Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMMONIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1995

Determination of ammonia in ear-lobe capillary blood is an alternative to arterial blood ammonia.

Blood ammonia determination is a laboratory test to diagnose hepatic encephalopathy. Arterial blood is superior to peripheral venous blood ammonia because of ammonia metabolism in muscle. We have compared capillary with arterial whole blood ammonia as capillary sampling is an attractive alternative. Ear-lobe capillary blood ammonia (ECA) was determined in all 173 persons studied, fingertip capillary blood ammonia (FCA) in 46 of these and arterial blood ammonia (AA) in 113. Of the 173, 60 were healthy (H), 64 were patients, not liver diseased (NLD) and 49 had liver disease (LD). Reference values, median and ranges, mumol NH3-N/l: AA, NLD, n = 64: 17 (7-42); ECA, H = NLD (P = 0.9), n = 124: 20 (7-45); FCA, H = NLD (P = 0.8), n = 33: 70 (29-151). Within the NLD group (n = 64) AA values (range 7-42) were little but significantly lower than the ECA values (range 7-45, P = 0.002). FCA NLD > AA NLD (n = 14, P < 0.0001); FCA H+NLD > ECA (n = 33, P < 0.0001). AA correlated very well with ECA, r = 0.87 (n = 113, P < 0.0001) and less well with FCA, r = 0.56 (n = 27, P < 0.01). ECA correlated with FCA, r = 0.51 (n = 46, P < 0.001). Ear-lobe capillary blood ammonia thus accurately reflects arterial ammonia and is an attractive alternative. The higher fingertip ammonia may be due to contamination with ammonia-rich sweat from finger grooves, regardless of the precautions taken.

Adolescent↗
PubMed1985

Effect of cortical-medullary gradient for ammonia on urinary excretion of ammonia.

Previous studies suggested that a portion of ammonia secreted into the proximal tubule may diffuse directly from Henle's loop into the medullary collecting duct. Since water is absorbed along the course of the descending portion of the loop, it was proposed that the concentration of ammonia increased in loop fluid, and that rapid diffusibility of the free base would facilitate the delivery of ammonia into medullary interstitium where a high level could be maintained by the countercurrent exchange process. In this schema it was proposed that there was an ammonia concentration gradient between medullary structures and cortex, and recovery of ammonia by the medullary collecting duct due to the low pH in tubule fluid at that site. The present study was designed to evaluate this hypothesis by estimating ammonia concentrations in medullary and cortical tissue, and by correlating medullary levels with secretion rate into the inner medullary collecting duct. In control animals the concentration of total ammonia (NH4+ + NH3+) in inner medullary vasa recta was 9.2 +/- 1.5 mumoles/ml, a level 100-fold higher than the cortical level of 0.10 +/- 0.01. During acute acidosis the medullary level rose to 22.5 +/- 2.7 mumoles/ml, but in acute acidosis during mannitol infusion the level fell to 8.0 +/- 1.2. The rate of ammonia secretion into inner medullary collecting duct fluid correlated directly with medullary vasa recta ammonia concentration. These data provide evidence for a steep ammonia concentration gradient between the medulla and cortex, and suggest that the diffusion gradient across collecting duct epithelium governs the rate of the addition of ammonia to collecting duct fluid.

Acidosis↗
PubMed2000

Gastric-juice ammonia assay for diagnosis of Helicobacter pylori infection and the relationship of ammonia concentration to gastritis severity.

