Record Information
Version1.0
Creation date2010-04-08 22:06:00 UTC
Update date2020-09-17 15:42:23 UTC
Primary IDFDB003908
Secondary Accession NumbersNot Available
Chemical Information
FooDB NameAmmonia
DescriptionAmmonia, also known as NH3 or amoniaco, belongs to the class of inorganic compounds known as homogeneous other non-metal compounds. These are inorganic non-metallic compounds in which the largest atom belongs to the class of 'other non-metals'. Ammonia is a colourless alkaline gas and is one of the most abundant nitrogen-containing compounds in the atmosphere. It is an irritant with a characteristic pungent odor that 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. Small amounts of ammonia are naturally formed in nearly all tissues and organs of the vertebrate organism. Ammonia is both a neurotoxin and a metabotoxin. In fact, it is the most common endogenous neurotoxin. A neurotoxin is a compound that causes damage to neural tissue and neural cells. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Ammonia is recognized to be central in the pathogenesis of a brain condition known as hepatic encephalopathy, which arises from various liver diseases and leads to a build-up ammonia in the blood (hyperammonemia). More than 40% of people with cirrhosis develop hepatic encephalopathy. Part of the neurotoxicity of ammonia arises from the fact that it easily crosses the blood-brain barrier and is absorbed and metabolized by the astrocytes, a population of cells in the brain that constitutes 30% of the cerebral cortex. Astrocytes use ammonia when synthesizing glutamine from glutamate. The increased levels of glutamine lead to an increase in osmotic pressure in the astrocytes, which become swollen. There is increased activity of the inhibitory gamma-aminobutyric acid (GABA) system, and the energy supply to other brain cells is decreased. This can be thought of as an example of brain edema. The source of the ammonia leading to hepatic encaphlopahy is not entirely clear. The gut produces ammonia, which is metabolized in the liver, and almost all organ systems are involved in ammonia metabolism. Colonic bacteria produce ammonia by splitting urea and other amino acids, however this does not fully explain hyperammonemia and hepatic encephalopathy. The alternative explanation is that hyperammonemia is the result of intestinal breakdown of amino acids, especially glutamine. The intestines have significant glutaminase activity, predominantly located in the enterocytes. On the other hand, intestinal tissues only have a little glutamine synthetase activity, making it a major glutamine-consuming organ. In addition to the intestine, the kidney is an important source of blood ammonia in patients with liver disease. Ammonia is also taken up by the muscle and brain in hepatic coma, and there is confirmation that ammonia is metabolized in muscle. Excessive formation of ammonia in the brains of Alzheimer's disease patients has also been demonstrated, and it has been shown that some Alzheimer's disease patients exhibit elevated blood ammonia concentrations. Ammonia is the most important natural modulator of lysosomal protein processing. Indeed, there is strong evidence for the involvement of aberrant lysosomal processing of beta-amyloid precursor protein (beta-APP) in the formation of amyloid deposits. Inflammatory processes and activation of microglia are widely believed to be implicated in the pathology of Alzheimer's disease. Ammonia is able to affect the characteristic functions of microglia, such as endocytosis, and cytokine production. Based on these facts, an ammonia-based hypothesis for Alzheimer's disease has been suggested (PMID: 17006913, 16167195, 15377862, 15369278). Chronically