Biochemical and Histopathological Effects of Aflatoxin on ...

2.4. Biotransformation <strong>of</strong><strong>Aflatoxin</strong> BI
The major hydroxylated metabolite <strong>of</strong> AFBI formed by cytochromes
P-450 are aflatoxin MI (AFM 1) , aflatoxin PI (AFP1) , aflatoxin Ql (AFQI)
<strong>and</strong> aflatoxin Bza (AFBza). Additional metabolites, which are generally
formed in smaller quantities depending on various conditions, include
aflatoxicol MI <strong>and</strong> aflatoxicol HI. These stable metabolites are considered to
be detoxified relative to AFBl, are more polar, <strong>and</strong> as such are more easily
extractable. The cyclopentanol aflatoxicol (AFL) is not a product <strong>of</strong>
oxidative metabolism, but rather a result <strong>of</strong> the reproductive metabolism <strong>of</strong>
AFB I catalyzed by soluble NADPH - dependent reductases (Wong <strong>and</strong>
Hsieh, 1978).
2.5. Biosynthesis <strong>of</strong><strong>Aflatoxin</strong>
As is the case for many other toxic secondary metabolites produced by
fungi, aflatoxins are synthesized by the polyketide route, wherein head-to­
tail condensation <strong>of</strong> acetate units proceed via poly-Bvketo-thiol ester
intermediate (Applebaum <strong>and</strong> Marth,1981). In this biosynthetic pathway, the
chain is initiated by acetyl coenzyme A, <strong>and</strong> malonyl COA is the source <strong>of</strong>
additional carbon units (Money, 1976). Relative to other polyketide-derived
mycotoxins, the synthesis <strong>of</strong> aflatoxins has been particularly difficult to
elucidate. It is now known that aflatoxins are derived from a C20 polyketide
(Smith <strong>and</strong> Moss, 1985).
2.6. Carcinogenicity <strong>of</strong><strong>Aflatoxin</strong>s
A requisite step in the toxic <strong>and</strong> carcinogenic action <strong>of</strong> AFBI is its
conversion to one or more metabolites in the various tissues <strong>of</strong> exposed
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