OBJECTIVES: To determine the test characteristics of gastric-juice ammonia concentration as measured by an ion-selective electrode and a rapid ammonia detection device for the diagnosis of Helicobacter pylori infection and to assess the relationship between gastric-juice ammonia concentration and the severity of gastritis. METHODS: Patients undergoing upper endoscopy had collection of gastric juice that was tested for ammonia using an ion-selective electrode and a rapid ammonia assay device that uses a pH-indicating membrane. A receiver operating characteristic curve was calculated for ammonia concentration. Severity of gastritis was graded using the Sydney classification (1) and correlated to gastric-juice ammonia concentration. Patients also underwent H. pylori testing by IgG serology, rapid urease testing, and histological special stain. Ammonia testing results were compared with a reference standard of two of three positive tests and with a second reference standard of a positive serology. RESULTS: 73 patients underwent endoscopy and collection of gastric juice. The receiver operating characteristic curve indicated an optimal cutoff value of 5 mM, yielding a sensitivity of 67%, specificity of 93%, positive predictive value of 67%, and negative predictive value of 93% (compared with the combined reference standard). The rapid NH3-testing device yielded a sensitivity of 83%, specificity 63%, positive predictive value 31%, and negative predictive value 95%. The severity of neutrophilic (p = 0.001) and mononuclear cell (p = 0.003) infiltration were significantly correlated with gastric-juice ammonia concentration. CONCLUSIONS: Measurement of gastric-juice ammonia concentration by ion-selective electrode or rapid detection device is a relatively insensitive and nonspecific means of H. pylori diagnosis. Gastritis severity increases with gastric-juice ammonia concentration.

Ammonia↗
PubMed2000

Partial pressure of ammonia versus ammonia in hepatic encephalopathy.

Ammonia is considered the major pathogenetic factor of cerebral dysfunction in hepatic failure. The correlation between total plasma ammonia and the severity of hepatic encephalopathy (HE), however, is variable. Because ammonia that is present in gaseous form readily enters the brain, the correlation with the grade of HE of the pH-dependent partial pressure of gaseous ammonia (pNH(3)) could be better than that of total arterial ammonia levels. To test this hypothesis, 56 cirrhotic patients with acute episodes of clinical HE (median age, 54 years; range, 21-75) were studied by clinical examination and by long-latency median-nerve sensory-evoked potentials (SEPs) N70 peak, an objective and sensitive electrophysiological measure of HE. pNH(3) was calculated from arterial blood according to published methods. The clinical grade of HE correlated (P <.001) with both pNH(3) and total ammonia, but correlation was stronger with pNH(3) (r =.79 vs.69, P =.01). A similar correlation was found for N70 peak latency (r =.71 with pNH(3) vs.64 with total ammonia, respectively, P =.08). In summary, arterial pNH(3) correlates more closely than total ammonia with the degree of clinical and electrophysiological abnormalities in HE. These findings support the ammonia hypothesis of HE and suggest that pNH(3) might be superior to total ammonia in the pathophysiological evaluation of HE.

Adult↗
PubMed1999

Sources and sinks for ammonia and nitrite on the early Earth and the reaction of nitrite with ammonia.

An analysis of sources and sinks for ammonia and nitrite on the early Earth was conducted. Rates of formation and destruction, and steady state concentrations of both species were determined by steady state kinetics. The importance of the reaction of nitrite with ammonia on the feasibility of ammonia formation from nitrite was evaluated. The analysis considered conditions such as temperature, ferrous iron concentration, and pH. For sinks we considered the reduction of nitrite to ammonia, reaction between nitrite and ammonia, photochemical destruction of both species, and destruction at hydrothermal vents. Under most environmental conditions, the primary sink for nitrite is reduction to ammonia. The reaction between ammonia and nitrite is not an important sink for either nitrite or ammonia. Destruction at hydrothermal vents is important at acidic pH's and at low ferrous iron concentrations. Photochemical destruction, even in a worst case scenario, is unimportant under many conditions except possibly under acidic, low iron concentration, or low temperature conditions. The primary sink for ammonia is photochemical destruction in the atmosphere. Under acidic conditions, more of the ammonia is tied up as ammonium (reducing its vapor pressure and keeping it in solution) and hydrothermal destruction becomes more important.

Ammonia↗
PubMed1992

Plasma ammonia is the principal source of ammonia in sweat.

