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1. Azane
2. 7664-41-7
3. Ammonia Gas
4. Nitro-sil
5. Spirit Of Hartshorn
6. Ammonia, Anhydrous
7. Ammoniakgas
8. Ammonia Anhydrous
9. Anhydrous Ammonia
10. Ammoniak
11. Am-fol
12. Liquid Ammonia
13. Ammonia Solution
14. Ammoniak Kconzentrierter
15. Amoniak [polish]
16. Ammoniac [french]
17. Ammoniak [german]
18. Ammoniac
19. Ammoniaca [italian]
20. Caswell No. 041
21. Ammonia (conc 20% Or Greater)
22. Refrigerent R717
23. Ccris 2278
24. Hsdb 162
25. Ammonia Solution, Strong
26. Nh3
27. Un 2073 (>44% Solution)
28. Un1005
29. Aminomethyl Polystyrene Resin
30. Epa Pesticide Chemical Code 005302
31. R 717 (ammonia)
32. Strong Ammonia Solution
33. R 717
34. Un 1005 (anhydrous Gas Or >50% Solution)
35. Un 2672 (between 12% And 44% Solution)
36. Ammonia, 7m In Methanol
37. Ammonia Anhydrous, 99.98%
38. Chebi:16134
39. Mfcd00011418
40. 5138q19f1x
41. Ammonia Solution, Strong (nf)
42. Ammonia Solution, Strong [nf]
43. Amoniaco
44. Ammoniaca
45. Amoniak
46. (aminomethyl)polystyrene
47. Einecs 231-635-3
48. Tertiaeres Amin
49. Aminyl Radical
50. Ammonia Ca
51. Primaeres Amin
52. Ammonia Inhalant
53. Ammonia,aromatic
54. Ammonia-solution
55. Ammoniacum Gummi
56. Sekundaeres Amin
57. Unii-5138q19f1x
58. Anyhydrous Ammonia
59. Ammonium Causticum
60. (aminomethyl)polystyrene, 100-200 Mesh, Extent Of Labeling: ~0.5 Mmol/g Amine Loading
61. Nh4
62. Unx
63. Strong-ammonia Solution
64. Ammonia [vandf]
65. Ammonia [inci]
66. Ammonia (8ci,9ci)
67. Ammonia Water (jp15)
68. Aromatic Ammonia Vaporole
69. Ammonia [ii]
70. Ammonia [mi]
71. Ammonia, 2m In Methanol
72. Dowex(r) 66 Free Base
73. Ammonia [who-dd]
74. Ammonia, 0.5m In Thf
75. Aromatic Ammonia, Vaporole
76. Ec 231-635-3
77. Ammonia Solution Strong (nf)
78. Ammonia Solution Strong [usan]
79. Ins No.527
80. N H3
81. Chembl1160819
82. Dtxsid0023872
83. Dtxsid80420101
84. Ins-527
85. [nh3]
86. Dtxsid801029786
87. Nh(3)
88. 2-methylamino-5-nitro-benzonitrile
89. Ammonia Solution, 0.4 M In Thf
90. Ammonia Solution, 4 M In Methanol
91. Ammonia Solution, 7 N In Methanol
92. Ammonia, Anhydrous, >=99.98%
93. Act02989
94. Ammonia Solution 2.0 M In Ethanol
95. Ammonia Solution 2.0 M In Methanol
96. Ammonia Solution, 0.5 M In Dioxane
97. Ammonia Solution, 2.0 M In Ethanol
98. Akos015916403
99. Ammonia Anhydrous 170g Lecture Bottle
100. Ammonia Solution, 2.0 M In Methanol
101. Ammonia Solution 2.0 M In Isopropanol
102. Ammonia 0.5m Solution In 1,4-dioxane
103. Ammonia Solution, 2.0 M In Isopropanol
104. Ammonia (includes Anhydrous Ammonia And Aqueous Ammonia From Water Dissociable Ammonium Salts And Other Sources; 10% Of Total Aqueous Ammonia Is Reportable Under This Listing)
105. Ammonia, Anhydrous, Liquefied Or Ammonia Solutions, Relative Density <0.880 At 15 C In Water, With >50% Ammonia [un1005] [nonflammable Gas]
106. Ammonia, Anhydrous, Liquefied Or Ammonia Solutions, Relative Density <0.880 At 15 C In Water, With >50% Ammonia [un1005] [poison Gas, Corrosive]
107. Ammonia, Puriss., Anhydrous, >=99.9%
108. Ammonia Solution 0.25m In Tetrahydrofuran
109. Ammonia, Puriss., Anhydrous, >=99.95%
110. E-527
111. Q4087
112. R-717
113. C00014
114. D02916
115. Dowex(r) Marathon(tm) Wba Free Base, Free Base
116. Q4832241
117. Q6004010
118. Q27110025
119. (aminomethyl)polystyrene, 100-200 Mesh, Extent Of Labeling: ~2 Mmol/g Amine Loading
