You are using an unsupported browser. Please upgrade your browser to a newer version to get the best experience on Toxin, Toxin Target Database.
Record Information
Version2.0
Creation Date2009-03-06 18:58:11 UTC
Update Date2018-03-21 17:46:11 UTC
Accession NumberT3D0157
Identification
Common NameAmmonia
ClassSmall Molecule
DescriptionAmmonia 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 encephalopathy 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 hyperammonemia 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 hyperammonemia 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.
Compound Type
  • Fertilizer
  • Food Toxin
  • Household Toxin
  • Industrial Precursor/Intermediate
  • Industrial/Workplace Toxin
  • Inorganic Compound
  • Lachrymator
  • Metabolite
  • Natural Compound
  • Non-Metal
  • Organic Compound
Chemical Structure
Thumb
Synonyms
Synonym
Ammonia anhydrous
Ammonia water
Anhydrous ammonia
Azane
Liquid ammonia
NH(3)
NH3
Spirit of hartshorn
Chemical FormulaH3N
Average Molecular Mass17.031 g/mol
Monoisotopic Mass17.027 g/mol
CAS Registry Number7664-41-7
IUPAC Nameammonia
Traditional Nameammonia
SMILESN
InChI IdentifierInChI=1S/H3N/h1H3
InChI KeyInChIKey=QGZKDVFQNNGYKY-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
Biological Properties
StatusDetected and Not Quantified
OriginEndogenous
Cellular Locations
  • Cytoplasm
  • Extracellular
Biofluid LocationsNot Available
Tissue Locations
  • All Tissues
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 Not Available
3-Hydroxy-3-Methylglutaryl-CoA Lyase DeficiencySMP00138 Not Available
ArgininemiaSMP00357 Not Available
Argininosuccinic AciduriaSMP00003 Not Available
Beta-Ketothiolase DeficiencySMP00173 Not Available
Biotinidase DeficiencySMP00174 Not Available
Carbamoyl Phosphate Synthetase DeficiencySMP00002 Not Available
Carnitine-acylcarnitine translocase deficiencySMP00517 Not Available
Citrullinemia Type ISMP00001 Not Available
Hyperinsulinism-Hyperammonemia SyndromeSMP00339 Not Available
Hyperornithinemia-hyperammonemia-homocitrullinuria [HHH-syndrome]SMP00506 Not Available
Isovaleric AciduriaSMP00238 Not Available
Lysinuric Protein IntoleranceSMP00197 Not Available
Malonic AciduriaSMP00198 Not Available
Methylmalonic AciduriaSMP00200 Not Available
Methylmalonic Aciduria Due to Cobalamin-Related DisordersSMP00201 Not Available
Propionic AcidemiaSMP00236 Not Available
Pyruvate Carboxylase DeficiencySMP00350 Not Available
Short Chain Acyl CoA Dehydrogenase Deficiency (SCAD Deficiency)SMP00235 Not Available
Applications
Biological Roles
Chemical Roles
Physical Properties
StateLiquid
AppearanceColorless gas.
Experimental Properties
PropertyValue
Melting Point-77.7°C
Boiling PointNot Available
Solubility482 mg/mL at 24°C [DEAN,JA (1985)]
LogPNot Available
Predicted Properties
PropertyValueSource
logP-0.98ChemAxon
pKa (Strongest Basic)8.86ChemAxon
Physiological Charge1ChemAxon
Hydrogen Acceptor Count1ChemAxon
Hydrogen Donor Count1ChemAxon
Polar Surface Area13.59 Å2ChemAxon
Rotatable Bond Count0ChemAxon
Refractivity15.51 m3·mol-1ChemAxon
Polarizability1.99 Å3ChemAxon
Number of Rings0ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Spectra
Spectrum TypeDescriptionSplash Key
Predicted GC-MSPredicted GC-MS Spectrum - GC-MSsplash10-014i-9000000000-92ab2d6b6fd9cfb23ac7View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-014i-9000000000-88ae09421d46f7dea1c5View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-014i-9000000000-88ae09421d46f7dea1c5View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-014i-9000000000-88ae09421d46f7dea1c5View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Negativesplash10-014i-9000000000-5e750288766bc8c562ffView in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Negativesplash10-014i-9000000000-5e750288766bc8c562ffView in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Negativesplash10-014i-9000000000-5e750288766bc8c562ffView in MoNA
MSMass Spectrum (Electron Ionization)splash10-014i-9000000000-e0a6e51ead158714099bView in MoNA
Toxicity Profile
Route of ExposureOral (30) ; inhalation (30) ; dermal (30)
Mechanism of ToxicityThe 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. (30)
MetabolismAmmonia 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. (30)
Toxicity ValuesLD50: 350 mg/kg (Oral, Rat) (2) LC50: 3360 mg/m3 over 1 hour (Inhalation, Mouse) (2) Severe hyperammonemia is characterized by serum ammonia levels greater than 1000 μmol/L
Lethal Dose2500 to 4500 ppm over 30 minutes for an adult human. (30)
Carcinogenicity (IARC Classification)No indication of carcinogenicity to humans (not listed by IARC).
