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PubMed1984

Ammonia toxicity for mammalian and avian lymphocytes from blood.

The effect of addition of ammonia to cultures of avian, bovine, cavian, equine, human, leporinae, murine, ovine and porcine blood lymphocytes was studied. The concentrations of ammonia in the lymphocyte cultures represented normal (0.01-0.5 mg/dl), subtoxic (0.5-1 mg/dl), and toxic (1-10 mg/dl) concentrations of ammonia in blood. Viability of the lymphocytes and their mitogenic reactivity were measured. In general, 1.0 and 10 mg/dl of ammonia (toxic concentrations) affected viability and mitogenic responsiveness of all lymphocytes from tested species. The lower concentrations of ammonia affected only avian, bovine and equine lymphocytes.

Ammonia↗
PubMed1996

Control of ammonia formation during Bacillus subtilis fermentation of legumes.

The control of ammonia formation during the Bacillus subtilis fermentation of autoclaved, roasted soybean cotyledons (Glycine max) and of autoclaved African locust bean cotyledons (Parkia spp.) was investigated. Addition of NaCl, 1.5 mol (kg wet cotyledons)-1, part way through the fermentation inhibited ammonia formation and softening of the cotyledons. Addition of glycerol, 1.7 mol (kg wet cotyledons)-1 part way through the fermentation inhibited alkalinisation and ammonia formation while allowing enzymic activity and softening of the cotyledons to continue. Restriction of the oxygen supply by incubating the cotyledons in a sealed container also prevented excessive ammonia production and increase in pH value. Fermentations conducted in sealed containers with an air to cotyledons ratio of approximately 130-175 ml air (g wet cotyledons)-1 supported good microbial growth and proteolysis without the formation of detectable ammonia aroma.

Ammonia↗
PubMed1986

Ammonia levels in the whelping nests of farmed raccoon dogs and polecats.

Ammonia concentrations were measured in the nests of farmed raccoon dogs (Nyctereutes-procyonoides Gray, 1834) and polecats (Mustela putorius) at weaning time. Ammonia levels in the nests of raccoon dogs and polecats varied from 1 to 43 ppm and from 0 to 5 ppm, respectively. In the raccoon dog, with increasing litter size, the ammonia concentrations tended to increase exponentially. In the polecat, no marked relationship between litter size and ammonia levels were found. The results show that no special adaptations are required in farm life because even the highest ammonia concentrations measured were below the harmful level.

Ammonia↗
PubMed1986

Ammonia absorption from different parts of chicken intestine and its quantitative evaluation in situ.

Ammonia was more rapidly absorbed from the ileum than the jejunum, and the lower the small intestine was, the more rapid was the absorption of lumen fluid. About 95% of ammonia-15N introduced into the intestinal sac having Meckel's diverticulum in the middle part disappeared in 30 min, of which 90% was recovered as non-protein-N in the blood of the mesenteric vein draining the sac and in the mucosa of the tested portion in 30 min. About 57% of ammonia which disappeared from the intestinal lumen was found as ammonia-N and 26% as other non-protein-N in the mesenteric blood. Maximal rates of appearance of total non-protein-15N and ammonia-15N in the mesenteric blood were found within 10 min and returned to the levels at 0-5 min in 30 min.

Ammonia↗
PubMed1996

Participation of NH4+ in total ammonia absorption across the rumen epithelium of sheep (Ovis aries).

1. Participation of NH4+ in total ammonia transport across sheep rumen wall was studied in vitro. 2. In Ussing-type chambers addition of NH4+ or K+ to the incubation solution on the mucosal side of the epithelium evoked positive short-circuit currents (ISC). 3. The K+ induced ISC but not the NH4+ induced ISC could be blocked by Ba2+ whereas both, K+ or NH4+ induced ISC were blocked by quinidine. 4. Transepithelial fluxes of ammonia were significantly reduced when quinidine was present in the incubation solution. 5. When the transepithelial potential difference was clamped to -25 mV (polarity on the serosal side) ammonia fluxes from the mucosal to the serosal side were significantly larger than fluxes of ammonia measured as a potential difference of +25 mV. 6. It is suggested that NH4+ takes part in ammonia transport across the rumen epithelium, most probably by using a K(+)-transport system.

Ammonia↗
PubMed1992

Ammonia: a possible promotor in Helicobacter pylori-related gastric carcinogenesis.

