Definition
Mycotoxin prod. by Aspergillus flavus and Aspergillus parasiticus
Description
Aflatoxin G is a mycotoxin produced by Aspergillus flavus and Aspergillus parasiticus Aflatoxin G belongs to the family of Difurocoumarolactone Series. These are polycyclic aromatic compounds containing a delta-valerolactone ring fused to the coumarin moiety of the difurocoumarin skeleton. Difurocoumarolactones are a subgroup of the aflatoxins and related compounds.
Top Gene Interactions
Related Pathways
General Information
- 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. (A2973)
- 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. (L1956)
- 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. (A704, L1956)
- Symptoms: A broad range of symptoms can be found depending upon dosage, including, vomiting, abdominal pain, hemorrhage, and pulmonary edema. (L1879)
- 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. (A704, L1879)
- Route of Exposure: Oral, dermal, inhalation, and parenteral (contaminated drugs). (A3101)
Mechanism of Action
Target Name | Mechanism of Action | References |
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DNA | 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. (L1877, A2859, A2972) |
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