high levels of ammonia in the blood are associated with nearly twenty different inborn errors of metabolism including: 3-hydroxy-3-methylglutaryl-CoA lyase deficiency, 3-methyl-crotonylglycinuria, argininemia, argininosuccinic aciduria, beta-ketothiolase deficiency, biotinidase deficiency, carbamoyl phosphate synthetase deficiency, carnitine-acylcarnitine translocase deficiency, citrullinemia type I, hyperinsulinism-hyperammonemia syndrome, hyperornithinemia-hyperammonemia-homocitrullinuria syndrome, isovaleric aciduria, lysinuric protein intolerance, malonic aciduria, methylmalonic aciduria, methylmalonic aciduria due to cobalamin-related disorders, propionic acidemia, pyruvate carboxylase deficiency, and short chain acyl CoA dehydrogenase deficiency (SCAD deficiency). Many of these inborn errors of metabolism are associated with urea cycle disorders or impairment to amino acid metabolism. High levels of ammonia in the blood (hyperammonemia) lead to the activation of NMDA receptors in the brain. This results in the depletion of brain ATP, which in turn leads to release of glutamate. Ammonia also leads to the impairment of mitochondrial function and calcium homeostasis, thereby decreasing ATP synthesis. Excess ammonia also increases the formation of nitric oxide (NO), which in turn reduces the activity of glutamine synthetase, and thereby decreases the elimination of ammonia in the brain (PMID: 12020609). As a neurotoxin, ammonia predominantly affects astrocytes. Disturbed mitochondrial function and oxidative stress, factors implicated in the induction of the mitochondrial permeability transition, appear to be involved in the mechanism of ammonia neurotoxicity. Ammonia can also affect the glutamatergic and GABAergic neuronal systems, the two prevailing neuronal systems of the cortical structures. All of these effects can lead to irreversible brain damage, coma, and/or death. Infants with urea cycle disorders and hyperammonia initially exhibit vomiting and increasing lethargy. If untreated, seizures, hypotonia (poor muscle tone, floppiness), respiratory distress (respiratory alkalosis), and coma can occur. Adults with urea cycle disorders and hyperammonia will exhibit episodes of disorientation, confusion, slurred speech, unusual and extreme combativeness or agitation, stroke-like symptoms, lethargy, and delirium. Ammonia also has toxic effects when an individual is exposed to ammonia solutions. Acute exposure to high levels of ammonia in air may be irritating to skin, eyes, throat, and lungs and cause coughing and burns. Lung damage and death may occur after exposure to very high concentrations of ammonia. Swallowing concentrated solutions of ammonia can cause burns in the mouth, throat, and stomach. Splashing ammonia into eyes can cause burns and even blindness.
CAS Number7664-41-7
Structure
Thumb
Synonyms
SynonymSource
[NH3]ChEBI
Am-folHMDB
Ammonia (CONC 20% or greater)HMDB
Ammonia anhydrousHMDB
Ammonia gasHMDB
Ammonia inhalantHMDB
Ammonia solutionHMDB
Ammonia solution strongHMDB
Ammonia solution strong (NF)HMDB
Ammonia water (jp15)HMDB
AmmoniacChEBI
Ammoniacum gummiHMDB
AmmoniakChEBI
Ammoniak kconzentrierterHMDB
AmmoniakgasHMDB
Ammonium ionHMDB
AmoniacoChEBI
Anhydrous ammoniamanual
Aromatic ammonia vaporoleHMDB
AzaneHMDB
Liquid ammoniaHMDB
NH(3)HMDB
NH3manual
Nitro-silHMDB
Primaeres aminHMDB
R-717ChEBI
Sekundaeres aminHMDB
Spirit OF hartshornChEBI
Tertiaeres aminHMDB
Predicted PropertiesNot Available
Chemical FormulaH3N
IUPAC name
InChI IdentifierInChI=1S/H3N/h1H3
InChI KeyQGZKDVFQNNGYKY-UHFFFAOYSA-N
Isomeric SMILESN
Average Molecular Weight17.0305
Monoisotopic Molecular Weight17.026549101
Classification
ClassificationNot classified
Ontology
Physiological effect