Helicobacter pylori (HP) has been shown to possibly be a pathogen of gastric carcinoma. HP has urease activity and produces ammonia in the stomach. In this study, the role of ammonia on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in rats. After 24 weeks pretreatment with MNNG (83 mg/l), 0.01% ammonia or tap water as a drinking water was administered for 24 weeks. The ammonia-treated rats showed a significantly higher incidence of gastric cancer (percent of animals with tumors and number of tumors per rat). Ammonia would thus appear to have an important role in HP-related human gastric carcinogenesis.

Adenocarcinoma↗
PubMed1990

Ammonia is endogenously generated in the brain in the presence of presumed and verified dementia of Alzheimer type.

The healthy, mature, non-starved brain was found to take up a small amount of ammonia on average 7.22 +/- 0.72 micrograms/100 g x min. In contrast, in patients thought to be suffering from incipient early-onset dementia of the Alzheimer type (DAT) the brain released a larger amount of ammonia on average 25.59 +/- 16.17 micrograms/100 g x min. In advanced DAT states, an average of 2.73 +/- 0.32 micrograms/100 g x min was released indicating the temporary nature of the severe loss of amino-N during the early stages of presumed DAT. Detrimental effects of endogenously formed ammonia on brain metabolism may affect the membrane potential, the excitability of neurons, and the energy metabolism. Ammonia may be assumed to be involved in the morphological changes in astrocytes and in the gliosis observed in early degeneration related to DAT. Endogenously generated brain ammonia thus may have a role in the cascade of cell damaging events in presumed incipient DAT.

Alzheimer Disease↗
PubMed1995

Abolition of the inhibitory effect of ethanol oxidation on gluconeogenesis from lactate by asparagine or low concentrations of ammonia.

When isolated hepatocytes from fasted rats were incubated with 10 mM lactate, the [lactate]/[pyruvate] ratio measured at the beginning of the incubation was raised above 70:1 but declined to a steady level of about 8:1 within 40 min. The rate of gluconeogenesis from lactate was initially slow but gradually increased over the incubation period becoming maximal by 30 min. The simultaneous addition of lactate and ethanol resulted in an initial [lactate]/[pyruvate] ratio above 250:1 which by 60 min had declined to a new steady-state level of approx. 60:1. The lactate, ethanol combination also brought about a prolongation of the lag phase before glucose synthesis became maximal; however, by 40 min the rate of gluconeogenesis was independent of the presence of ethanol. Thus the inhibitory effect of ethanol on glucose synthesis was manifest only over the early portion of the incubation period. When asparagine, a precursor of malate/aspartate components, was added to the incubation mixture, the lag before maximal rates of glucose formation from lactate in the absence or presence of ethanol was almost abolished. The presence of asparagine also rapidly lowered the [lactate]/[pyruvate] ratio of hepatocytes incubated with lactate plus ethanol establishing a steady-state level of 15:1 within 10-15 min. Asparagine enhanced the rate of lactate-stimulated ethanol oxidation, particularly during the early part of the incubation. In endeavouring to elucidate which of the products of asparagine catabolism (i.e. ammonia and aspartate) were responsible for these effects, we found that a small and constant level of ammonia, formed by the degradation of urea by urease, almost reproduced the effects of asparagine on the [lactate]/[pyruvate] ratio, glucose synthesis and ethanol oxidation. A bolus addition of 10 mM aspartate or 4 mM ammonia to cells metabolising lactate and ethanol were less effective than a steady-state low ammonia concentration, generated from urea/urease. Our studies suggest that asparagine or a low concentration of ammonia, by providing components of the malate/aspartate shuttle, can ameliorate some of the metabolic effects of ethanol on the liver.

Ammonia↗
PubMed1983

Aerobic and anaerobic ammonia production by fish.

1. In comparison to other vertebrates, a relatively large part of energy consumption in fish is covered by protein catabolism. 2. In Teleosts, ammonia is the major component of nitrogen excretion, its production rate being directly related to the rate of protein oxidation, while urea is almost exclusively produced from nucleotides by uricolysis. 3. Aerobic ammonia excretion arises from extraction of blood ammonia by the gill. 4. Under aerobic conditions, ammonia originates mainly in the liver by transdeamination and the hydrolysis of imino groups, while an additional quantity is formed in working skeletal muscles by purine nucleotide cycling. 5. During a decline of environmental oxygen, the contribution of the liver to total ammonia production seems to be lowered, while that of skeletal muscles is increased. 6. Anaerobic ammoniogenesis seems to proceed via at least 4 different mechanisms, all occurring in goldfish: deamination of adenylates via adenylate deaminase, deamination of aspartate via the purine nucleotide cycle, breakdown of alanine to ethanol, CO2 and NH3, and oxidation of glutamate via a slowly spinning Krebs-cycle. 7. In goldfish, the combination of these mechanisms is able to sustain an anaerobic rate of ammoniogenesis being equal to that observed under normoxic conditions.