Uses/SourcesAmmonia 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. (30)
Minimum Risk LevelAcute Inhalation: 1.7 ppm (29) Chronic Inhalation: 0.1 ppm (29)
Health EffectsAcute 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. (30) Chronically high levels of ammonia in the blood are associated with nearly 20 different inborn errors of metabolism including: 3-Hydroxy-3-Methylglutaryl-CoA Lyase Deficiency, 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). Hyperammonemia is one of the metabolic derangements that contribute to hepatic encephalopathy.
SymptomsAcute exposure leads to irritation and burning at the site of exposure. (30) Symptoms include cough, chest pain (severe), chest tightness, difficulty breathing and wheezing, tearing and burning of eyes, temporary blindness, throat pain (severe), mouth pain, lip swelling, heart and blood, rapid, weak pulse, collapse and shock. Chronic exposure: Symptoms of hyperammonia include: lethargy, irritability, poor feeding, vomiting and seizures. Signs and symptoms of late-onset hyperammonemia (later in life) may include intermittent ataxia, intellectual impairment, failure to thrive, gait abnormality, behavior disturbances, epilepsy, recurrent Reye syndrome and protein avoidance.
TreatmentAcute Exposure: EYES: irrigate opened eyes for several minutes under running water. INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice. SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention. INHALATION: supply fresh air. If required provide artificial respiration. Chronic Exposure: Intravenous arginine (argininosuccinase deficiency), sodium phenylbutyrate and sodium benzoate (ornithine transcarbamoylase deficiency) are pharmacologic agents commonly used as adjunctive therapy to treat hyperammonemia in patients.
Normal Concentrations
Not Available
Abnormal Concentrations
Not Available
DrugBank IDNot Available
HMDB IDHMDB00051
PubChem Compound ID222
ChEMBL IDCHEMBL1160819
ChemSpider ID217
KEGG IDC00014
UniProt IDNot Available
OMIM ID102770 , 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
ChEBI ID16134
BioCyc IDAMMONIA
CTD IDD000641
Stitch IDAmmonia
PDB IDNH3
ACToR ID6151
Wikipedia LinkAmmonia
References
Synthesis ReferenceMohr, Rudolf. Ammonia separation from offgas obtained from melamine synthesis. U.S. (1971), 5 pp. CODEN: USXXAM US 3555784 19710119 CAN 77:50902 AN 1972:450902
MSDSLink
General References
  1. Lemberg A, Fernandez MA: Hepatic encephalopathy, ammonia, glutamate, glutamine and oxidative stress. Ann Hepatol. 2009 Apr-Jun;8(2):95-102. [19502650 ]
  2. Azzi A, Boscoboinik D, Clement S, Marilley D, Ozer NK, Ricciarelli R, Tasinato A: Alpha-tocopherol as a modulator of smooth muscle cell proliferation. Prostaglandins Leukot Essent Fatty Acids. 1997 Oct;57(4-5):507-14. [9430404 ]
  3. Albrecht J, Norenberg MD: Glutamine: a Trojan horse in ammonia neurotoxicity. Hepatology. 2006 Oct;44(4):788-94. [17006913 ]
  4. 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. [16167195 ]
  5. Norenberg MD, Rama Rao KV, Jayakumar AR: Ammonia neurotoxicity and the mitochondrial permeability transition. J Bioenerg Biomembr. 2004 Aug;36(4):303-7. [15377862 ]
  6. 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. [15369278 ]
