by PET that separates scar from viable tissue. METHODS AND RESULTS: In a group of 25 patients with impaired regional wall motion at baseline as measured by radionuclide ventriculography, we examined the relationship between myocardial blood flow and functional outcome of myocardial segments in patients who underwent coronary revascularization within 2 months after PET. Regional wall motion was graded on a 5-point scale, from normal to dyskinetic. Regional nitrogen 13 (N-13) ammonia uptake values were expressed as a percentage of maximal myocardial N-13 ammonia uptake and compared with values obtained from healthy volunteers. Results were displayed as polar maps, on which regions of interest were placed corresponding to revascularized vascular territories. We were able to show a statistically significant relationship between regional wall motion abnormalities and decreasing blood flow by N-13 ammonia uptake. An N-13 ammonia uptake of greater than 80% for any given segment was highly accurate in predicting normal or nearly normal postoperative regional wall motion, whereas severely decreased ammonia uptake less than 40% showed normalization of regional wall motion in only 13% of segments. CONCLUSIONS: Relative ammonia uptake of greater than 80% and less than 40% preoperatively had excellent predictive value for functional outcome, but intermediate quantitative ammonia uptake (between 40% to 80%) necessitates additional information to accurately predict functional recovery.

Adult↗
PubMed1979

Effect of ammonia on the glutamate dehydrogenase catalyzed oxidative deamination of L-glutamate. The steady state.

Ammonia is known to inhibit the steady-state rate of oxidation of L-glutamate catalyzed by glutamate dehydrogenase. We reported previously [Brown, A., Colen, A. H., & Fisher, H. F. (1978) Biochemistry 17, 2031] kinetic evidence supporting the formation in the initial rapid phase of a complex which is composed of enzyme, reduced coenzyme, alpha-ketoglutarate, and ammonia. We show here that the effects of ammonia on the steady-state reaction can be correlated with transient-state kinetic effects related to the concentration of that ammonia-containing complex. These results indicate the existence of alternate reaction pathways which become important at high ammonia concentrations. These new pathways provide an additional route for the release of NADPH from the enzyme surface. The expanded mechanism shows that the noncompetitive product inhibition by ammonia can occur without the simultaneous presence of ammonia and L-glutamate on the enzyme. This mechanism also accommodates the observed substrate inhibition by L-glutamate.

Ammonia↗
PubMedDate not supplied

Effects of ammonia and glucosamine on the heterogeneity of erythropoietin glycoforms.

Recombinant human erythropoietin (EPO) is a glycoprotein produced as a therapeutic agent from mammalian cell cultures for the treatment of anemia associated with severe kidney damage. The EPO structure has a high glycan content which is essential for bioactivity but shows considerable molecular heterogeneity. The cell culture conditions that affect the heterogeneity of the glycoforms of EPO are not well understood. However, the accumulation of ammonia in culture is one factor that has been associated with an enhanced heterogeneity of glycoforms. In this report we investigate the metabolic perturbations associated with ammonia and glucosamine that may give rise to an altered pattern of EPO glycosylation. Recombinant human erythropoietin was synthesized in serum-free cultures of transfected Chinese hamster ovary (CHO) cells. The molecular heterogeneity of erythropoietin was increased by supplementation of cultures with either ammonia or glucosamine. The enhanced molecular heterogeneity was shown to be due to variable glycosylation that resulted in EPO with an enhanced molecular weight and isoelectric point range. Enzymatic removal of the glycan moiety of EPO in all cases resulted in a single molecular form with a molecular weight of 18 000, which corresponded to non-glycosylated EPO. The variable glycosylation was consistent with reduced sialylation and antennarity of the carbohydrate structures present on the three N-linked sites of EPO. In the presence of ammonia (>30 mM) the proportion of tetrasialylated and tetraantennary glycan structures were reduced by 73% and 57%, respectively, as determined by HPLC analysis. Such changes were also observed, although to a lesser extent (41% and 37%), by an increase in the glucosamine concentration (>10 mM) in the medium. The enhanced heterogeneity of the glycan structures coincided with a significant increase in the intracellular UDP-N-acetylhexosamine (UDP-GNAc) pool. The measured UDP-GNAc level was up to 2 orders of magnitude higher in the presence of either glucosamine or ammonia. However, the changes in the glycosylation profiles induced by either glucosamine or ammonia were significantly different even at the same intracellular UDP-GNAc concentration. This suggests that the enhanced EPO heterogeneity could not be mediated solely by the increased UDP-GNAc level. Glucosamine (but not ammonia) was shown to cause significant inhibition of glucose transport into the cells, which could induce a different pattern of primary metabolism.