Amino Acids↗
PubMed1987

Incorporation of intraportal ammonia-N into blood and tissue nitrogenous compounds in chickens fed low and high protein diets.

1. 15N-Percentage of the amide of glutamine in total blood non-protein-15N was 42 and 48% in chickens fed 5 and 20% protein diets, respectively, when 15N-ammonia was intraportally-infused for 6 hr. 2. The infused ammonia-15N also appeared in the amide of free glutamine in the liver and kidney in large amounts at both levels of protein intake. 3. The 15N incorporated into glutamine-amide in the blood, liver and kidney and non-protein-15N in plasma were greater in chickens fed the low protein diet than in those fed the high protein diet (P less than 0.05 except kidney of P less than 0.01). 4. About 60% of the amide-N of the glutamine which was increased during 6 hr infusion of ammonia was derived from infused ammonia-N and the remainder from endogenous nitrogen, irrespective of protein intake. 5. These results suggest that glutamine is the most important intermediate in detoxication of intraportal ammonia in chickens.

Ammonia↗
PubMed1988

Ammonia production from amino acids and urea in the caecal contents of the chicken.

1. Ammonia production from urea and amino acids in the caecal contents of the chicken was evaluated using 15N-labeled nitrogenous compounds. 2. About 43% of each of urea nitrogen and glutamine amide nitrogen was converted to ammonia nitrogen, but only 25% of epsilon-nitrogen of the added arginine, a precursor of urea, was found in ammonia. 3. Amino nitrogen of the separately added glutamic acid and glycine to be converted to ammonia was 19-20% of their added amounts, whereas that of alpha-alanine was 11%. 4. It is concluded that dietary and urinary amino acids and urea which find their ways into the caeca are useful nitrogen sources for ammonia production by microflora in the caeca of the chicken.

Amino Acids↗
PubMed1985

Functional relationship of ammonia to DNA, RNA and protein in brain.

The functional significance of the production of ammonia during neuronal activity is not known, although a number of studies are available concerning the mechanism of of ammonia toxicity in brain. Hyperammonemia without behavioural change was induced in experimental rats by i.p. administration of either a single dose of ammonium acetate or 6 doses with an interval of 1 h during the day or one single dose daily for 7 days. No significant change was observed in the content of DNA, RNA and protein in cerebral cortex, cerebellum and brain stem following the administration of a single dose. There was a marked decreased in the content of DNA in all three brain regions after the administration of 6 hourly doses of ammonium acetate. Under these conditions the RNA was found to increase in all three brain regions. A decrease in the content of protein per gram wet weight was observed in cerebral cortex and brain stem while the change in cerebellum was found to be insignificant. However, the content of RNA and protein was found to show a very significant increase when expressed per microgram of DNA for each region under these conditions, indicating an increase in RNA and protein in the cells surviving the toxic damage caused by ammonia. A marked and significant increase in the content of RNA and protein was observed in all three brain regions following the administration of a single dose per day for 7 days. These results are discussed not only with respect to toxic damage to the glial cells by ammonia, but also with respect to the probable effect of ammonia liberated during neuronal activity on inhibition of lysosomal degradation of protein, and on its stimulatory effects of transcriptional and translational activities. The increased RNA and protein under these conditions may be contributing not only in the proliferation of glial cells (Alzheimer Type II cells) but also in the dendritic spinous growth.

Acetates↗
PubMed1984

The metabolic basis for the genesis of seizures: the role of the potassium-ammonia axis.

A conceptual approach to the understanding of the pathogenesis of idiopathic seizures is presented. Hypokalemia and/or alkalosis promotes the elaboration of an alkaline urine, which increases the renal return of ammonia and exposes the brain to chronically higher concentrations of ammonia. In the brain, ammonia is preferentially detoxified to glutamine and therefore depletes the available glutamic acid, which is also a precursor of GABA, the major mediator of central inhibition. Mild chronic elevations of ammonia may also result in long-term nutritional alterations of amino-acid precursors of other brain neurotransmitters. A linkage thus exists for the metabolic basis of seizures: the role of the potassium-ammonia axis may be important in the selective depletion of GABA, the major mediator of central inhibition.

Alkalosis↗
PubMed1984

The metabolic basis for the genesis of seizures: the role of the potassium-ammonia axis.

