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Record Information
Version2.0
Creation Date2010-04-14 00:54:38 UTC
Update Date2014-12-24 20:26:19 UTC
Accession NumberT3D3668
Identification
Common NameDeoxynivalenol
ClassSmall Molecule
DescriptionDeoxynivalenol is found in cereals and cereal products. Deoxynivalenol is produced by Fusarium graminearum and Fusarium roseum, responsible for headblight in cereals Vomitoxin, also known as deoxynivalenol (DON), is a type B trichothecene, an epoxy-sesquiterpeneoid. This mycotoxin occurs predominantly in grains such as wheat, barley, oats, rye, and maize, and less often in rice, sorghum, and triticale. The occurrence of deoxynivalenol is associated primarily with Fusarium graminearum (Gibberella zeae) and F. culmorum, both of which are important plant pathogens which cause Fusarium head blight in wheat and Gibberella ear rot in maize. Deoxynivalenol is a direct relationship between the incidence of Fusarium head blight and contamination of wheat with deoxynivalenol has been established. The incidence of Fusarium head blight is strongly associated with moisture at the time of flowering (anthesis), and the timing of rainfall, rather than the amount, is the most critical factor. Furthermore, deoxynivalenol contents are significantly affected by the susceptibility of cultivars towards Fusarium species, previous crop, tillage practices, and fungicide use Deoxynivalenol belongs to the family of Trichothecenes. These are sesquiterpene mycotoxins structurally characterized by the presence of an epoxide ring and a benzoyran derivative with a variant number of hydroxyl, acetly, or other substituents [1]. (Reference: [1] http://www.inchem.org/documents/ehc/ehc/ehc105.htm).
Compound Type
  • Ester
  • Ether
  • Food Toxin
  • Fungal Toxin
  • Lachrymator
  • Metabolite
  • Mycotoxin
  • Natural Compound
  • Organic Compound
  • Pesticide
Chemical Structure
Thumb
Synonyms
Synonym
Rd toxin
Vomitoxin
Chemical FormulaC15H20O6
Average Molecular Mass296.316 g/mol
Monoisotopic Mass296.126 g/mol
CAS Registry Number51481-10-8
IUPAC Name3',10'-dihydroxy-2'-(hydroxymethyl)-1',5'-dimethyl-8'-oxaspiro[oxirane-2,12'-tricyclo[7.2.1.0²,⁷]dodecan]-5'-en-4'-one
Traditional Name3',10'-dihydroxy-2'-(hydroxymethyl)-1',5'-dimethyl-8'-oxaspiro[oxirane-2,12'-tricyclo[7.2.1.0²,⁷]dodecan]-5'-en-4'-one
SMILESCC1=CC2OC3C(O)CC(C)(C33CO3)C2(CO)C(O)C1=O
InChI IdentifierInChI=1/C15H20O6/c1-7-3-9-14(5-16,11(19)10(7)18)13(2)4-8(17)12(21-9)15(13)6-20-15/h3,8-9,11-12,16-17,19H,4-6H2,1-2H3
InChI KeyInChIKey=LINOMUASTDIRTM-UHFFFAOYNA-N
Chemical Taxonomy
Description belongs to the class of organic compounds known as trichothecenes. These are sesquiterpene mycotoxins structurally characterized by the presence of an epoxide ring and a benzopyran derivative with a variant number of hydroxyl, acetyl, or other substituents. The most important structural features causing the biological activities of trichothecenes are the 12,13-epoxy ring, the presence of hydroxyl or acetyl groups at appropriate positions on the trichothecene nucleus and the structure and position of the side-chain.
KingdomOrganic compounds
Super ClassLipids and lipid-like molecules
ClassPrenol lipids
Sub ClassSesquiterpenoids
Direct ParentTrichothecenes
Alternative Parents
Substituents
  • Trichothecene skeleton
  • Cyclohexenone
  • Oxepane
  • Oxane
  • Cyclic alcohol
  • Ketone
  • Secondary alcohol
  • Cyclic ketone
  • Dialkyl ether
  • Oxirane
  • Ether
  • Oxacycle
  • Organoheterocyclic compound
  • Organic oxide
  • Carbonyl group
  • Organooxygen compound
  • Hydrocarbon derivative
  • Organic oxygen compound
  • Primary alcohol
  • Alcohol
  • Aliphatic heteropolycyclic compound
Molecular FrameworkAliphatic heteropolycyclic compounds
External DescriptorsNot Available
Biological Properties
StatusDetected and Not Quantified
OriginExogenous
Cellular Locations
  • Cytoplasm
  • Extracellular
Biofluid LocationsNot Available
Tissue LocationsNot Available
PathwaysNot Available
ApplicationsNot Available
Biological RolesNot Available
Chemical RolesNot Available
Physical Properties
StateSolid
AppearanceWhite crystalline solid.
