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T3D3671 - Aflatoxin G2
| Record Information | |
|---|---|
| Version | 1.0 |
| Creation Date | 2010-04-15 17:12:34 UTC |
| Update Date | 2013-04-25 08:48:30 UTC |
| Accession Number | T3D3671 |
| Identification | |
| Common Name | Aflatoxin G2 |
| Description | Aflatoxin G2 is a naturally occurring mycotoxin that is produced by Aspergillus parasiticus. Aflatoxins are toxic and probably among the most carcinogenic substances known. They are common and widespread in nature and can colonize and contaminate grain before harvest or during storage. (W819) |
| Compound Type |
|
| Chemical Structure |
|
| Synonyms |
|
| Chemical Formula | C18H18ClNO4 |
| Average Molecular Weight | 347.793 |
| Monoisotopic Molecular Weight | 347.092435776 |
| Chemical IUPAC Name | 3-{4-[(3-chlorophenyl)methoxy]phenyl}-5-(methoxymethyl)-1,3-oxazolidin-2-one |
| CAS Registry Number | 7241-98-7 |
| SMILES | COCC1CN(C(=O)O1)C1=CC=C(OCC2=CC(Cl)=CC=C2)C=C1 |
| InChI Identifier | InChI=1S/C18H18ClNO4/c1-22-12-17-10-20(18(21)24-17)15-5-7-16(8-6-15)23-11-13-3-2-4-14(19)9-13/h2-9,17H,10-12H2,1H3 |
| InChI Key | InChIKey=BHCOKYJYXDKTPG-UHFFFAOYSA-N |
| Chemical Taxonomy | |
| Kingdom | Organic Compounds |
| Super Class | Benzenoids |
| Class | Benzene and Substituted Derivatives |
| Sub Class | Benzylethers |
| Direct Parent | Benzylethers |
| Alternative Parents |
|
| Molecular Framework | Aromatic Heteropolycyclic Compounds |
| Substituents |
|
| External Descriptors | Not Available |
| External Links | |
| DrugBank ID | Not Available |
| PubChem Compound ID | 23670  |
| KEGG ID | Not Available |
| UniProt ID | Not Available |
| OMIM ID | Not Available |
| ChEBI ID | Not Available |
| BioCyc ID | Not Available |
| CTD ID | Not Available |
| Stitch ID | Not Available |
| PDB ID | Not Available |
| ACToR ID | Not Available |
| Wikipedia Link | http://en.wikipedia.org/wiki/Aflatoxin |
| Physical Properties | |
| Appearance | Crystals with green fluorescence from ethanol. |
| Melting Point | Not Available |
| Solubility | Not Available |
| Predicted LogP | 3.7064265343333327 |
| Toxicity Profile | |
| Route of Exposure | Oral, dermal, inhalation, and parenteral (contaminated drugs). (W967) |
| Mechanism of Action | Aflatoxins produce singlet oxygen upon their exposure to UV (365-nm) light. Singlet oxygen in turn activates them to mutagens and DNA binding species. Aflatoxin metabolites can intercalate into DNA and alkylate the bases through their epoxide moiety, binding particularity to N7-guanine bases. In addition to randomly mutating DNA, this is thought to cause mutations in the p53 gene, an important gene in preventing cell cycle progression when there are DNA mutations, or signaling apoptosis. (W572, W575, W820) |
| Metabolism | Aflatoxins are metabolized in the liver by the cytochrome P-450-dependent polysubstrate mono-oxygenase system to less toxic metabolites. The main reactions in aflatoxin metabolism are hydroxylation, oxidation, and demethylation. (W821) |
| Toxicity Values | Not Available |
| Lethal Dose | Not Available |
| Carcinogenicity (IARC Classification) | Not Available |
| Uses/Sources | The native habitat of Aspergillus is in soil, decaying vegetation, hay, and grains undergoing microbiological deterioration and it invades all types of organic substrates whenever conditions are favorable for its growth. Crops which are frequently affected include cereals (maize, sorghum, pearl millet, rice, wheat), oilseeds (peanut, soybean, sunflower, cotton), spices (chile peppers, black pepper, coriander, turmeric, ginger), and tree nuts (almond, pistachio, walnut, coconut, brazil nut). The toxin can also be found in the milk of animals which are fed contaminated feed. Thus, aflatoxins are usually encountered in thecontext of chronic exposure, via food intake or secondary to the handling of foodstuffs. (W819) |
| Minimum Risk Level | Not Available |
| Health Effects | The main target organ in mammals is the liver so aflatoxicosis is primarily a hepatic disease. Protracted exposure to aflatoxins may cause liver damage and necrosis, cholestasis, and hepatomas. Moreover, protracted exposure to aflatoxins has been associated with hepatocellular carcinoma, acute hepatitis, Reye's syndrome, bile duct cell proliferation, periportal fibrosis, hemorrhages, mucous membrane jaundice, fatty liver changes, cirrhosis in malnourished children, and kwashiorkor. However, aflatoxins accumulate in the presence of liver disease, and the association with hepatic cancer is confounded by the occurrence of hepatitis-B. Thus, it is not clear in these various instances whether aflatoxin is a primary cause of the disease, is an innocent bystander which accumulates secondary to the disease process, or is a contributing cause in conjunction with other factors. It is also mutagenic and teratogenic. Inhaled aflatoxins may produce pulmonary adenomatosis. Aflatoxins modify the immune system by affecting antibody formation, complement, cell-mediated immunity, and phagocytosis. (W574, W819) |
| Symptoms | A broad range of symptoms can be found depending upon dosage, including, vomiting, abdominal pain, hemorrhage, and pulmonary edema. (W584) |
| Treatment | Administration of phonobarbital enhances hepatic transformation activities and also protects against AFB-induced toxicity, carcinogenicity and DNA binding in vivo. In cases of ingestion, feeding large quantities of an adsorbent such as activated charcoal may be used. Antioxidants such as ellagic acid and inducers of some cytochromes P450, such as indole-3-carbinol, may give a protective effect. (W574, W584) |
| References | |
| General References |
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Targets
1. Cytokine receptor common subunit beta
High affinity receptor for interleukin-3, interleukin-5 and granulocyte-macrophage colony-stimulating factor.
Aflatoxins produce singlet oxygen upon their exposure to UV (365-nm) light. Singlet oxygen in turn activates them to mutagens and DNA binding species. Aflatoxin metabolites can intercalate into DNA and alkylate the bases through their epoxide moiety, binding particularity to N7-guanine bases. In addition to randomly mutating DNA, this is thought to cause mutations in the p53 gene, an important gene in preventing cell cycle progression when there are DNA mutations, or signaling apoptosis. (W572, W575, W820)UniProt ID: P32927
Gene: CSF2RB
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report
References:
- W572 — International Agency for Research on Cancer (IARC) - Summaries & Evaluations AFLATOXINS [Link]
- W575 — Stark AA, Liberman DF. Synergism between aflatoxins in covalent binding to DNA and in mutagenesis in the photoactivation system. Mutat Res. 1991 Mar;247(1):77-86.
[1900569 ]
- W820 — Eaton DL, Gallagher EP. Mechanisms of aflatoxin carcinogenesis. Annu Rev Pharmacol Toxicol. 1994;34:135-72.
[8042848 ]