Ammonia↗
PubMed2002

Breath ammonia measurement in Helicobacter pylori infection.

Our aim was to define the utility of breath ammonia measurement in assessing Helicobacter pylori infection. Volunteers breathed into a device containing three fiberoptic NH3 sensors at baseline and after ingesting 300 mg of urea. Breath ammonia levels were compared to the [14C]urea breath test. Thirteen subjects were tested. Before urea ingestion, H. pylori-positive subjects had significantly lower breath ammonia levels than negative subjects (mean +/- SD, 0.04 ppm +/- 0.09 vs 0.49 ppm +/- 0.24, P = 0.002) and had a significantly greater increases in breath ammonia after urea ingestion (range 198-1,494% vs 6-98%). One H. pylori-positive subject underwent treatment and breath ammonia levels shifted from the pattern seen in positive subjects to that seen in negative subjects. In conclusion, breath ammonia measurement for H. Pylori-positive and negative subjects showed distinct patterns. Breath ammonia measurement may be feasible as a diagnostic test for H. pylori.

Adult↗
PubMed1998

Ammonia and manganese increase arginine uptake in cultured astrocytes.

Recent work has suggested a possible role for nitric oxide (NO) in the development of hepatic encephalopathy (HE). In this study, we examined the effect of ammonia and manganese, factors implicated in the pathogenesis of HE, on the transport of arginine (a precursor of NO) into primary cultures of astrocytes. Treatment with 5 mM ammonia for 1-4 days produced a maximal (53%) increase in L-arginine uptake at 3 days when compared to untreated cells. Kinetic analysis following 4-day treatment with 5 mM ammonia revealed an 82% increase in the Vmax and a 61% increase in the Km value. Similar analysis with 100 microM manganese showed a 101% increase in Vmax and a 131% increase in the Km value. These results suggest that both manganese and ammonia alter L-arginine uptake by modifying the transporter for arginine. A decrease of 32% in the non-saturable component of L-arginine transport was also observed following treatment with ammonia. When cultures were treated separately with 5 mM ammonia and 100 microM manganese for 2 days, the uptake of L-arginine increased by 41% and 57%, respectively. Combined exposure led to no further increase in uptake. Our results suggest that ammonia and manganese may contribute to the pathogenesis of HE by influencing arginine transport and thus possibly NO synthesis in astrocytes.

Ammonia↗
PubMed2004

Ammonia neurotoxicity and the mitochondrial permeability transition.

Ammonia is a neurotoxin that predominantly affects astrocytes. Disturbed mitochondrial function and oxidative stress, factors implicated in the induction of the mitochondrial permeability transition (MPT), appear to be involved in the mechanism of ammonia neurotoxicity. We have recently shown that ammonia induces the MPT in cultured astrocytes. To elucidate the mechanisms of the MPT, we examined the role of oxidative stress and glutamine, a byproduct of ammonia metabolism. The ammonia-induced MPT was blocked by antioxidants, suggesting a causal role of oxidative stress. Direct application of glutamine (4.5-7.0 mM) to cultured astrocytes increased free radical production and induced the MPT. Treatment of astrocytes with the mitochondrial glutaminase inhibitor, 6-diazo-5-oxo-L-norleucine, completely blocked free radical formation and the MPT, suggesting that high ammonia concentrations in mitochondria resulting from glutamine hydrolysis may be responsible for the effects of glutamine. These studies suggest that oxidative stress and glutamine play major roles in the induction of the MPT associated with ammonia neurotoxicity.

