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.

SourceResearch connectionFrom yearThrough year

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

At least 703 records · Page 39Linked to original sources

PubMed1975

Relationship between ruminal ammonia and nonprotein nitrogen utilization by ruminants. II. Application of published evidence to the development of theoretical model for predicting nonprotein nitrogen utilization.

Results from published experiments dealing with several aspects of nitrogen utilization by ruminants were used to test the concept of zero utilization of nonprotein nitrogen under conditions where more ammonia (greater than 5 mg ammonia nitrogen/100 ml) is in the rumen than can be converted to microbial protein. Results from experiments where the flow of non-ammonia nitrogen to the abomasum of sheep was measured indicate that when urea was the source of supplemental nitrogen, a constant quantity of amino acids reached the abomasum for all rations ranging from 10 to 23% crude protein. From growth studies, addition of nonprotein nitrogen to low protein, high energy rations caused an improved rate of gain. Additions of nonprotein nitrogen to rations resulting in predicted ruminal ammonia concentrations greater than 5 mg ammonia nitrogen/100 ml rumen fluid were without benefit. From lactation studies, nonprotein nitrogen supplementation did not improve milk production if the ration contained more than 12.5% crude protein prior to supplementation or if the predicted ruminal ammonia concentration was greater than 4 mg ammonia nitrogen/100 ml rumen fluid. The importance of the amino acid requirement of the animal as well as the composition of the ration in designing and evaluating nitrogen supplementation studies is discussed.

Ammonia↗

PubMed1987

Concentration of ammonia across cell membranes of mixed rumen bacteria.

When mixed ruminal bacteria were provided with growth rate limiting amounts of mixed carbohydrates, more than 50 mg ammonia/L were required for maximal protein synthesis. Microbial protein synthesis declined when ammonia concentration was less than 50 mg/L and unfermented carbohydrates increased. Ammonia starvation also decreased growth efficiency. Intracellular ammonia increased as a linear function of extracellular ammonia, but the intracellular concentration was always at least 160 mg/L higher than the extracellular concentration. Maximal protein synthesis was not observed until intracellular ammonia was greater than 220 mg/L. The concentration gradient of ammonia across cell membranes ranged from 15-fold to 1.8-fold and indicated that some of the ruminal bacteria may have active transport mechanisms for ammonia. These concentration gradients were, however, far less than those reported for bacteria from other habitats. The ruminal bacteria left more than 12 mg ammonia/L when carbohydrates were still available, and this observation was consistent with the assumption that active ammonium transport was not readily or maximally induced.

Ammonia↗

PubMed2003

Chronic ammonia inhalation and interstitial pulmonary fibrosis: a case report and review of the literature.

Ammonia is an irritant gas with a characteristic pungent odor, which is widely used in industry. Inasmuch as ammonia is highly soluble in water and, upon inhalation, is deposited in the upper airways, occupational exposures to ammonia have commonly been associated with sinusitis, upper airway irritation, and eye irritation. Acute exposures to high levels of ammonia have also been associated with diseases of the lower airways and interstitial lung. In this study, the authors report on a patient with long-term, repetitive occupational exposure to ammonia at levels at or above odor recognition who developed interstitial lung disease. The scientific literature on inhaled ammonia exposure is reviewed and discussed. The authors conclude that the taking of a careful occupational exposure history for patients presenting with shortness of breath associated with ammonia exposure may assist with an early diagnosis, thus allowing for treatment early in the disease process and prevention of further exposure.

Administration, Inhalation↗

PubMed1996

Evaluation of chemical amendments to reduce ammonia volatilization from poultry litter.

Ammonia volatilization from poultry litter often causes high levels of atmospheric ammonia in poultry houses, which is detrimental to both farm workers and birds. Ammonia emissions from houses also aggravate environmental problems, such as acid rain, and result in a loss of fertilizer nitrogen. The objectives of this study were to determine the effect of litter amendments on ammonia volatilization and to determine the effect of these amendments on nitrogen and phosphorus content in litter. The results of this research indicate that alum [Al2(SO4)3.18H2O], ferrous sulfate (FeSO4.7H2O), and phosphoric acid (H3PO4) dramatically reduce ammonia volatilization form litter. The amount of ammonia lost from litter treated with sodium bisulfate (NaHSO4) and a proprietory product made of Ca-Fe silicate with a phosphoric acid coating was not different from the control (untreated litter). Aluminum sulfate (alum) and ferrous sulfate also reduced water soluble P concentrations in litter, whereas phosphoric acid greatly increased water-soluble P levels. The most effective compound evaluated with respect to reducing both ammonia loss and P solubility was alum.

