**3. The metabolism of mycotoxins**

Examination of the metabolic fate of aflatoxin B1 can be used to illustrate the importance of the metabolic process in determining toxicity, and as a means of determining exposure to mycotoxins, by measuring; mycotoxin-macromolecular conjugates, the parent mycotoxin and a biochemical change initiated by the mycotoxin, respectively (Coker 1999).

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converted to aflatoxin B1 -dihydrodiol (Figure 8) (Baertschi et al., 1989; Coker, 1999; Kremer

Fig. 7. The biotransformation of aflatoxin B1 (Baertschi et al., 1998)

protein amino groups to produce Schiff base adduct (Autrup et al., 1987).

Aflatoxin B1 is converted to at least seven metabolites, including a proposed unstable metabolite, the aflatoxin B1 -8,9-epoxide, which is the so called ultimate carcinogenic form (Hsieh and Wong, 1994; Magan et al., 2010). Aflatoxin M1 occurs in milk of cows fed on aflatoxin B1-containing feeds. This metabolite is found in the liver, kidneys and urine of sheep and in the livers of rats treated with aflatoxin B1 (Appleton et al., 1982; Micco et al., 1991). The carcinogenicity of aflatoxin B1 arises from interaction with guanine moiety of DNA, to produce the aflatoxin-N7-guanine adduct (Baerstchi et al., 1989), whereas the acute toxicity of aflatoxin B1 is believed to stem from interaction between the dihydrodiol and

et al., 2007)
