Record Information
Version1.0
Created at2020-03-18 23:22:07 UTC
Updated at2020-12-07 19:06:57 UTC
CannabisDB IDCDB006161
Secondary Accession NumbersNot Available
Cannabis Compound Identification
Common 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.
Structure
Thumb
Synonyms
ValueSource
[NH3]ChEBI
AmmoniacChEBI
AmmoniakChEBI
AmoniacoChEBI
NH3ChEBI
R-717ChEBI
Spirit OF hartshornChEBI
Ammonia anhydrousHMDB
Ammonia inhalantHMDB
Ammonia solution strongHMDB
Ammonia waterHMDB
Liquid ammoniaHMDB
Am-folHMDB
Ammonia (CONC 20% or greater)HMDB
Ammonia gasHMDB
Ammonia solutionHMDB
Ammonia solution strong (NF)HMDB
Ammonia water (JP15)HMDB
Ammoniacum gummiHMDB
Ammoniak kconzentrierterHMDB
AmmoniakgasHMDB
Ammonium ionHMDB
Anhydrous ammoniaHMDB
Aromatic ammonia vaporoleHMDB
AzaneHMDB
NH(3)HMDB
Nitro-silHMDB
Primaeres aminHMDB
Sekundaeres aminHMDB
Tertiaeres aminHMDB
Chemical FormulaH3N
Average Molecular Weight17.03
Monoisotopic Molecular Weight17.0265
IUPAC Nameammonia
Traditional Nameammonia
CAS Registry Number15194-15-7
SMILES
N
InChI Identifier
InChI=1S/H3N/h1H3
InChI KeyQGZKDVFQNNGYKY-UHFFFAOYSA-N
Chemical Taxonomy
Description 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'.
KingdomInorganic compounds
Super ClassHomogeneous non-metal compounds
ClassHomogeneous other non-metal compounds
Sub ClassNot Available
Direct ParentHomogeneous other non-metal compounds
Alternative ParentsNot Available
Substituents
  • Homogeneous other non metal
Molecular FrameworkNot Available
External Descriptors
Ontology
Physiological effect

Organoleptic effect:

Health effect:

Disposition

Route of exposure:

Source:

Biological location:

Role

Indirect biological role:

Biological role:

Environmental role:

Industrial application:

Physical Properties
StateSolid
Experimental Properties
PropertyValueReference
Melting Point-77.7 °CNot Available
Boiling Point−33.34 °CWikipedia
Water Solubility482 mg/mL at 24 °CNot Available
logPNot AvailableNot Available
Predicted Properties
PropertyValueSource
logP-0.98ChemAxon
pKa (Strongest Basic)8.86ChemAxon
Physiological Charge1ChemAxon
Hydrogen Acceptor Count1ChemAxon
Hydrogen Donor Count1ChemAxon
Polar Surface Area13.59 ŲChemAxon
Rotatable Bond Count0ChemAxon
Refractivity15.51 m³·mol⁻¹ChemAxon
Polarizability1.99 ųChemAxon
Number of Rings0ChemAxon
BioavailabilityYesChemAxon
Rule of FiveYesChemAxon
Ghose FilterNoChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleNoChemAxon
Spectra
EI-MS/GC-MS
TypeDescriptionSplash KeyView
EI-MSMass Spectrum (Electron Ionization)splash10-014i-9000000000-e0a6e51ead158714099bSpectrum
Predicted GC-MSAmmonia, non-derivatized, Predicted GC-MS Spectrum - 70eV, Positivesplash10-014i-9000000000-92ab2d6b6fd9cfb23ac7Spectrum
MS/MS
TypeDescriptionSplash KeyView
Predicted MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-014i-9000000000-88ae09421d46f7dea1c5Spectrum
Predicted MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-014i-9000000000-88ae09421d46f7dea1c5Spectrum
Predicted MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-014i-9000000000-88ae09421d46f7dea1c5Spectrum
Predicted MS/MSPredicted LC-MS/MS Spectrum - 10V, Negativesplash10-014i-9000000000-5e750288766bc8c562ffSpectrum
Predicted MS/MSPredicted LC-MS/MS Spectrum - 20V, Negativesplash10-014i-9000000000-5e750288766bc8c562ffSpectrum
Predicted MS/MSPredicted LC-MS/MS Spectrum - 40V, Negativesplash10-014i-9000000000-5e750288766bc8c562ffSpectrum
NMR
TypeDescriptionView
Pathways
Pathways
Protein Targets
EnzymesNot Available
TransportersNot Available
Metal BindingsNot Available
ReceptorsNot Available
Transcriptional FactorsNot Available
Concentrations Data
Not Available
HMDB IDHMDB0000051
DrugBank IDDBMET01482
Phenol Explorer Compound IDNot Available
FoodDB IDFDB003908
KNApSAcK IDC00007267
Chemspider ID217
KEGG Compound IDC00014
BioCyc IDAMMONIA
BiGG IDNot Available
Wikipedia LinkAmmonia
METLIN ID3189
PubChem Compound222
PDB IDNot Available
ChEBI ID16134
References
General References
  1. Albrecht J, Norenberg MD: Glutamine: a Trojan horse in ammonia neurotoxicity. Hepatology. 2006 Oct;44(4):788-94. doi: 10.1002/hep.21357. [PubMed:17006913 ]
  2. Shawcross DL, Olde Damink SW, Butterworth RF, Jalan R: Ammonia and hepatic encephalopathy: the more things change, the more they remain the same. Metab Brain Dis. 2005 Sep;20(3):169-79. doi: 10.1007/s11011-005-7205-0. [PubMed:16167195 ]
  3. Norenberg MD, Rama Rao KV, Jayakumar AR: Ammonia neurotoxicity and the mitochondrial permeability transition. J Bioenerg Biomembr. 2004 Aug;36(4):303-7. doi: 10.1023/B:JOBB.0000041758.20071.19. [PubMed:15377862 ]
  4. Brautbar N, Wu MP, Richter ED: Chronic ammonia inhalation and interstitial pulmonary fibrosis: a case report and review of the literature. Arch Environ Health. 2003 Sep;58(9):592-6. doi: 10.3200/AEOH.58.9.592-596. [PubMed:15369278 ]
  5. Monfort P, Kosenko E, Erceg S, Canales JJ, Felipo V: Molecular mechanism of acute ammonia toxicity: role of NMDA receptors. Neurochem Int. 2002 Aug-Sep;41(2-3):95-102. doi: 10.1016/s0197-0186(02)00029-3. [PubMed:12020609 ]