Air Pollution↗

PubMed1976

Ammonia absorption from the rumen to the systemic circulation with urea poisoning in goats.

To confirm the transfer of ammonia leaking from the rumen content via the liver to the perid by laparotomy. When ammonia leakage from the hepatic vein occurred, it was followed by an increase in ammonia concentration in the jugular vein. There were increases of ammonia concentration in the intestinal vein and in the thoracic duct after urea drenching. These increases suggested neither trapping ammonia in the peritoneal fluid nor responsibility for increases of ammonia in the systemic circulation, respectively. At times when respiration ceased due to urea poisoning, the peritoneal fluids wee in the fluid. The hypothesis of the peritoneal cavity-thoracic duct route of ammonia absorption, presented by some of previous workers on urea toxicity, was not supported in the present study.

Ammonia↗

PubMed1992

[Effect of a long-term oral ammonia administration on immunoreactive-somatostatin concentrations of rat stomach].

The effect of a long-term oral ammonia administration on immunoreactive-somatostatin concentrations was investigated in rat stomach. The gastric ir-somatostatin concentrations in the group treated with 0.01% ammonia (pH 9.6) for four weeks were significantly higher than those in both the group treated with 0.1% ammonia (pH 10.4), 0.1 mM-NaOH (pH 9.6), or distilled water (pH 7.0) for four weeks and the group treated with 0.01% ammonia for two weeks. On the contrary, ir-somatostatin levels in the gastric juice and serum tended to decrease with ammonia administration. Further, ammonia administration significantly induced the decrease in mucosal thickness in the pyloric gland area and parietal cell numbers in a dose- and time-dependent manner. From these findings, it was suggested that a long-term oral treatment with 0.01% ammonia, which was clinically estimated as the concentration of the gastric juice in patients with Helicobacter pylori infection, induced not only atrophic changes on gastric mucosa, but the inhibitory effect on somatostatin secretion in rat stomach.

Administration, Oral↗

PubMed2003

[Ammonia and GABA-ergic neurotransmission in pathogenesis of hepatic encephalopathy].

Pathogenesis of hepatic encephalopathy has not been fully revealed and there are many factors which may affect its development. Ammonia and changes in GABA-ergic neurotransmission seem to be the most essential of these factors. Hepatic encephalopathy is frequently, though not always, accompanied by elevated blood ammonia level. Due to the changes in permeability of blood-brain barrier the ammonia level in the brain also increases which results in both stimulating and inhibitory neurotransmission disturbances. Ammonia also affects abnormal interaction of metabolic neurones and astrocytes as well as glutamine-serotonin balance. Another essential factor affecting hepatic encephalopathy development are disturbances in GABA-ergic neurotransmission connected with GABAA receptor complex. When the liver is damaged GABA-ergic neurotransmission increases due to a higher GABA level, natural benzodiazepine receptor agonists as well as neurosteroids synthesised in astrocytes. Many studies point to the fact that ammonia and GABA-ergic neurotransmission disturbances interrelate with each other. There is a concept saying that both these factors cause hepatic encephalopathy. Ammonia may indirectly increase GABA-ergic neurotransmission and also inhibit the function of the central nervous system by synergistic activity with benzodiazepine receptor ligands. So far it is not known whether GABA-ergic neurotransmission is affected by ammonia only or by other factors as well.

Ammonia↗

PubMed2005

[Identification of ammonia oxidation Streptomyces strain A2 and study of its autotrophic ammonium oxidation characteristics].

Streptomyces strain A2 was isolated from a nitrification reactor. According to the characteristics of morphology, cultivation, physiology, (G + C)mol% content, 16S rDNA sequence and DNA-DNA hybridization. it was identified as Streptomyces bikiniensis. Strain A2 could heterotrophically grow on YD medium and could also autotrophically grow on inorganic medium. The heterotrophical growth rate (0.39mg/L.d) was higher than the autotrophical growth rate (0.22mg/L.d). During heterotrophical growth ammonia was mainly assimilated. During autotrophical growth, however, one part of ammonia was assimilated and other part of ammonia was converted into nitrite. When grown on the inorganic medium, the maximum ammonium oxidation rate reached at ammonium concentration of 118mgN/L. The optimal pH for growth and ammonia oxidation was 9.36 and 9.29, respectively. The optimal temperature for growth and ammonia oxidation was 31 degrees C and 40.6 degrees C, respectively. A high concentration of dissolved oxygen was good for growth and ammonia oxidation, and growth was more sensitive to dissolved oxygen change than to ammonia oxidation.