  7. Seiler N: Ammonia and Alzheimer's disease. Neurochem Int. 2002 Aug-Sep;41(2-3):189-207. [12020619 ]
  8. Yoshida Y, Higashi T, Nouso K, Nakatsukasa H, Nakamura SI, Watanabe A, Tsuji T: Effects of zinc deficiency/zinc supplementation on ammonia metabolism in patients with decompensated liver cirrhosis. Acta Med Okayama. 2001 Dec;55(6):349-55. [11779097 ]
  9. Huizenga JR, Teelken AW, Tangerman A, de Jager AE, Gips CH, Jansen PL: Determination of ammonia in cerebrospinal fluid using the indophenol direct method. Mol Chem Neuropathol. 1998 Jun-Aug;34(2-3):169-77. [10327416 ]
  10. Cohen BI: The significance of ammonia/gamma-aminobutyric acid (GABA) ratio for normality and liver disorders. Med Hypotheses. 2002 Dec;59(6):757-8. [12445521 ]
  11. Kochar DK, Agarwal P, Kochar SK, Jain R, Rawat N, Pokharna RK, Kachhawa S, Srivastava T: Hepatocyte dysfunction and hepatic encephalopathy in Plasmodium falciparum malaria. QJM. 2003 Jul;96(7):505-12. [12881593 ]
  12. Zupke C, Sinskey AJ, Stephanopoulos G: Intracellular flux analysis applied to the effect of dissolved oxygen on hybridomas. Appl Microbiol Biotechnol. 1995 Dec;44(1-2):27-36. [8579834 ]
  13. Cooper AJ: Role of glutamine in cerebral nitrogen metabolism and ammonia neurotoxicity. Ment Retard Dev Disabil Res Rev. 2001;7(4):280-6. [11754523 ]
  14. Remer T: Influence of nutrition on acid-base balance--metabolic aspects. Eur J Nutr. 2001 Oct;40(5):214-20. [11842946 ]
  15. Kaiho T, Tanaka T, Tsuchiya S, Yanagisawa S, Takeuchi O, Miura M, Saigusa N, Miyazaki M: Effect of the herbal medicine Dai-kenchu-to for serum ammonia in hepatectomized patients. Hepatogastroenterology. 2005 Jan-Feb;52(61):161-5. [15783019 ]
  16. Nybo L, Dalsgaard MK, Steensberg A, Moller K, Secher NH: Cerebral ammonia uptake and accumulation during prolonged exercise in humans. J Physiol. 2005 Feb 15;563(Pt 1):285-90. Epub 2004 Dec 20. [15611036 ]
  17. Huizenga JR, Vissink A, Kuipers EJ, Gips CH: Helicobacter pylori and ammonia concentrations of whole, parotid and submandibular/sublingual saliva. Clin Oral Investig. 1999 Jun;3(2):84-7. [10803116 ]
  18. Satoh M, Yokoya S, Hachiya Y, Hachiya M, Fujisawa T, Hoshino K, Saji T: Two hyperandrogenic adolescent girls with congenital portosystemic shunt. Eur J Pediatr. 2001 May;160(5):307-11. [11388600 ]
  19. Suarez I, Bodega G, Fernandez B: Glutamine synthetase in brain: effect of ammonia. Neurochem Int. 2002 Aug-Sep;41(2-3):123-42. [12020613 ]
  20. Helewski K, Kowalczyk-Ziomek G, Konecki J: [Ammonia and GABA-ergic neurotransmission in pathogenesis of hepatic encephalopathy]. Wiad Lek. 2003;56(11-12):560-3. [15058165 ]
  21. Grasten SM, Juntunen KS, Poutanen KS, Gylling HK, Miettinen TA, Mykkanen HM: Rye bread improves bowel function and decreases the concentrations of some compounds that are putative colon cancer risk markers in middle-aged women and men. J Nutr. 2000 Sep;130(9):2215-21. [10958815 ]
  22. Pita AM, Wakabayashi Y, Fernandez-Bustos MA, Virgili N, Riudor E, Soler J, Farriol M: Plasma urea-cycle-related amino acids, ammonium levels, and urinary orotic acid excretion in short-bowel patients managed with an oral diet. Clin Nutr. 2003 Feb;22(1):93-8. [12553956 ]
  23. Geier M, Bosch OJ, Boeckh J: Ammonia as an attractive component of host odour for the yellow fever mosquito, Aedes aegypti. Chem Senses. 1999 Dec;24(6):647-53. [10587497 ]