Sweat contains ammonia. However, neither its source nor factors affecting its concentration in the sweat are known. The aim of this study was to examine the effect of plasma concentrations of ammonia and urea on the concentration of ammonia in the sweat. Four groups of male volunteers were examined: one control, two after ingestion of ammonium chloride, three cirrhotic, hyperammonaemic, four uraemic. Sweat was collected from each subject from the palmar side of the forearm using gauze pads, after previous iontophoresis of pilocarpine. Ammonia and urea concentrations were determined in the sweat and in the plasma. It was found that elevated plasma ammonia concentration in healthy subjects after ingestion of ammonium chloride as well in the cirrhotic patients resulted in an increase of ammonia concentration in the sweat. High plasma and sweat urea concentration in the uraemic subjects did not affect the concentration of ammonia in the sweat. It was concluded that plasma ammonia was the principal source of ammonia in the sweat.

Administration, Oral↗
PubMed2003

Evaluation of ammonia metabolism in the skeletal muscles of patients with cirrhosis using N-13 ammonia PET.

OBJECTIVE: Skeletal muscle is said to compensate for the decreased ammonia metabolism in patients with cirrhosis. Branched-chain amino acids (BCAA) are being used as a treatment for hyperammonemia, and are believed to decrease blood ammonia by consumption of BCAA in skeletal muscles. We examined ammonia metabolism of the skeletal muscles in patients with liver cirrhosis after administration of BCAA using 13N-ammonia positron emission tomography (PET). METHODS: The subjects were patients with compensated or decompensated liver cirrhosis. PET studies were performed before and 2 hours after injection of BCAA. Serial dynamic PET scans (2 min x 10 frames) were started simultaneously with 13N-ammonia injection. The standardized uptake value (SUV) of both thighs was calculated. RESULTS: In the patient with compensated liver cirrhosis, there was little difference in the rate of increase in SUV before to after administration of BCAA. However, in the patient with decompensated liver cirrhosis, the rate of increase in SUV after administration was higher than that before administration of BCAA. CONCLUSION: Ammonia metabolism in the muscle of patients with liver cirrhosis could be examined noninvasively under physiological conditions using 13N-ammonia PET. The muscles were found to metabolize ammonia partially, and the role of this contribution to metabolism of ammonia in patients with decompensated liver cirrhosis is particularly important.

Aged↗
PubMed1995

Prenatal exposure of rats to ammonia impairs NMDA receptor function and affords delayed protection against ammonia toxicity and glutamate neurotoxicity.

The aim of this work was to assess whether perinatal hyperammonemia impairs the function of NMDA receptors and whether this impairment affords protection against acute ammonia toxicity and glutamate and NMDA neurotoxicity. Rats were exposed to ammonia during the prenatal and lactation periods by feeding the female rats an ammonium-containing diet since day 1 of pregnancy. After weaning (at postnatal day 21), the pups were fed a normal diet with no ammonia added. This treatment resulted in a marked decrease of the growth rate of the animals, which was maintained even 1 month after normalization of ammonia levels. Rats exposed to ammonia were more resistant than controls to acute ammonia toxicity 13 days after feeding a normal diet but not at 3 months. Primary cultures of cerebellar neurons from hyperammonemic rats showed decreased binding of [3H]MK-801 and were remarkably more resistant than controls to glutamate and NMDA toxicities. Also, the increase in aspartate aminotransferase activity induced by low concentrations of NMDA was not produced in such cultures. These results indicate that exposure to ammonia during the prenatal and lactation periods results in long-lasting impairment of NMDA receptor function. This would be the reason for the delayed protection afforded by exposure to low ammonia levels against acute ammonia toxicity in animals and against glutamate and NMDA toxicity in neuronal cultures.

Aging↗
PubMed1981

Purification and properties of adenylyl sulphate:ammonia adenylyltransferase from Chlorella catalysing the formation of adenosine 5' -phosphoramidate from adenosine 5' -phosphosulphate and ammonia.