Ammonia↗

PubMed1988

Venous, arterial, and arterialized-venous blood ammonia levels and their relationship to hepatic encephalopathy after propranolol.

To assess side effects of propranolol in the treatment of portal hypertension, we measured blood ammonia in 14 cirrhotics before and after administration of propranolol, and in six cirrhotics before and after placebo. We evaluated ammonia blood levels obtained from three sites: venous, arterial, and arterialized-venous, obtained by warming the forearm. Ammonia concentration of arterial and arterialized-venous blood were abnormal for all cirrhotics studied and significantly greater than the ammonia concentration of venous blood (p less than 0.01). When propranolol was administered to patients with alcoholic cirrhosis and marginal liver function, as reflected by ammonia levels above 60 microM, it caused a significant increase in ammonia levels in arterialized-venous and arterial, but not in venous, blood (p less than 0.05). Propranolol caused a significant increase in the time required to perform sensitive psychometric tests (p less than 0.05). Encephalopathy usually became clinically apparent when the mean of the arterial and arterialized-venous blood ammonia levels rose above 122 microM.

Ammonia↗

PubMed1984

[Concentration of ammonia in the urine of dairy cows given green feed rations and winter feed rations].

The concentration of ammonia in urine at a known level of energy yielding nutrients offered in feed rations was determined in 987 dairy cows in four summer feeding seasons and 1420 cows in three winter feeding seasons. The long-term average ammonia levels in urine showed no significant variation with the two types of feed rations. Different feed rations in the feeding seasons had no significant influence on ammonia concentration in the urine of lactating cows. On a long term-average as well as in the overwhelming majority of the winter and summer feeding seasons, high-pregnant cows had significantly higher ammonia contents in urine than the cows in the first and second lactation stage. At feeding rations complying with Czechoslovak Standard CSN 46 7070 the content of ammonia in the urine of lactating cows was lower than the recorded long-time averages and averages for individual stages; on the other hand, in high-pregnant cows the ammonia level was higher in both types of feed rations and the difference from lactating cows increased 3.25 times. This suggests that neither do the feed rations currently used in practice nor those strictly adhering to the Czechoslovak Standard meet the biological demand of high-pregnant cows and often lead to the injury of hepatal parenchyma. Ammonia concentration of 11.7 to 58.7 mmol per litre of urine is considered as a tolerable limit.

Ammonia↗

PubMed1983

Indocyanine green clearance and ammonia tolerance in partially hepatectomized and hepatic devascularized, anesthetized dogs.

Indocyanine green clearance and ammonia tolerance were measured in anesthetized dogs with 60% hepatectomy, 40% hepatectomy, portacaval shunt, and hepatic artery ligation. With a dose of 0.5 mg of indocyanine green/kg of body weight, plasma clearance of the dye was significantly (P less than 0.001) delayed only in dogs with 60% hepatectomy. Ammonia tolerance was abnormal in dogs in this group, because after they were given a gastric challenge load of an ammonium salt, they had a 5-fold increase in plasma ammonia concentration, compared with a 2.5-fold increase in the control group. Before challenge loading, base-line plasma ammonia concentration was significantly (P less than 0.05) increased within 5 minutes after surgical preparation of the portacaval shunt. After challenge loading the stomach with an ammonium salt, dogs with portacaval shunt had increased plasma ammonia concentration, but the amount was not significantly different from postchallenge-loading values in control dogs. Dogs with 40% hepatectomy and with hepatic artery ligation could not be differentiated from control dogs by indocyanine green clearance or by ammonia tolerance testing. Abnormal tolerance to a challenge gastric load of an ammonium salt or delayed clearance of indocyanine green may indicate marked loss of functional hepatic mass, but normal tolerance or normal dye clearance may not exclude liver disease or dysfunction. Seemingly, base-line plasma ammonia concentration was a sensitive indicator of abnormal portal circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Ammonia↗

PubMed1981

Effects of atmospheric ammonia on young pigs experimentally infected with Bordetella bronchiseptica.