  24. Iwata H, Ueda Y: Pharmacokinetic considerations in development of a bioartificial liver. Clin Pharmacokinet. 2004;43(4):211-25. [15005636 ]
  25. Ohmoto K, Miyake I, Tsuduki M, Ohno S, Yamamoto S: Control of solitary gastric fundal varices and portosystemic encephalopathy accompanying liver cirrhosis by balloon-occluded retrograde transvenous obliteration (B-RTO): a case report. Hepatogastroenterology. 1999 Mar-Apr;46(26):1249-52. [10370701 ]
  26. Verrotti A, Greco R, Morgese G, Chiarelli F: Carnitine deficiency and hyperammonemia in children receiving valproic acid with and without other anticonvulsant drugs. Int J Clin Lab Res. 1999;29(1):36-40. [10356662 ]
  27. Hussein HS, Flickinger EA, Fahey GC Jr: Petfood applications of inulin and oligofructose. J Nutr. 1999 Jul;129(7 Suppl):1454S-6S. [10395620 ]
  28. Environment Canada (1981). Tech Info for Problem Spills: Ammonia (Draft).
  29. 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]
  30. 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]
  31. Wikipedia. Ammonia. Last Updated 28 June 2009. [Link]
Gene Regulation
Up-Regulated Genes
GeneGene SymbolGene IDInteractionChromosomeDetails
Down-Regulated Genes
GeneGene SymbolGene IDInteractionChromosomeDetails

Targets

General Function:
Receptor binding
Specific Function:
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. In chronic inflammation, acts as a chemoattractant for neutrophils (By similarity). It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.C3-beta-c: Acts as a chemoattractant for neutrophils in chronic inflammation.Acylation stimulating protein: 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 C5AR2. Promotes the phosphorylation, ARRB2-mediated internalization and recycling of C5AR2 (PubMed:8376604, PubMed:2909530, PubMed:9059512, PubMed:10432298, PubMed:15833747, PubMed:16333141, PubMed:19615750).
Gene Name:
C3
Uniprot ID:
P01024
Molecular Weight:
187146.73 Da
References
  1. 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]
General Function:
Temperature-gated cation channel activity
Specific Function:
Receptor-activated non-selective cation channel involved in detection of pain and possibly also in cold perception and inner ear function (PubMed:25389312, PubMed:25855297). Has a central role in the pain response to endogenous inflammatory mediators and to a diverse array of volatile irritants, such as mustard oil, cinnamaldehyde, garlic and acrolein, an irritant from tears gas and vehicule exhaust fumes (PubMed:25389312, PubMed:20547126). Is also activated by menthol (in vitro)(PubMed:25389312). Acts also as a ionotropic cannabinoid receptor by being activated by delta(9)-tetrahydrocannabinol (THC), the psychoactive component of marijuana (PubMed:25389312). May be a component for the mechanosensitive transduction channel of hair cells in inner ear, thereby participating in the perception of sounds. Probably operated by a phosphatidylinositol second messenger system (By similarity).
Gene Name:
TRPA1
Uniprot ID:
O75762
Molecular Weight:
127499.88 Da
References
  1. Nilius B, Prenen J, Owsianik G: Irritating channels: the case of TRPA1. J Physiol. 2011 Apr 1;589(Pt 7):1543-9. doi: 10.1113/jphysiol.2010.200717. Epub 2010 Nov 15. [21078588 ]