Extracts of Chlorella pyrenoidosa, Euglena gracilis var. bacillaris, spinach, barley, Dictyostelium discoideum and Escherichia coli form an unknown compound enzymically from adenosine 5'-phosphosulphate in the presence of ammonia. This unknown compound shares the following properties with adenosine 5'-phosphoramidate: molar proportions of constituent parts (1 adenine:1 ribose:1 phosphate:1 ammonia released at low pH), co-electrophoresis in all buffers tested including borate, formation of AMP at low pH through release of ammonia, mass and i.r. spectra and conversion into 5'-AMP by phosphodiesterase. This unknown compound therefore appears to be identical with adenosine 5'-phosphoramidate. The enzyme that catalyses the formation of adenosine 5'-phosphoramidate from ammonia and adenosine 5'-phosphosulphate was purified 1800-fold (to homogeneity) from Chlorella by using (NH(4))(2)SO(4) precipitation and DEAE-cellulose, Sephadex and Reactive Blue 2-agarose chromatography. The purified enzyme shows one band of protein, coincident with activity, at a position corresponding to 60000-65000 molecular weight, on polyacrylamide-gel electrophoresis, and yields three subunits on sodium dodecyl sulphate/polyacrylamide-gel electrophoresis of 26000, 21000 and 17000 molecular weight, consistent with a molecular weight of 64000 for the native enzyme. Isoelectrofocusing yields one band of pI4.2. The pH optimum of the enzyme-catalysed reaction is 8.8. ATP, ADP or adenosine 3'-phosphate 5'-phosphosulphate will not replace adenosine 5'-phosphosulphate, and the apparent K(m) for the last-mentioned compound is 0.82mm. The apparent K(m) for ammonia (assuming NH(3) to be the active species) is about 10mm. A large variety of primary, secondary and tertiary amines or amides will not replace ammonia. One mol.prop. of adenosine 5'-phosphosulphate reacts with 1 mol.prop. of ammonia to yield 1 mol.prop. each of adenosine 5'-phosphoramidate and sulphate; no AMP is found. The highly purified enzyme does not catalyse any of the known reactions of adenosine 5'-phosphosulphate, including those catalysed by ATP sulphurylase, adenosine 5'-phosphosulphate kinase, adenosine 5'-phosphosulphate sulphotransferase or ADP sulphurylase. Adenosine 5'-phosphoramidate is found in old samples of the ammonium salt of adenosine 5'-phosphosulphate and can be formed non-enzymically if adenosine 5'-phosphosulphate and ammonia are boiled. In the non-enzymic reaction both adenosine 5'-phosphoramidate and AMP are formed. Thus the enzyme forms adenosine 5'-phosphoramidate by selectively speeding up an already favoured reaction.

Adenosine Monophosphate↗
PubMed1999

Effect of lactitol on blood ammonia response to oral glutamine challenge in cirrhotic patients: evidence for an effect of nonabsorbable disaccharides on small intestine ammonia generation.