120. (aminomethyl)polystyrene, 200-400 Mesh, Extent Of Labeling: ~0.6 Mmol/g Amine Loading
121. (aminomethyl)polystyrene, 200-400 Mesh, Extent Of Labeling: ~1.5 Mmol/g Amine Loading
122. (aminomethyl)polystyrene, 400-500 Mum, Extent Of Labeling: 1-2 Mmol/g Amine Loading
123. (aminomethyl)polystyrene, 100-200 Mesh, Extent Of Labeling: 0.5-1.0 Mmol/g N Loading, 1 % Cross-linked
124. (aminomethyl)polystyrene, 100-200 Mesh, Extent Of Labeling: 1.0 Mmol/g N Loading, 1 % Cross-linked
125. (aminomethyl)polystyrene, 200-400 Mesh, Extent Of Labeling: 1.0-1.5 Mmol/g N Loading, 1 % Cross-linked
126. (aminomethyl)polystyrene, 200-400 Mesh, Extent Of Labeling: 1.0-2.0 Mmol/g Loading, 2 % Cross-linked
127. (aminomethyl)polystyrene, 200-400 Mesh, Extent Of Labeling: 4.0 Mmol/g Loading, 2 % Cross-linked
128. (aminomethyl)polystyrene, 50-100 Mesh, Extent Of Labeling: 2.0 Mmol/g Loading, 1 % Cross-linked
129. (aminomethyl)polystyrene, 70-90 Mesh, Extent Of Labeling: 1.0-1.5 Mmol/g N Loading, 1 % Cross-linked
130. (aminomethyl)polystyrene, 70-90 Mesh, Extent Of Labeling: 1.5-2.0 Mmol/g N Loading, 1 % Cross-linked
131. (aminomethyl)polystyrene, Macroporous, 30-60 Mesh, Extent Of Labeling: 1.5-3.0 Mmol/g Loading
132. (aminomethyl)polystyrene, Macroporous, 70-90 Mesh, Extent Of Labeling: 1.5-3.0 Mmol/g Loading
133. 8007-57-6
134. Ammonia (includes Anhydrous Ammonia And Aqueous Ammonia From Water Dissociable Ammonium Salts And Other Sources 10% Of Total Aqueous Ammonia Is Reportable Under This Listing)
135. Ammonia, Anhydrous, Liquefied Or Ammonia Solutions, Relative Density <0.880 At 15 C In Water, With >50% Ammonia
136. Ammonia, Anhydrous, Liquefied Or Ammonia Solutions, Relative Density <0.880 At 15 C In Water, With >50% Ammonia [un1005] [nonflammable Gas]
137. Ammonia, Anhydrous, Liquefied Or Ammonia Solutions, Relative Density <0.880 At 15 C In Water, With >50% Ammonia [un1005] [poison Gas, Corrosive]
138. Stratospheres(tm) Pl-ams Resin, 100-200 Mesh, Extent Of Labeling: ~1.0 Mmol/g Loading, 1 % Cross-linked With Divinylbenzene
139. Stratospheres(tm) Pl-ams Resin, 100-200 Mesh, Extent Of Labeling: 2.0 Mmol/g Loading, 1 % Cross-linked
140. Stratospheres(tm) Pl-ams Resin, 30-40 Mesh, Extent Of Labeling: 1.0 Mmol/g Loading, 1 % Cross-linked
141. Stratospheres(tm) Pl-ams Resin, 30-40 Mesh, Extent Of Labeling: 2.0 Mmol/g Loading, 1 % Cross-linked
142. Stratospheres(tm) Pl-ams Resin, 50-100 Mesh, Extent Of Labeling: 2.0 Mmol/g Loading, 1 % Cross-linked
| Molecular Weight | 17.031 g/mol |
|---|---|
| Molecular Formula | H3N |
| XLogP3 | -0.7 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 1 |
| Rotatable Bond Count | 0 |
| Exact Mass | 17.026549100 g/mol |
| Monoisotopic Mass | 17.026549100 g/mol |
| Topological Polar Surface Area | 1 Ų |
| Heavy Atom Count | 1 |
| Formal Charge | 0 |
| Complexity | 0 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Reflex respiratory stimulant. /Ammonia water-10%/
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 84
Caution: Irritating to skin and mucous membranes. /Ammonia water-10%/
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 84
- Indicated for use as a smelling salt to treat or prevent fainting. - (when radiolabelled) Indicated for diagnostic PET imaging of the myocardium under rest or pharmacologic stress conditions to evaluate myocardial perfusion in patients with suspected or existing coronary artery disease.