Effects of atmospheric ammonia on performance and respiratory tract health of young pigs experimentally infected with Bordetella bronchiseptica were studied. Treatments were: (1) control, (2) Bordetella inoculation (approx 10(9) bacteria/naris) alone, (3) Bordetella inoculation plus exposure to atmospheric ammonia at 34.7 mg/m3 (50 ppm), and (4) Bordetella inoculation plus exposure to atmospheric ammonia at 69.4 mg/m3 (100 ppm). Pigs weighted 8.01 kg (av) at start of treatment. Body weight and feed disappearance were measured weekly. After 4 weeks, all pigs were killed and examined grossly, and appropriate specimens were obtained for histopathologic examination. Regression models were fitted to growth, feed disappearance, and gain-to-feed data. The growth model indicated that Bordetella-inoculated pigs gained 26% less body weight than did controls, regardless of atmospheric ammonia concentration. Bordetella inoculation, regardless of ammonia exposure, reduced feed disappearance 12% below the control rate. Treatment difference was not noted in gain/feed data. Shrunken turbinates were observed in Bordetella-inoculated pigs. Shrinkage also appeared to be related directly to ammonia concentration. Rhinitis was confirmed histopathologically, and its severity was related with atmospheric ammonia concentration, but no difference was seen in the osseous core of the turbinates.

Air Pollutants↗

PubMed1981

Effects of atmospheric ammonia on young pigs experimentally infected with Ascaris suum.

Effects of atmospheric ammonia at 69.4 mg/m3 (100 ppm) on productive performance and respiratory tract health of young pigs (starting body weight averaged 7.5 kg) experimentally infected with Ascaris suum (50,000 embryonated ova administered by gavage when pigs were 5 weeks of age) were studied in 5 trials of 4 weeks each (when pigs were 5 to 9 weeks of age). Effects of atmospheric-ammonia exposure and ascarid infection on growth were additive. Compared with controls, percentage reductions in average daily gain were 32%, 28%, and 61% for ammonia-exposed, ascarid-infected, and combined ammonia plus ascarid groups, respectively. Ammonia exposure or ascarid infection alone depressed feed disappearance by 18%. Effects of the 2 factors were additive, resulting in a 35% reduction in feed disappearance. Pigs exposed to the combined factors had an average gain/feed ratio of 0.518, which was less than that of control pigs (0.546), but was greater than that of pigs exposed to atmospheric ammonia (0.489) or pigs infected with ascarids (0.501) alone. Liver scarring, due to larval migration, was not affected by ammonia exposure. Larval migration through the respiratory tract was not confirmed histopathologically in pigs killed 4 weeks after inoculation. A supplementary experiment was conducted which demonstrated that residual evidence of previous pulmonary larval migration was present 2 weeks after inoculation.

Air Pollutants↗

PubMed1995

Effect of ammonia on cell-cycle progression of human gastric cancer cells.

AIM: Ammonia is a cytotoxic factor of Helicobacter pylori that is involved in gastric mucosal injury. This study was designed to show whether ammonia has an effect on the cell-cycle progression in human gastric cells in vitro. MATERIALS AND METHODS: We studied the effects of ammonia and ammonium chloride on cell growth and cell-cycle progression of the human gastric cancer cell line HGC-27. We cultured HGC-27 cells and counted viable cells by trypan blue dye exclusion 24 h after the addition of various concentrations of ammonia or ammonium chloride. DNA contents of nuclei were analysed by flow-cytometry. RESULTS: Ammonia and ammonium chloride inhibited the proliferation of HGC-27 cells dose-dependently. Flow-cytometric analysis showed S-phase accumulation of HGC-27 cells treated with ammonia and ammonium chloride at cytostatic doses. CONCLUSIONS: These results suggest that ammonia and ammonium chloride inhibit the growth of gastric cells in S phase. This mechanism may make a significant contribution to the pathogenesis of Helicobacter pylori-associated gastric mucosal atrophy.

Ammonia↗

PubMedDate not supplied

Some metabolic effects of ammonia on astrocytes and neurons in primary cultures.