OBJECTIVE: Nonabsorbable disaccharides are widely used to decrease blood ammonia concentration. Their principal mode of action is the modification of pH and bacterial flora in the colon. The aim of the present study was to test the hypothesis that these drugs may also reduce small intestine ammonia generation. METHODS: Eight male cirrhotics without overt hepatic encephalopathy received 20 g of glutamine in 100 ml of water. Venous samples for whole blood ammonia were taken before, 30 and 60 min after the load. Immediately after the last blood sample the patients were submitted to the following psychometric tests: number connection test, Posner's attention test, and Sternberg paradigm. After the first glutamine load, patients were started on lactitol (initial dose 20 g, three times a day). Once two bowel movements/day were obtained and maintained for at least 5 days, oral glutamine challenge and psychometric tests were repeated. RESULTS: Ammonia increased significantly after the glutamine load (from 83 +/- 13 to 164 +/- 30 microg/dl at 30 min and 210 +/- 29 microg/dl at 60 min; mean +/- SE; p = 0.006 analysis of variance) but not after glutamine load after lactitol treatment (from 77 +/- 17 to 111 +/- 21 microg/dl and 142 +/- 24 microg/dl; p = not significant). The peak increment (127 +/- 24 vs 65 +/- 18 microg/dl; p = 0.008) of ammonia elevation was significantly smaller during lactitol administration. The patients' psychometric performance after the glutamine load did not differ significantly after lactitol treatment. CONCLUSIONS: Lactitol reduces the elevation in blood ammonia that follows oral glutamine challenge. Because enterally administered glutamine is efficiently absorbed in the jejunum and, in part, metabolized to ammonia we suggest that lactitol affects small intestine ammonia generation probably by shortening the residence time of intestinal contents.

Administration, Oral↗
PubMed2002

Combined effect of oxygen and ammonia on the kinetics of ammonia elimination and oxygen consumption of adherent rat liver cells.

Oxygen is essential for the survival of isolated liver cells and its concentration is known to affect their viability and function. Recent reports have also shown that ammonia is eliminated at a rate depending on its concentration and that high ammonia concentrations may be cytotoxic to rat liver cells. Nonetheless, little quantitative information on the effect of either metabolite on liver cell reaction kinetics is available although important to the design of bioreactors for bioartificial livers (BALs). In this investigation, we characterized the dependence of the rate of oxygen consumption (OCR), ammonia elimination (AER) and urea synthesis (USR) on ammonia concentration at physiological (i.e., 43 and 72 mmHg) and supra-physiological (i.e., 134 mmHg) dissolved oxygen tensions. To this purpose, isolated rat liver cells were cultured in adhesion on collagen in a continuous-flow bioreactor optimised for the kinetic characterisation of liver cell metabolic reactions. Rates of the investigated reactions generally increased with increasing ammonia concentrations. OCR and USR significantly increased with increasing dissolved oxygen tensions, particularly at high ammonia concentrations. The actual dissolved oxygen tension significantly influenced also OCR and USR dependence on ammonia concentration. The best-fit rate equations were used to show that, at the beginning of the treatment with a bioreactor packed with primary liver cells, high ammonia concentration in the blood may cause large hypoxic zones in the bioreactor as a result of its effect on OCR. This suggests that plasma (or blood) detoxification prior to entering the bioreactor might enhance BAL efficacy by preserving a large fraction of the available cell activity for longer times.

Ammonia↗
PubMed1976

[Studies on the adsorption removal of ammonia gas. 1) Adsorption of ammonia gas on several kinds of activated carbons (author's transl)].

The present study was designed to secure some fundamental informations on the adsorption removal of ammonia gas by the static method. In order to find out the suitable activated carbons for the adsorption removal of ammonia gas, amounts of ammonia gas adsorbed on twelve kinds of activated carbons were measured at 30 degrees C and up to 70,000 ppm of ammonia gas. The relations between the amounts of ammonia gas adsorbed on the activated carbons and the physical properties of them were discussed through the results of specific surface area, pore volume, mean pore radius, scanning electron micrograph, pH, and amount of base. The results were as follows: 1) Among the twelve kinds of activated carbons, the activated carbons No. 2, No. 3, and No. 6 adsorbed larger amount of ammonia gas than the others. 2) Adsorption of ammonia gas on the activated carbons seemed to be mainly physical as judged from the values of heat of adsorption. 3) The adsorption capacity of the used activated carbons can be recovered to the original capacity by some treatment. 4) The period to reach adsorption equilibrium was about 5 minutes. 5) It may be concluded that adsorption of ammonia gas on the activated carbons was decided mainly by the surface properties (pH and amount of base) of the activated carbons rather than their porous structures.

