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T3D0157 - Ammonia

Record Information
Version 1.0
Creation Date 2009-03-06 18:58:11 UTC
Update Date 2013-04-25 08:33:04 UTC
Accession Number T3D0157
Identification
Common Name Ammonia
Description Ammonia is a gas that occurs naturally in nature (produced by bacteria) and may also be synthetically manufactured. It is an important source of nitrogen, which is needed by plants and animals, thus it often serves as a precursor to foodstuffs and fertilizers. It may also be applied directly to some crops. Ammonia is a building block for the synthesis of many pharmaceuticals, and is also used in commercial cleaning products. (S307, S308)
Compound Type
  • Organic Compound
  • Industrial Precursor/Intermediate
  • Fertilizer
Chemical Structure
Thumb
MOL SDF SMILES InChI
Synonyms
  1. Ammonia anhydrous
  2. Ammonia gas
  3. Ammonia inhalant
  4. Ammonia solution
  5. Ammonia solution, strong [usan]
  6. Ammonia water
  7. Ammonia, anhydrous
  8. Ammoniac [french]
  9. Ammoniaca [italian]
  10. Ammoniacum gummi
  11. Ammoniak kconzentrierter
  12. Ammoniak [german]
  13. Ammoniakgas
  14. Amoniak [polish]
  15. Anhydrous ammonia
  16. Aromatic ammonia, vaporole
  17. Azane
  18. Liquid ammonia
  19. Nitro-sil
  20. Primaeres amin
  21. Sekundaeres amin
  22. Spirit of hartshorn
  23. Tertiaeres amin
Chemical Formula H3N
Average Molecular Weight 17.0305
Monoisotopic Molecular Weight 17.026549101
Chemical IUPAC Name
ammonia
CAS Registry Number 7664-41-7
SMILES
N
InChI Identifier
InChI=1S/H3N/h1H3
InChI Key InChIKey=QGZKDVFQNNGYKY-UHFFFAOYSA-N
Chemical Taxonomy
Kingdom Inorganic Compounds
Super Class Homogeneous Non-metal Compounds
Class Other Non-metal Organides
Sub Class Other Non-metal Hydrides
Direct Parent Other Non-metal Hydrides
Alternative Parents Not Available
Molecular Framework Acyclic Compounds
Substituents Not Available
External Descriptors
  • a small molecule(Cyc)
  • mononuclear parent hydride(ChEBI)
  • azane(ChEBI)
DrugBank ID Not Available
PubChem Compound ID 222 Link_out
KEGG ID C00014 Link_out
UniProt ID Not Available
OMIM ID 102770 124450 138130 138290 139260 179800 180297 182128 201450 207800 207900 212138 215700 222700 232600 235800 237300 237310 238700 238970 245349 258870 261600 266150 309000 311250 312170 600346 601003 602268 603859 604618 605381 605899 606673 606762 607079 608158 608285 608307 608310 608490 609060 609457 610021 610505 611261 611470 611719 Link_out
ChEBI ID 16134 Link_out
BioCyc ID AMMONIA Link_out
CTD ID D000641 Link_out
Stitch ID Ammonia Link_out
PDB ID Not Available
ACToR ID 6151
Wikipedia Link http://en.wikipedia.org/wiki/Ammonia Link_out
Physical Properties
Appearance Colorless gas.
Melting Point -77.7 C
Solubility 482 mg/mL at 24 °C [DEAN,JA (1985)]
Predicted LogP -0.9779999999999999
Toxicity Profile
Route of Exposure Oral (S307) ; inhalation (S307) ; dermal (S307)
Mechanism of Action The topical damage caused by ammonia is probably due mainly to its alkaline properties. Its high water solubility allows it to dissolve in moisture on the mucous membranes, skin, and eyes, forming ammonium hydroxide. Ammonium hydroxide causes saponification of cell membrane lipids, resulting in cell disruption and death. Additionally, it extracts water from the cells and initiates an inflammatory response, which further damages the surrounding tissues. Excess circulating levels of ammonia (hyperammonemia) can cause serious neurological effects. This is thought to involve the alteration of glutamate metabolism in the brain and resultant increased activation of NMDA receptors, which causes decreased protein kinase C-mediated phosphorylation of Na+/K+ ATPase, increased activity of Na+/K+ ATPase, and depletion of ATP. Ammonia can chemically interact with an internal thiolester bond of complement 3 (C3). This causes a conformation change in C3, which activates the alternative complement pathway, causing the release of chemoattractants and the assembly of the membrane attack complex of complement. The altered C3 can also bind directly to phagocyte complement receptors, which causes the release of toxic oxygen species. (S307)
Metabolism Ammonia can be absorbed by inhalation and oral routes exposure, and also to a much lesser extent through the skin and eyes. Most of the inhaled ammonia is retained in the upper respiratory tract and is subsequently eliminated in expired air, while ingested ammonia is 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. Ammonia is mainly excreted in the urine. (S307)
Toxicity Values LD50: 350 mg/kg (Oral, Rat) (S309) LC50: 3360 mg/m3 over 1 hour (Inhalation, Mouse) (S309)
Lethal Dose 2500 to 4500 ppm over 30 minutes for an adult human. (S307)
Carcinogenicity (IARC Classification) Not Available
Uses/Sources Ammonia is used directly on farm crops, and is also a precursor to foodstuffs and fertilizers. It is also found in many household and industrial cleaners. (S307)
Minimum Risk Level Acute Inhalation: 1.7 ppm (R260) Chronic Inhalation: 0.1 ppm (R260)
Health Effects 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 mouth, throat, and stomach. Splashing ammonia into eyes can cause burns and even blindness. (S307)
Symptoms Exposure to high levels of ammonia can cause irritation and burning at the site of exposure. (S307)
Treatment Not Available
References
General References
  • S307 — ATSDR - Agency for Toxic Substances and Disease Registry (2004). Toxicological profile for ammonia. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
  • S308 — Wikipedia. Ammonia. Last Updated 28 June 2009. [Link]
  • S309 — Environment Canada (1981). Tech Info for Problem Spills: Ammonia (Draft).
  • R260 — ATSDR - Agency for Toxic Substances and Disease Registry (2001). Minimal Risk Levels (MRLs) for Hazardous Substances. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
  • S310 — Lemberg A, Fernandez MA: Hepatic encephalopathy, ammonia, glutamate, glutamine and oxidative stress. Ann Hepatol. 2009 Apr-Jun;8(2):95-102. [19502650 Link_out]

Targets

1. Complement C3

C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind covalently, via its reactive thioester, to cell surface carbohydrates or immune aggregates. Derived from proteolytic degradation of complement C3, C3a anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes. Acylation stimulating protein (ASP): adipogenic hormone that stimulates triglyceride (TG) synthesis and glucose transport in adipocytes, regulating fat storage and playing a role in postprandial TG clearance. Appears to stimulate TG synthesis via activation of the PLC, MAPK and AKT signaling pathways. Ligand for GPR77. Promotes the phosphorylation, ARRB2-mediated internalization and recycling of GPR77.

Ammonia can chemically interact with an internal thiolester bond of complement 3 (C3). This causes a conformation change in C3, which activates the alternative complement pathway, causing the release of chemoattractants and the assembly of the membrane attack complex of complement. The altered C3 can also bind directly to phagocyte complement receptors, which causes the release of toxic oxygen species. (S307)
UniProt ID: P01024 Link_out
Gene: C3 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out
References:
  • S307 — ATSDR - Agency for Toxic Substances and Disease Registry (2004). Toxicological profile for ammonia. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]