Ammonia↗
PubMed2002

Ammonia threshold--comparison to lactate threshold, correlation to other physiological parameters and response to training.

During standard graded exercise, blood lactate and blood ammonia levels increase in parallel and the two thresholds appear at the same relative intensity. The first part of this study aimed at comparing ammonia threshold to lactate threshold with five different graded exercise protocols. A significant difference between the two thresholds was found only in the continuous protocol with 4-min steps in which ammonia threshold appeared at a higher intensity than lactate threshold. The second part of the study investigated the correlation of ammonia threshold to some common physiological measurements. Correlation was significant with lactate threshold, ventilation threshold and endurance time. No correlation was found the anaerobic power, anaerobic capacity measurement and peak VO2. Ammonia threshold was also studied before and after endurance training and sprint training. The 8-week endurance training program was able to delay the appearance of ammonia threshold, but not the 8-week sprint training program. Findings in this study demonstrate that ammonia threshold is a physiological parameter that should be recognized and has potential to be applied for the evaluation of exercise capacity and the effectiveness of endurance training programs.

Adult↗
PubMed1980

Adaptive change in ammonia excretion in renal insufficiency.

Experiments were performed to study the mechanism of the compensatory increase in the excretion of metabolic acid by residual nephrons after reduction in renal mass. Despite a decrease in nephron population to 20% of control, total excretion of acid remained similar to pair-fed controls due to an increase in nephron excretion from 5.4 +/- 0.5 in controls to 22.3 +/- 1.9 nEq/24 hr (P < 0.25), including a threefold rise in ammonia excretion and a ninefold increase in excretion of titratable acid. Further studies showed that the in vivo production of ammonia by residual nephrons paralleled, in general, the nephron excretion rate, and increased from the control value of 0.23 +/- 0.02 to 0.54 +/- 0.09 ng/min (P < 0.05). Because the production rate of ammonia per milligram of DNA was not increased in experimental animals above control and because changes were not found in enzymes and substrates associated with increased ammoniagenesis in the rat, these data suggest that formation of additional ammonia-producing cells, due to hyperplasia, plays a role in the compensatory increase in ammonia excretion by residual nephrons. During acute acidosis, cellular ammonia production rose in a parallel manner in control and experimental kidneys, indicating that the capacity to form ammonia is not impaired in chronic renal insufficiency.

Acidosis↗
PubMed1981

Mechanism by which enhanced ammonia production reduces urinary potassium excretion.

To determine the mechanism whereby an increase in ammonia production decreases urinary potassium excretion, we perfused isolated rat kidneys at a pH of either 7.0 or 7.4. After 45 min of perfusion at either pH, glutamine or ammonium chloride was added to the perfusate to result in concentration of 5 and 0.8 mM, respectively and observations were continued for 50 min. Control kidneys were perfused at both pH's without further additions to the perfusate. At pH 7.0 glutamine increased ammonia production and increased urinary ammonium excretion strikingly; whereas the addition of ammonium chloride did not change ammonia production but increased urinary ammonium excretion to a comparably degree. Both maneuvers resulted in a reciprocal fall in urinary potassium excretion in comparison with control perfusions. The decreases in potassium excretion could not be accounted for by differences in perfusate or urinary acid-base parameters, or by changes in urinary sodium, water, or chloride excretion. At pH 7.4, glutamine also significantly increased ammonia production and perfusate ammonia concentration. In contrast to the studied at pH 7.0 in which the urine pH was acid (5.9), the urine remained alkaline (pH 7.2), and both urinary ammonium excretion and urinary potassium excretion were unaltered. Thus, potassium sparing is not a nonspecific effect of glutamine, its metabolism to ammonia, or perfusate ammonia concentration but is directly related to an increase in urinary ammonium excretion.

Ammonia↗
PubMed1981

Ammonia partitioning between glutamine and urea: interorgan participation in metabolic acidosis.