FDA Label
As a gas, ammonia is a natural byproduct and respiratory stimulant. Its renal metabolism plays a role in whole body acid-base balance.
Absorption
Ammonia can be absorbed via oral or inhalation route. Inhales ammonia is temporarily dissolved in the mucus of the upper respiratory tract, however the majority of the gas is released back into the air via expiration. In healthy male subjects under exposure to 500 ppm ammonia for 10-27 minutes, about 70-80% of total inspired ammonia was expired. In extrahepatic tissues such as the intestine, ammonia is incorporated into nontoxic glutamine and released into blood, where it is transported to the liver for ureagenesis.
Route of Elimination
It is mainly excreted through expired air or renal elimination.
Studies suggest that ammonia can be absorbed by the inhalation and oral routes of exposure, but there is less certainty regarding absorption through the skin. Absorption through the eye has been documented. Most of the inhaled ammonia is retained in the upper respiratory tract and is subsequently eliminated in expired air. Almost all of the ammonia produced endogenously in the intestinal tract is absorbed. Exogenous ammonia is also readily absorbed in the intestinal tract. Ammonia that reaches the circulation is widely distributed to all body compartments although substantial first pass metabolism occurs in the liver where it is transformed into urea and glutamine. Ammonia or ammonium ion reaching the tissues is taken up by glutamic acid, which participates in transamination and other reactions. The principal means of excretion of ammonia that reaches the circulation in mammals is as urinary urea; minimal amounts are excreted in the feces and in expired air.
HHS/ATSDR; Toxicological Profile for Ammonia p.78 (September 2004) TP126. Available from, as of May 24, 2016: https://www.atsdr.cdc.gov/toxprofiles/index.asp
Experiments with volunteers show that ammonia, regardless of its tested concentration in air (range, 57-500 ppm), is almost completely retained in the nasal mucosa (83-92%) during short-term exposure, i.e., up to 120 sec. However, longer-term exposure (10-27 min) to a concentration of 500 ppm resulted in lower retention (4-30%), with 350-400 ppm eliminated in expired air by the end of the exposure period, suggesting an adaptive capability or saturation of the absorptive process. Nasal and pharyngeal irritation, but not tracheal irritation, suggests that ammonia is retained in the upper respiratory tract. Unchanged levels of blood-urea-nitrogen (BUN), non-protein nitrogen, urinary-urea, and urinary-ammonia are evidence of low absorption into the blood. Exposure to common occupational limits of ammonia in air (25 ppm) with 30% retention (and assuming this quantity is absorbed into the blood stream) would yield an increase in blood ammonium concentration of 0.09 mg/L. This calculated rise is only 10% above fasting levels.
HHS/ATSDR; Toxicological Profile for Ammonia p.79 (September 2004) TP126. Available from, as of May 24, 2016: https://www.atsdr.cdc.gov/toxprofiles/index.asp
Animal data provide supporting evidence for high-percentage nasal retention, thus protecting the lower respiratory tract from exposure (rabbit, dog). Continuous exposure of rats for 24 hr to concentrations up to 32 ppm resulted in significant increase in blood ammonia levels. Exposures to 310-1,157 ppm led to significantly increased blood concentrations of ammonia within 8 hr of exposure initiation, but blood ammonia returned to pre-exposure values within 12 hr of continuous exposure and remained so over the remaining of the 24 hr exposure period. This suggests an adaptive response mechanism may be activated with longerterm exposure.