Adsorption↗
PubMed1991

Neurotoxicity of ammonia and fatty acids: differential inhibition of mitochondrial dehydrogenases by ammonia and fatty acyl coenzyme A derivatives.

In several metabolic encephalopathies, hyperammonemia and organic acidemia are consistently found. Ammonia and fatty acids (FAs) are neurotoxic: previous workers have shown that ammonia and FAs can act singly, in combination, or synergistically, in inducing coma in experimental animals. However, the biochemical mechanisms underlying the neurotoxicity of ammonia and FAs have not been fully elucidated. FAs are normally converted to their corresponding CoA derivatives (CoAs) once they enter cells and it is known that these fatty acyl CoAs can alter intermediary metabolism. The present study was initiated to determine the effects of ammonia and fatty acyl CoAs on brain mitochondrial dehydrogenases. At a pathophysiological level (2 mM), ammonia is a potent inhibitor of brain mitochondrial alpha-ketoglutarate dehydrogenase complex (KGDHC). Only at toxicological levels (10-20 mM) does ammonia inhibit brain mitochondrial NAD(+)- and NADP(+)- linked isocitrate dehydrogenase (NAD-ICDH, NADP-ICDH), and NAD(+)-linked malate dehydrogenase (MDH) and liver mitochondrial NAD-ICDH. Butyryl- (BCoA), octanoyl- (OCoA), and palmitoyl (PCoA) CoA were potent inhibitors of brain mitochondrial KGDHC, with IC50 values of 11, 20, and 25 microM, respectively; moreover, the inhibitory effect of fatty acyl CoAs and ammonia were additive. At levels of 250 microM or higher, both OCoA (IC50 = 1.15 mM) and PCoA (IC50 = 470 microM) inhibit brain mitochondrial NADP-ICDH; only at higher levels (0.5-1 mM) does BCoA inhibit this enzyme (by 30-45%). Much less sensitive than KGDHC and NADP-ICDH, brain mitochondrial NAD-ICDH is only inhibited by 1 mM BCoA, OCoA, and PCoA by 22%, 35%, and 44%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acyl Coenzyme A↗
PubMed2001

Diversity of ammonia monooxygenase operon in autotrophic ammonia-oxidizing bacteria.

Autotrophic ammonia-oxidizing bacteria use the essential enzyme ammonia monooxygenase (AMO) to transform ammonia to hydroxylamine. The amo operon consists of at least three genes, amoC, amoA, and amoB; amoA encodes the subunit containing the putative enzyme active site. The use of the amo genes as functional markers for ammonia-oxidizing bacteria in environmental applications requires knowledge of the diversity of the amo operon on several levels: (1) the copy number of the operon in the genome, (2) the arrangement of the three genes in an individual operon, and (3) the primary sequence of the individual genes. We present a database of amo gene sequences for pure cultures of ammonia-oxidizing bacteria representing both the beta- and the gamma-subdivision of Proteobacteria in the following genera: Nitrosospira (6 strains), Nitrosomonas (5 strains) and Nitrosococcus (2 strains). The amo operon was found in multiple (2-3) nearly identical copies in the beta-subdivision representatives but in single copies in the gamma-subdivision ammonia oxidizers. The analysis of the deduced amino acid sequence revealed strong conservation for all three Amo peptides in both primary and secondary structures. For the amoA gene within the beta-subdivision, nucleotide identity values are approximately 85% within the Nitrosomonas or the Nitrosospira groups, but approximately 75% when comparing between these groups. Conserved regions in amoA and amoC were identified and used as primer sites for PCR amplification of amo genes from pure cultures, enrichments and the soil environment. The intergenic region between amoC and amoA is variable in length and may be used to profile the community of ammonia-oxidizing bacteria in environmental samples. Electronic supplementary material to this paper can be obtained by using the Springer LINK server located at http://dx.doi.org/10.1007/s00203-001-0369-z.

Amino Acid Sequence↗