A conceptual approach to the understanding of the pathogenesis of idiopathic seizures is presented. Hypokalemia and/or alkalosis promotes the elaboration of an alkaline urine, which increases the renal return of ammonia and exposes the brain to chronically higher concentrations of ammonia. In the brain, ammonia is preferentially detoxified to glutamine and therefore depletes the available glutamic acid, which is also a precursor of GABA, the major mediator of central inhibition. Mild chronic elevations of ammonia may also result in long-term nutritional alterations of amino-acid precursors of other brain neurotransmitters. A linkage thus exists for the metabolic basis of seizures: the role of the potassium-ammonia axis may be important in the selective depletion of GABA, the major mediator of central inhibition.

Alkalosis↗
PubMed1985

Cot-death: the ammonia factor.

Wet nappies at night could cause infants at risk to die. Tyler first suspected this ten years ago when his head was jerked back from his infant son's cot by the pungent odour of ammonia gas. This theory is consistent with the full epidemiology of cot-death. Ammonia is an insidious poison which has a wide and varied range of effects on the respiratory and nervous systems according to concentration and length of exposure. At its mildest it irritates the tissues. In larger doses ammonia can cause pulmonary oedema and pneumonitis. It can also cause stenosis of affected organs. Its chief danger lies in its potential to disrupt oxygenation at every level throughout the body. Acute and chronic poisoning profiles indicate the possibility that numbers of infants reported as dying from gastro-intestinal or respiratory disease could have been ammonia poisoning victims. Predisposing factors, such as smoking during pregnancy, are shown to contribute to the vulnerability of the infant to ammonia poisoning. The theory provides the framework for the development of an effective programme of infant death prevention.

Ammonia↗
PubMed1986

The pathogenesis of vascular headaches in patients with hypertension; the role of the ammonia-potassium axis.

Headaches may occur in as many as 25% of hypertensive patients and generally bears little relationship to level of diastolic blood pressure. Previous observations, in normotensive patients, suggested that abnormalities in both potassium and ammonia metabolism might be related to the pathogenesis of these headaches. The present study was undertaken to see whether these factors also occurred in hypertensive patients with headaches. The present observations were made in thirteen hypertensive patients with vascular headaches. The major findings include potassium levels of 3.45 +/- 0.25 mEq/L; CO2, 29.85 +/- 1.21 mEq/L; blood ammonia, 41 +/- 8.40 U mol/L and an alkaline pH of the urine. The blood ammonia levels, when factored by the BUN, yielded elevated ammonia to BUN ratios (3.81 +/- 1.82). These findings are similar to those previously observed in normotensive patients with vascular headaches. The profile of hypokalemia and/or alkalosis, increased blood ammonia to BUN ratios and a relatively alkaline urine appears to be a commonly observed pattern in patients with vascular headaches. These data suggest that a biochemical basis exists for the genesis of vascular headaches in patients with hypertension.

Ammonia↗
PubMed1992

Accumulation of radioactivity in the pancreas after intravenous administration of [13N]ammonia.

A biodistribution study of [13N]ammonia in rats showed a high accumulation of radioactivity in the pancreas soon after the intravenous injection of this tracer. In humans, the pancreas was also clearly visualized by dynamic positron emission tomography soon after the intravenous injection of [13N]ammonia. To investigate the mechanism of the pancreatic accumulation of [13N]ammonia, in vitro studies with pancreatic slices and in vivo biodistribution and metabolism studies were carried out in rats. The results indicated that [13N]ammonia enters the pancreas from the blood by diffusion at a rate dependent on local blood flow, and then is rapidly incorporated into the amino acid fraction (mainly the glutamine fraction), followed by its incorporation into protein. These findings suggest that [13N]ammonia could be useful for diagnostic imaging of the pancreas.

Ammonia↗
PubMed2004

Characteristics of anaerobic ammonia removal by a mixed culture of hydrogen producing photosynthetic bacteria.

It is known that the presence of ammonia inhibits hydrogen production by photosynthetic bacteria. In order to avoid it, a two-step process containing ammonia removal and hydrogen production was investigated in this study. Firstly, the effects of carbonate presence on ammonia removal by photosynthetic bacteria were investigated by the vial tests because it is known that the uptake of volatile fatty acids (VFAs) sometimes requires carbonate. The results of them showed that the presence of carbonate promoted the uptake of VFAs and ammonia. Especially, the uptake of propionate and/or butyrate required the presence of carbonate. The results of the batch experiments of two-step hydrogen production showed that the depletion of ammonia triggered hydrogen evolution. Herein, the presence of albumin did not inhibit hydrogen evolution and preferably it increased the hydrogen production rate. And the VFA-C/NH4-N ratio in substrate fed into two-step hydrogen production process should be more than 6.0.

Albumins↗