HHS/ATSDR; Toxicological Profile for Ammonia p.79 (September 2004) TP126. Available from, as of May 24, 2016: https://www.atsdr.cdc.gov/toxprofiles/index.asp
Absorption data from human inhalation exposure suggest that only small amounts of ammonia are absorbed into the systemic circulation. Initial retention of inhaled ammonia in the mucus of the upper respiratory tract may be 80% or more, but after equilibrium is established (within 30 min) 70-80% of inspired ammonia is expired in exhaled air. The lack of change in blood nitrogen compounds and urinary-ammonia compounds lends further support to a limited absorption into the systemic circulation. Toxic effects reported from inhalation exposure suggest local damage, or changes resulting from necrotic tissue degradation, rather than the presence of elevated levels of NH4+, per se, in tissues other than the respiratory/pharyngeal tissues. Information on the distribution of endogenously-produced ammonia suggests that any NH4+ absorbed through inhalation would be distributed to all body compartments via the blood, where it would be used in protein synthesis or as a buffer, and that excess levels would be reduced to normal by urinary excretion, or converted by the liver to glutamine and urea. If present in quantities that overtax these organs, NH4+ is distributed to other tissues and is known to be detoxified in the brain. /NH4+/
HHS/ATSDR; Toxicological Profile for Ammonia p.81 (September 2004) TP126. Available from, as of May 24, 2016: https://www.atsdr.cdc.gov/toxprofiles/index.asp
For more Absorption, Distribution and Excretion (Complete) data for Ammonia (16 total), please visit the HSDB record page.
Healthy hepatocytes detoxify ammonia where hepatic glutaminase, glutamine synthetase and the urea cycle enzymes act as major enzymes for ammonia metabolism. Ammonia is converted to urea in the liver and other tissues. Glutaminase and glutamine synthetase catalyze the condensation of ammonia with glutamate to glutamine, which is a common nontoxic carrier of ammonia. In case of hepatic dysfunction or impairment, detoxification capacity decreases and may cause severe pathologies from hyperammonemia, such as hepatic encephalopathy.
Human adults produce around 1000 mmol of ammonia daily. Some is reutilized in biosynthesis. The remainder is waste and neurotoxic. Eventually most is excreted in urine as urea, together with ammonia used as a buffer. In extrahepatic tissues, ammonia is incorporated into nontoxic glutamine and released into blood. Large amounts are metabolized by the kidneys and small intestine. In the intestine, this yields ammonia, which is sequestered in portal blood and transported to the liver for ureagenesis, and citrulline, which is converted to arginine by the kidneys. The amazing developments in NMR imaging and spectroscopy and molecular biology have confirmed concepts derived from early studies in animals and cell cultures. The processes involved are exquisitely tuned. When they are faulty, ammonia accumulates. Severe acute hyperammonemia causes a rapidly progressive, often fatal, encephalopathy with brain edema. Chronic milder hyperammonemia causes a neuropsychiatric illness. Survivors of severe neonatal hyperammonemia have structural brain damage. Proposed explanations for brain edema are an increase in astrocyte osmolality, generally attributed to glutamine accumulation, and cytotoxic oxidative/nitrosative damage. However, ammonia neurotoxicity is multifactorial, with disturbances also in neurotransmitters, energy production, anaplerosis, cerebral blood flow, potassium, and sodium. Around 90% of hyperammonemic patients have liver disease. Inherited defects are rare. They are being recognized increasingly in adults. Deficiencies of urea cycle enzymes, citrin, and pyruvate carboxylase demonstrate the roles of isolated pathways in ammonia metabolism. Phenylbutyrate is used routinely to treat inherited urea cycle disorders, and its use for hepatic encephalopathy is under investigation. /Hyperammonemia/
PMID:25735860 Walker V; Adv Clin Chem 67: 73-150 (2014)
The inhibitory effects of ammonia on two different degradation pathways of methanogenic acetate were evaluated using a pure culture (Methanosaeta thermophila strain PT) and defined co-culture (Methanothermobacter thermautotrophicus strain TM and Thermacetogenium phaeum strain PB), which represented aceticlastic and syntrophic methanogenesis, respectively. Growth experiments with high concentrations of ammonia clearly demonstrated that sensitivity to ammonia stress was markedly higher in M. thermophila PT than in the syntrophic co-culture. M. thermophila PT also exhibited higher sensitivity to high pH stress, which indicated that an inability to maintain pH homeostasis is an underlying cause of ammonia inhibition. Methanogenesis was inhibited in the resting cells of M. thermophila PT with moderate concentrations of ammonia, suggesting that the inhibition of enzymes involved in methanogenesis may be one of the major factors responsible for ammonia toxicity. Transcriptomic analysis revealed a broad range of disturbances in M. thermophila PT cells under ammonia stress conditions, including protein denaturation, oxidative stress, and intracellular cation imbalances. The results of the present study clearly demonstrated that syntrophic acetate degradation dominated over aceticlastic methanogenesis under ammonia stress conditions, which is consistent with the findings of previous studies on complex microbial community systems. Our results also imply that the co-existence of multiple metabolic pathways and their different sensitivities to stress factors confer resiliency on methanogenic processes.