Health effect:

Disposition

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Process

Naturally occurring process:

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Indirect biological role:

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Physico-Chemical Properties - Experimental
Physico-Chemical Properties - Experimental
PropertyValueReference
Physical stateLiquid
Physical DescriptionNot Available
Mass CompositionNot Available
Melting Point-77.7 oC
Boiling PointNot Available
Experimental Water Solubility482 mg/mL at 24 oCDEAN,JA (1985)
Experimental logPNot Available
Experimental pKa9.25
Isoelectric pointNot Available
ChargeNot Available
Optical RotationNot Available
Spectroscopic UV DataNot Available
DensityNot Available
Refractive IndexNot Available
Spectra
Spectra
EI-MS/GC-MSNot Available
MS/MSNot Available
NMRNot Available
ChemSpider ID217
ChEMBL IDCHEMBL1160819
KEGG Compound IDC00014
Pubchem Compound ID222
Pubchem Substance IDNot Available
ChEBI ID16134
Phenol-Explorer IDNot Available
DrugBank IDNot Available
HMDB IDHMDB00051
CRC / DFC (Dictionary of Food Compounds) IDNot Available
EAFUS IDNot Available
Dr. Duke IDAMMONIA|NH3
BIGG IDNot Available
KNApSAcK IDC00007267
HET IDNH3
Food Biomarker OntologyNot Available
VMH IDNot Available
Flavornet IDNot Available
GoodScent IDrw1097731
SuperScent IDNot Available
Wikipedia IDAmmonia
Phenol-Explorer Metabolite IDNot Available
Duplicate IDSNot Available
Old DFC IDSNot Available
Associated Foods
FoodContent Range AverageReference
FoodReference
Biological Effects and Interactions
Health Effects / Bioactivities
DescriptorIDDefinitionReference
neurotoxic50910 A poison that interferes with the functions of the nervous system.CHEBI
Enzymes
NameGene NameUniProt ID
Adenosine deaminaseADAP00813
BiotinidaseBTDP43251
Aminomethyltransferase, mitochondrialAMTP48728
Glycine cleavage system H protein, mitochondrialGCSHP23434
Kynurenine--oxoglutarate transaminase 3CCBL2Q6YP21
Selenocysteine lyaseSCLYQ96I15
5-phosphohydroxy-L-lysine phospho-lyaseAGXT2L2Q8IUZ5
Fatty-acid amide hydrolase 1FAAHO00519
Fatty-acid amide hydrolase 2FAAH2Q6GMR7
Isoaspartyl peptidase/L-asparaginaseASRGL1Q7L266
60 kDa lysophospholipaseASPGQ86U10
Histidine ammonia-lyaseHALP42357
Cystathionine gamma-lyaseCTHP32929
L-serine dehydratase/L-threonine deaminaseSDSP20132
Serine dehydratase-likeSDSLQ96GA7
Kynurenine--oxoglutarate transaminase 1CCBL1Q16773
Carbamoyl-phosphate synthase [ammonia], mitochondrialCPS1P31327
AMP deaminase 3AMPD3Q01432
AMP deaminase 2AMPD2Q01433
AMP deaminase 1AMPD1P23109
Glutamine synthetaseGLULP15104
Glutaminase liver isoform, mitochondrialGLS2Q9UI32
GMP reductase 2GMPR2Q9P2T1
Glutaminase kidney isoform, mitochondrialGLSO94925
GMP reductase 1GMPRP36959
Formimidoyltransferase-cyclodeaminaseFTCDO95954
Ammonium transporter Rh type ARHAGQ02094
AIDAIDQ546Y9
Ethanolamine-phosphate phospho-lyaseAGXT2L1Q8TBG4
CTP synthase 2CTPS2Q9NRF8
Serine racemaseSRRQ9GZT4
Glucosamine-6-phosphate isomerase 2GNPDA2Q8TDQ7
DNA dC->dU-editing enzyme APOBEC-3HAPOBEC3HQ6NTF7
Pathways
NameSMPDB LinkKEGG Link
Amino Sugar MetabolismSMP00045 map00520
Ammonia RecyclingSMP00009 map00910
Arginine and Proline MetabolismSMP00020 map00330
D-Arginine and D-Ornithine MetabolismSMP00036 map00472
Folate MetabolismSMP00053 map00670
Glucose-Alanine CycleSMP00127 Not Available
Glutamate MetabolismSMP00072 map00250
Glycine and Serine MetabolismSMP00004 map00260
Homocysteine DegradationSMP00455 Not Available
Phenylalanine and Tyrosine MetabolismSMP00008 map00360
Threonine and 2-Oxobutanoate DegradationSMP00452 Not Available
Urea CycleSMP00059 map00330
MetabolismNot Available
BiosynthesisNot Available
Organoleptic Properties
Flavours
FlavorCitations
ammoniacal
  1. The Good Scents Company (2009). Flavor and fragrance information catalog. <http://www.thegoodscentscompany.com/allprod.html> Accessed 15.10.23.
Files
MSDSshow
References
Synthesis ReferenceNot Available
General ReferenceNot Available
Content Reference— Duke, James. 'Dr. Duke's Phytochemical and Ethnobotanical Databases. United States Department of Agriculture.' Agricultural Research Service, Accessed April 27 (2004).