Experimental Properties
PropertyValue
Melting Point151 - 153°C
Boiling PointNot Available
SolubilityNot Available
LogPNot Available
Predicted Properties
PropertyValueSource
Water Solubility36.0 mg/mLALOGPS
logP-0.76ALOGPS
logP-0.97ChemAxon
logS-0.92ALOGPS
pKa (Strongest Acidic)12.68ChemAxon
pKa (Strongest Basic)-2.8ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count6ChemAxon
Hydrogen Donor Count3ChemAxon
Polar Surface Area99.52 Å2ChemAxon
Rotatable Bond Count1ChemAxon
Refractivity71.62 m3·mol-1ChemAxon
Polarizability29.3 Å3ChemAxon
Number of Rings4ChemAxon
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-9280000000-119212ca3f60c571bf83View in MoNA
Predicted GC-MSPredicted GC-MS Spectrum - GC-MS (3 TMS)splash10-03ka-6472900000-c31690653d6bee33225fView in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-004j-0090000000-34421174a0594b953987View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-01tc-0690000000-788fb9e234c649fd8b59View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-03fr-3690000000-6371a33a18e6e72609a8View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Negativesplash10-0002-0090000000-ed5069f39fe0effbb249View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Negativesplash10-016s-0390000000-23b417561faf609d9da0View in MoNA
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Negativesplash10-000e-5900000000-9f78eae3599b3edc1e36View in MoNA
Toxicity Profile
Route of ExposureOral, dermal, inhalation, and parenteral (contaminated drugs). (5)
Mechanism of ToxicityUnlike many other mycotoxins, trichothecenes do not require metabolic activation to exert their biological activity, instead directly reacting with cellular components. Trichothecenes are cytotoxic to most eukaryotic cells due to their powerful ability to inhibit protein synthesis. They do this by freely moving across the plasma membrane and binding specifically to ribosomes with high-affinity. Specifically, they interfere with the active site of peptidyl transferase at the 3'-end of large 28S ribosomal RNA and inhibit the initiation, elongation or termination step of protein synthesis, as well as cause polyribosomal disaggregation. Protein synthesis is an essential function in all tissues, but tissues where cells are actively and rapidly growing and dividing are very susceptible to the toxins. Additionally, binding to ribosomes is thought to activate proteins in downstream signalling events related to immune response and apoptosis, such as mitogen-activated protein kinases. This is known as ribotoxic stress response. Trichothecenes may also induce some alterations in membrane structure, leading to increased lipid peroxidation and inhibition of electron transport activity in the mitochondria. They can further induce apoptosis through generation of reactive oxygen species. Further secondary effects of trichothecenes include inhibition of RNA and DNA synthesis, and also inhibition of mitosis. (15, 16, 1, 2, 3, 4)
MetabolismTrichothecenes are lipophilic and thus easily absorbed through the skin, gut, and pulmonary mucosa. They are metabolized mainly by cytochrome P-450 and trichothecene-specific carboxylesterase activity in the liver, although other tissues such as the kidney, spleen, and intestine also show some metabolic activity. Trichothecenes are metabolically transformed to less toxic metabolites by such reactions as hydrolysis, hydroxylation, de-epoxidation, and glucuronidation. Deoxynivalenol is metabolized mainly to the de-epoxy metabolite. Metabolites are excreted in the urine and feces. (14, 16, 6)
Toxicity ValuesLD50: 70 mg/kg (Intraperitoneal, Mouse) (11) LD50: 46 mg/kg (Oral, Mouse) (12) LD50: 43 mg/kg (Subcutaneous, Mouse) (16)
Lethal DoseNot Available
Carcinogenicity (IARC Classification)3, not classifiable as to its carcinogenicity to humans. (18)
Uses/SourcesVomitoxin, also known as deoxynivalenol (DON), is a type B trichothecene, an epoxy-sesquiterpeneoid. Trichothecenes are a very large family of chemically related mycotoxins produced by various species of Fusarium, Myrothecium, Trichoderma, Trichothecium, Cephalosporium, Verticimonosporium, and Stachybotrys. Vomitoxin occurs predominantly in grains such as wheat, barley, oats, rye, and maize, and less often in rice, sorghum, and triticale. The occurrence of deoxynivalenol is associated primarily with Fusarium graminearum (Gibberella zeae) and F. culmorum, both of which are important plant pathogens which cause Fusarium head blight in wheat and Gibberella ear rot in maize. (15, 17)
Minimum Risk LevelNot Available
Health EffectsTrichothecenes have multiorgan effects including anoerxia and weight loss, growth retardation, nervous disorders, cardiovascular alterations, immunodepression, hemostatic derangements, skin toxicity, decreased reproductive capacity, bone marrow damage, and alimentary toxic aleukia. (15, 16, 3)