The distribution of precursor nitrogen between urea and glutamine was studied in control and acidotic rats. Acidosis, either acutely induced with hydrochloric acid or chronically induced with ammonium chloride, resulted in a rise in ammonia and a fall in urinary urea excretion; the percent of urinary nitrogen excreted as ammonia rose from 3.5 +/- 0.4 and 4.9 +/- 0.5 in fed and pair-fed controls to 25.9 +/- 3.9 and 37 +/- 5 in acidosis induced by hydrochloric acid and ammonium chloride. Hepatoportal vein urea concentration differences were significantly reduced, whereas glutamine concentration differences were significantly elevated, consistent with a shift of nitrogen from ureagenesis to glutamine; alanine and ammonia concentration differences were significantly decreased and increased respectively in the acidotic animals, suggesting that former supported urea synthesis whereas ammonia may preferentially support glutamine synthesis. Evidence of a feed-forward involvement of the gut in influencing hepatic nitrogen distribution was suggested by an increased ammonia and decreased alanine release in acidotic rats. Bilateral ureteral ligation was performed on control and acidotic rats to determine the fate of the redirected urinary ammonia. Ammonia did not accumulate in the blood, rather it was initially incorporated into glutamine, elevating the plasma level, and then it was subsequently deposited into urea. The shift of nitrogen back into urea in acidotic animals was confirmed by the greater postligation urea production rates supported by hepatic uptake of both alanine and glutamine. These results are discussed in terms of interorgan participation involving the liver, gut, and muscle in the partitioning of nitrogen between glutamine and urea.

Acidosis, Renal Tubular↗
PubMed2004

Methylamine, but not ammonia, is hypophagic in mouse by interaction with brain Kv1.6 channel subtype.

Ammonia and methylamine (MET) are endogenous compounds increased during liver and renal failure, Alzheimer's disease, vascular dementia and diabetes, where they alter some neurobehavioural functions probably acting as potassium channel blockers. We have already described that potassium channel blockers including tetraethylammonium (TEA), ammonia and MET are hypophagic in mice. Antisense oligonucleotides (aODNs) against Shaker-like Kv1.1 gene abolished the effect of TEA but not of ammonia and MET. The central effects elicited in fasted mice by ammonia and MET were further studied. For MET, an ED(50) value 71.4+/-1.8 nmol mouse(-1) was calculated. The slope of the dose-response curves for these two compounds and the partial hypophagic effect elicited by ammonia indicated a different action mechanism for these amines. The aODNs pretreatments capable of temporarily reducing the expression of all seven known subtypes of Shaker-like gene or to inactivate specifically the Kv1.6 subtype abolished the hypophagic effect of MET but not that of ammonia. Reverse transcription-polymerase chain reaction, Western blot and immunohistochemical results indicate that a full expression in the brain of Kv1.6 is required only for the activity of MET, and confirms the different action mechanism of ammonia and MET.

Ammonia↗
PubMed1983

The purine nucleotide cycle and ammonia formation from glutamine by rat kidney slices.

To test the significance of the purine nucleotide cycle in renal ammoniagenesis, studies were conducted with rat kidney cortical slices using glutamate or glutamine labelled in the alpha-amino group with 15N. Glucose production by normal kidney slices with 2 mM-glutamine was equal to that with 3 mM-glutamate. With L-[15N]glutamate as sole substrate, one-third of the total ammonia produced by kidney slices was labelled, indicating significant deamination of glutamate or other amino acids from the cellular pool. Ammonia produced from the amino group of L-[alpha-15N]glutamine was 4-fold higher than from glutamate at similar glucose production rates. Glucose and ammonia formation from glutamine by kidney slices obtained from rats with chronic metabolic acidosis was found to be 70% higher than by normal kidney slices. The contribution of the amino group of glutamine to total ammonia production was similar in both types of kidneys. No 15N was found in the amino group of adenine nucleotides after incubation of kidney slices from normal or chronically acidotic rats with labelled glutamine. Addition of Pi, a strong inhibitor of AMP deaminase, had no effect on ammonia formation from glutamine. Likewise, fructose, which may induce a decrease in endogenous Pi, had no effect on ammonia formation. The data obtained suggest that the contribution of the purine nucleotide cycle to ammonia formation from glutamine in rat renal tissue is insignificant.

Ammonia↗