PMID:24920170 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4103522 Kato S et al; Microbes Environ 29 (2): 162-7 (2014)
Recently, spatial-temporal/metabolic mathematical models have been established that allow the simulation of metabolic processes in tissues. We applied these models to decipher ammonia detoxification mechanisms in the liver. An integrated metabolic-spatial-temporal model was used to generate hypotheses of ammonia metabolism. Predicted mechanisms were validated using time-resolved analyses of nitrogen metabolism, activity analyses, immunostaining and gene expression after induction of liver damage in mice. Moreover, blood from the portal vein, liver vein and mixed venous blood was analyzed in a time dependent manner. Modeling revealed an underestimation of ammonia consumption after liver damage when only the currently established mechanisms of ammonia detoxification were simulated. By iterative cycles of modeling and experiments, the reductive amidation of alpha-ketoglutarate (alpha-KG) via glutamate dehydrogenase (GDH) was identified as the lacking component. GDH is released from damaged hepatocytes into the blood where it consumes ammonia to generate glutamate, thereby providing systemic protection against hyperammonemia. This mechanism was exploited therapeutically in a mouse model of hyperammonemia by injecting GDH together with optimized doses of cofactors. Intravenous injection of GDH (720 U/kg), alpha-KG (280 mg/kg) and NADPH (180 mg/kg) reduced the elevated blood ammonia concentrations (>200 uM) to levels close to normal within only 15 min. If successfully translated to patients the GDH-based therapy might provide a less aggressive therapeutic alternative for patients with severe hyperammonemia. /Hyperammonemia/
PMID:26639393 Ghallab A et al; J Hepatol 64 (4): 860-71 (2016)
The rodent liver eliminates toxic ammonia. In mammals, three enzymes (or enzyme systems) are involved in this process: glutaminase, glutamine synthetase and the urea cycle enzymes, represented by carbamoyl phosphate synthetase. The distribution of these enzymes for optimal ammonia detoxification was determined by numerical optimization. This in silico approach predicted that the enzymes have to be zonated in order to achieve maximal removal of toxic ammonia and minimal changes in glutamine concentration. Using 13 compartments, representing hepatocytes, the following predictions were generated: glutamine synthetase is active only within a narrow pericentral zone. Glutaminase and carbamoyl phosphate synthetase are located in the periportal zone in a non-homogeneous distribution. This correlates well with the paradoxical observation that in a first step glutamine-bound ammonia is released (by glutaminase) although one of the functions of the liver is detoxification by ammonia fixation. The in silico approach correctly predicted the in vivo enzyme distributions also for non-physiological conditions (e.g. starvation) and during regeneration after tetrachloromethane (CCl4) intoxication. Metabolite concentrations of glutamine, ammonia and urea in each compartment, representing individual hepatocytes, were predicted. Finally, a sensitivity analysis showed a striking robustness of the results. These bioinformatics predictions were validated experimentally by immunohistochemistry and are supported by the literature. In summary, optimization approaches like the one applied can provide valuable explanations and high-quality predictions for in vivo enzyme and metabolite distributions in tissues and can reveal unknown metabolic functions.
PMID:26438405 Bartl M, Arch Toxicol 89 (11): 2069-78 (2015)
For more Metabolism/Metabolites (Complete) data for Ammonia (17 total), please visit the HSDB record page.
In normal rat brain, blood-derived ammonia was rapidly converted to glutamine, indicating very short half-life of less than 3 seconds.
Whole body (following ingestion): 1-2 days; [TDR, p. 88]
TDR - Ryan RP, Terry CE, Leffingwell SS (eds). Toxicology Desk Reference: The Toxic Exposure and Medical Monitoring Index, 5th Ed. Washington DC: Taylor & Francis, 1999., p. 88
... The rate of turnover of blood derived ammonia to glutamine in normal rat brain is extremely rapid (half-life < or = 3 s), but is slowed in the brains of chronically (12-14 wk portacaval shunted) or acutely (urease treated) hyperammonemic rats (half-life < or = 10 s). ...
PMID:2888066 Cooper AJ, Lai JC; Neurochem Pathol 6 (1-2): 67-95 (1987).