SymptomsAfter direct dermal application or oral ingestion, the trichothecene mycotoxins can cause rapid irritation to the skin or intestinal mucosa, including skin irritation, burning and itching, rash or blisters, and bleeding. Eye contact can cause tearing, eye pain, conjunctivitis, burning sensations about the eyes, and blurred vision for up to 1 week. Symptoms also include nausea, vomiting, fatigue, dyspnea, and acute vascular effects leading to hypotension and shock. (15, 16)
TreatmentThere are no known antidotes to trichothecene mycotoxins. Treatments are directed at supporting hemopoietic abnormalities, gastrointestinal damage, and skin damage. Administer charcoal as a slurry in case of acute oral exposure. In case of inhalation: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of eye exposure, Irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. In case of dermal exposure, Remove contaminated clothing and wash exposed area thoroughly with soap and water. (7)
Normal Concentrations
Not Available
Abnormal Concentrations
Not Available
DrugBank IDNot Available
HMDB IDHMDB36156
PubChem Compound ID430147
ChEMBL IDNot Available
ChemSpider ID380420
KEGG IDC09747
UniProt IDNot Available
OMIM ID
ChEBI IDNot Available
BioCyc IDNot Available
CTD IDNot Available
Stitch IDNot Available
PDB IDNot Available
ACToR IDNot Available
Wikipedia LinkDeoxynivalenol
References
Synthesis ReferenceNot Available
MSDST3D3668.pdf
General References
  1. Pestka JJ: Mechanisms of deoxynivalenol-induced gene expression and apoptosis. Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2008 Sep;25(9):1128-40. [19238623 ]
  2. Nusuetrong P, Pengsuparp T, Meksuriyen D, Tanitsu M, Kikuchi H, Mizugaki M, Shimazu K, Oshima Y, Nakahata N, Yoshida M: Satratoxin H generates reactive oxygen species and lipid peroxides in PC12 cells. Biol Pharm Bull. 2008 Jun;31(6):1115-20. [18520041 ]
  3. Rocha O, Ansari K, Doohan FM: Effects of trichothecene mycotoxins on eukaryotic cells: a review. Food Addit Contam. 2005 Apr;22(4):369-78. [16019807 ]
  4. Bae HK, Pestka JJ: Deoxynivalenol induces p38 interaction with the ribosome in monocytes and macrophages. Toxicol Sci. 2008 Sep;105(1):59-66. doi: 10.1093/toxsci/kfn102. Epub 2008 May 22. [18502741 ]
  5. Peraica M, Domijan AM: Contamination of food with mycotoxins and human health. Arh Hig Rada Toksikol. 2001 Mar;52(1):23-35. [11370295 ]
  6. Wang SJ: Caffeine facilitation of glutamate release from rat cerebral cortex nerve terminals (synaptosomes) through activation protein kinase C pathway: an interaction with presynaptic adenosine A1 receptors. Synapse. 2007 Jun;61(6):401-11. [17372967 ]
  7. Grond S, Sablotzki A: Clinical pharmacology of tramadol. Clin Pharmacokinet. 2004;43(13):879-923. [15509185 ]
  8. Rumack BH POISINDEX(R) Information System Micromedex, Inc., Englewood, CO, 2010; CCIS Volume 143, edition expires Feb, 2010. Hall AH & Rumack BH (Eds): TOMES(R) Information System Micromedex, Inc., Englewood, CO, 2010; CCIS Volume 143, edition expires Feb, 2010.
  9. IPCS. INCHEM. Deoxynivalenol
  10. Langford RE; Introduction to Weapons of Mass Destruction p.182 (2004)
  11. O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 1789
  12. Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 3392
  13. Yannai, Shmuel. (2004) Dictionary of food compounds with CD-ROM: Additives, flavors, and ingredients. Boca Raton: Chapman & Hall/CRC.
  14. WHO; Environ Health Criteria 105: Selected Mycotoxins: Ochratoxins, Trichothecenes, Ergot (1990). [Link]
  15. Wikipedia. Trichothecene. Last Updated 30 March 2010. [Link]
  16. Wannemacher, R.W. JR., and Wiener, S.L. (1997). Chapter 34: Trichothecene Mycotoxins. In R. Zajtchuk (Ed.), Medical Aspects of Chemical and Biological Warfare. Maryland: Office of The Surgeon General. [Link]
  17. Wikipedia. Vomitoxin. Last Updated 20 January 2010. [Link]
  18. International Agency for Research on Cancer (2014). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. [Link]
Gene Regulation
Up-Regulated GenesNot Available
Down-Regulated GenesNot Available

Targets

General Function:
Structural constituent of ribosome
Specific Function:
Not Available
Gene Name:
MRPS5
Uniprot ID:
P82675
Molecular Weight:
48006.135 Da
References
  1. Pestka JJ: Mechanisms of deoxynivalenol-induced gene expression and apoptosis. Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2008 Sep;25(9):1128-40. [19238623 ]
  2. Bae HK, Pestka JJ: Deoxynivalenol induces p38 interaction with the ribosome in monocytes and macrophages. Toxicol Sci. 2008 Sep;105(1):59-66. doi: 10.1093/toxsci/kfn102. Epub 2008 May 22. [18502741 ]
  3. Wannemacher, R.W. JR., and Wiener, S.L. (1997). Chapter 34: Trichothecene Mycotoxins. In R. Zajtchuk (Ed.), Medical Aspects of Chemical and Biological Warfare. Maryland: Office of The Surgeon General. [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 ]