Some metabolic effects on primary cultures of neurons or astrocytes were studied following acute or chronic exposure to pathophysiological concentrations (usually 3 mM) of ammonia. Three parameters were investigated: (1) 14CO2 production from 14C-labeled substrates [glucose, pyruvate, branched-chain amino acids (leucine, valine, isoleucine), and glutamate]; (2) interconversion between glutamate and glutamine; and (3) incorporation of label from labeled branched-chain amino acids into proteins. Neither acute nor chronic exposure to ammonia had any effect on 14CO2 production from [U-14C]glucose in astrocytes and neurons, whereas under certain conditions 14CO2 production from [1-14C]pyruvate in astrocytes was inhibited by ammonia. Production of 14CO2 from [1-14C]branched-chain amino acids was inhibited by acute, but stimulated by chronic, exposure to ammonia (3 mM) in astrocytes, with less effect in neurons. Production of 14CO2 from [1-14C]glutamate in both astrocytes and neurons was inhibited by acute exposure to ammonia. In astrocytes, glutamate levels tended to decrease and glutamine levels tended to increase following acute exposure to ammonia; in neurons, both glutamine and glutamate levels decreased. Protein content (per culture dish) increased in astrocytes but not in neurons, after chronic exposure to ammonia, possibly as a result of enhanced protein synthesis and/or by inhibition of protein degradation.

Amino Acids↗

PubMed1990

Effects of ammonia on periphytic communities.

Laboratory tests were conducted to evaluate the chronic effects of ammonia on periphytic communities. Species richness of the protozoan component of these communities was affected at un-ionized ammonia concentrations of </= 0.01 mg NH3 litre(-1). A biologically important concentration was defined as the concentration of ammonia affecting 20% of species and was estimated from a concentration-response regression as 0.011 mg litre(-1). A comparable value based on literature reports of chronic toxicity to fish and invertebrates was 0.0126 mg litre(-1). Other non-taxonomic responses were equally sensitive to ammonia. Biomass (ash-free dry weight) and algal biomass (in vivo fluorescence) were significantly reduced even at the lowest tested ammonia treatment, 0.01 mg litre(-1), but the abundance of bacteria was reduced only in the highest treatment group, 0.43 mg litre(-1). Net community metabolism was reduced in all ammonia treatments. Periphyton communities were affected at levels below the USEPA chronic criterion of 0.027 mg litre(-1) (temperature = 8.8 degrees C and pH = 8.1). Successional maturity or age of the periphytic community affected the amount of biomass and algal biomass, but did not modify sensitivity to ammonia.

Journal Article↗

PubMed2000

Evolution of ammonia and urea tolerance in Drosophila melanogaster: resistance and cross-tolerance.

We examined whether populations of Drosophila melanogaster could evolve a genetically based tolerance to high levels of toxic compounds (urea or ammonia) added to their larval food medium. We also examined whether tolerance to one compound may impart cross-tolerance to other compounds. Five populations selected for ammonia tolerance (AX), five populations selected for urea tolerance (UX), and five unselected controls (AUC) were assayed for developmental time, viability, and female fertility. These characteristics were measured on each of the 15 populations reared on one of three larval food conditions (plain banana-molasses, 0.35 M NH(4)Cl, or 0.266 M urea). On urea-supplemented media, the urea-selected populations developed fastest and expressed the highest viability; the ammonia-selected populations developed significantly faster and had a higher viability than the controls. Similarly, on ammonia-supplemented media, the ammonia-selected populations developed fastest and expressed the highest viability; the urea-selected populations developed significantly faster and had a higher viability than the controls. This suggests that a cross-tolerance exists for resisting different toxic compounds. Urea-selected females reared on urea-containing food media displayed superior fecundity, without any observable cross-tolerance effect. When all populations were reared on food containing 0.266 M urea, the urea-selected populations had the lowest levels of urea in their tissues. All populations reared on food containing 0.37 M ammonia or 0.266 M urea, contained more ammonia in their tissues than did populations reared on plain food.

Journal Article↗

PubMed2000

The preferences of laying hens for different concentrations of atmospheric ammonia.

Ammonia gas is one of the most abundant aerial pollutants of modern poultry buildings. The current chronic exposure limit for ammonia of 25 ppm is set for human safety rather than animal welfare. This study assessed the behavioural preferences of laying hens (Gallus gallus domesticus) for different concentrations of ammonia found in commercial poultry houses. Six groups, each of six laying hens, were given the choice of three concentrations of ammonia ( approximately 0, 25 and 45 ppm) in a preference chamber over a period of 6 days and their location and behaviour recorded every 15 min. Hens foraged (p=0.018), preened (p=0.009) and rested (p=0.029) significantly more in fresh air than in the ammonia-polluted environments. There was a significant difference between the responses in 0 and 25 ppm (p<0.05) but not between 25 and 45 ppm (p>0.05). This suggests that ammonia may be aversive to hens with a threshold for this aversion between 0 and 25 ppm. Future studies should explore graded concentrations of ammonia between 0 and 25 ppm in order to suggest a new chronic exposure limit on the basis of animal welfare.

Journal Article↗