Renal excretion and metabolism of ammonia is critical in regulation of acid-base balance by generating bicarbonate ions and promoting renal net acid excretion, both under basal conditions and in response to acid-base disturbances. There is evidence that acute ammonia exposure activates NMDA receptor signalling pathways, and high concentrations of ammonia resulting from urea cycle enzyme deficiencies are associated with changes in astrocyte morphology due to glutamine accumulation, changes in the expression of key astrocyte proteins, and increased concentrations of neuroactive L-tryptophan metabolites.
... Ammonia plays a key role in the pathogenesis of hepatic encephalopathy, which manifests as a neuropsychiatric syndrome accompanying acute and chronic liver failure. One consequence of ammonia action on the brain is astrocyte swelling, which triggers the generation of oxidative/nitrosative stress at the level of NADPH oxidase, nitric oxide synthases and the mitochondria. A self-amplifying signaling loop between oxidative stress and astrocyte swelling has been proposed. Consequences of the ammonia-induced oxidative/nitrosative stress response are protein modifications through nitration of tyrosine residues and oxidation of astrocytic and neuronal RNA. Nitrosative stress also mobilizes zinc from intracellular stores with impact on gene expression. These alterations may at least in part mediate cerebral ammonia toxicity through disturbances of intracellular and intercellular signaling and of synaptic plasticity. Oxidative/nitrosative stress and a low-grade cerebral edema as key events in the pathogenesis of ammonia toxicity and hepatic encephalopathy may offer potential new strategies for treatment. Ammonia-induced oxidation of RNA and proteins may impair postsynaptic protein synthesis, which is critically involved in learning and memory consolidation. RNA oxidation offers a novel explanation for multiple disturbances of neurotransmitter systems and gene expression and the cognitive deficits observed in hepatic encephalopathy.
PMID:19904201 Haussinger D, Gorg B; Curr Opin Clin Nutr Metab Care 13 (1): 87-92 (2010)
SRP: Ammonia in an aqueous environment exists in equilibrium between ionized ammonium cation and the non-ionized ammonia. This equilibrium can be affected by buffers, pH, temperature, and salinity. Thus in many cases it is not possible to assign the associated toxicity to the ionized or non-ionized form of the ammonia-nitrogen. /Aqueous ammonia/
Mechanisms involved in hepatic encephalopathy (HE) still remain poorly understood. It is generally accepted that ammonia plays a major role in this disorder, and that astrocytes represent the principal target of ammonia neurotoxicity. In recent years, studies from several laboratories have uncovered a number of factors and pathways that appear to be critically involved in the pathogenesis of this disorder. Foremost is oxidative and nitrosative stress (ONS), which is largely initiated by an ammonia-induced increase in intracellular Ca(2+). Such increase in Ca(2+) activates a number of enzymes that promote the synthesis of reactive oxygen-nitrogen species, including constitutive nitric oxide synthase, NADPH oxidase and phospholipase A2. ONS subsequently induces the mitochondrial permeability transition, and activates mitogen-activated protein kinases and the transcription factor, nuclear factor-kappaB (NF-kappaB). These factors act to generate additional reactive oxygen-nitrogen species, to phosphorylate various proteins and transcription factors, and to cause mitochondrial dysfunction. This article reviews the role of these factors in the mechanism of HE and ammonia toxicity with a focus on astrocyte swelling and glutamate uptake, which are important consequences of ammonia neurotoxicity....
PMID:19104923 Norenberg MD et al; Metab Brain Dis 24 (1): 103-17 (2009)
A new model for ammonia excretion in freshwater fish and its variable linkage to Na(+) uptake and acid excretion /is proposed/. In this model, /the Rhesus protein/ Rhag facilitates NH(3) flux out of the erythrocyte, Rhbg moves it across the basolateral membrane of the branchial ionocyte, and an apical Na(+)/NH (+)(4) exchange complex consisting of several membrane transporters (Rhcg, V-type H(+)-ATPase, Na(+)/H(+) exchanger NHE-2 and/or NHE-3, Na(+) channel) working together as a metabolon provides an acid trapping mechanism for apical excretion. Intracellular carbonic anhydrase (CA-2) and basolateral Na(+)/HCO (-)(3) cotransporter (NBC-1) and Na(+)/K(+)-ATPase play indirect roles. These mechanisms are normally superimposed on a substantial outward movement of NH(3) by simple diffusion, which is probably dependent on acid trapping in boundary layer water by H(+) ions created by the catalyzed or non-catalyzed hydration of expired metabolic CO2 ...
PMID:19617422 Wright P, Wood C; J Exper Biol 212 (Pt 15): 2303-12 (2009)
For more Mechanism of Action (Complete) data for Ammonia (9 total), please visit the HSDB record page.
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