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Aflatoxins are toxic metabolites produced by certain fungi in/on foods and feeds . They are probably the best known and most intensively researched mycotoxins in the world. Aflatoxins have been associated with various diseases , such as aflatoxicosis , in livestock , domestic animals and humans throughout the world . The occurence of aflatoxins is influenced by certain environmental factors ; hence the extent of contamination will vary with geographic location , agricultural and agronomic practices, and the susceptibility of commodities to fungal invasion during preharvest , storage, and/or processing periods . Aflatoxins have received greater attention than any other mycotoxins because of their demonstrated potent carcinogenic effect in susceptible laboratory animals and their acute toxicological effects in humans . As it is realized that absolute safety is never achieved , many countries have attempted to limit exposure to aflatoxins by imposing regulatory limits on commodities intended for use as food and feed .

In the 1960 more than 100,000 young turkeys on poultry farms in England died in the course of a few months from an apparently new disease that was termed "Turkey X disease" . It was soon found that the difficulty was not limited to turkeys . Ducklings and young pheasants were also affected and heavy mortality was experienced .
A careful survey of the early outbreaks showed that they were all associated with feeds, namely Brazilian peanut meal . An intensive investigation of the suspect peanut meal was undertaken and it was quickly found that this peanut meal was highly toxic to poultry and ducklings with symptoms typical of Turkey X disease .
Speculations made during 1960 regarding the nature of the toxin suggested that it might be of fungal origin. In fact, the toxin-producing fungus was identified as Aspergillus flavus (1961) and the toxin was given the name Aflatoxin by virtue of its origin (A.flavis--> Afla).

This discovery has led to a growing awareness of the potential hazards of these substances as contaminants of food and feed causing illness and even death in humans and other mammals. Studies that are summarized in the following sections revealed that aflatoxins are produced primarily by some strains of A. Flavus and by most , if not all , strains of A. parasiticus , plus related species, A. nomius and A. niger . Moreover , these studies also revealed that there are four major aflatoxins : B1 , B2 , G1 , G2 plus two additional metabolic products , M1 and M2 , that are of significance as direct contaminants of foods and feeds . The aflatoxins M1 and M2 were first isolated from milk of lactating animals fed aflatoxin preparations ; hence , the M designation . Whereas the B designation of aflatoxins B1 and B2 resulted from the exhibition of blue fluorescence under UV-light , while the G designation refers to the yellow-green fluorescence of the relevant structures under UV-light . These toxins have closely similar structures and form a unique group of highly oxygenated, naturally occuring heterocyclic compounds . Their molecular formulas as established from elementary analyses and mass spectrometric determinations are :

Aflatoxins B2 and G2 were established as the dihydroxy derivatives of B1 and G1 , respectively . Whereas , aflatoxin M1 is 4-hydroxy aflatoxin B1 and aflatoxin M2 is 4-dihydroxy aflatoxin B2 .

Although aflatoxins are known to cause cancer (carcinogenic) in animals, the Federal Drug Administration (FDA) allows them at low levels because they are considered "unavoidable contaminants" of these foods. To help minimize risk, the FDA tests foods that may contain aflatoxin. Peanuts and peanut butter are some of the most rigorously tested products by FDA because they frequently contain aflatoxins and are widely consumed.

The FDA believes the occasional consumption of small amounts of aflatoxin pose little risk over a lifetime. It is not practical to attempt to remove aflatoxin from contaminated food products in order to make them edible.

Aflatoxin B1

Aflatoxin G1






  1. Aflatoxin, hepatitis and worldwide liver cancer risks.

  2. Effect of processing on aflatoxin.

  3. Interindividual differences in response to chemoprotection against aflatoxin -induced hepatocarcinogenesis: implications for human biotransformation enzyme polymorphisms.

  4. The chemistry and biology of aflatoxin B(1): from mutational spectrometry to carcinogenesis.

  5. Mechanisms of aflatoxin B1 lung tumorigenesis.

  6. Aflatoxin and liver cancer.

  7. Dietary clay in the chemoprevention of aflatoxin-induced disease.

  8. Regulation of rat glutathione S-transferase A5 by cancer chemopreventive agents: mechanisms of inducible resistance to aflatoxin B1.

  9. Use of aflatoxin adducts as intermediate endpoints to assess the efficacy of chemopreventive interventions in animals and man.

  10. Activation and detoxication of aflatoxin B1.





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This page was done by a student of Bioinformatics, Open University Jerusalem Israel, in a homage to Fermentek and to Dr Berend.

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