Biochemical and Histopathological Effects of Aflatoxin on ...

However, only aflatoxinls, is considered by the international agency for
research on cancer (IARC) as having produced sufficient evidence <strong>of</strong>
carcinogenicity in experimental animal to be identified as a carcinogen.
In a 12 month feeding study <strong>of</strong> rainbow trout, the hepatocarcinogenic
activity <strong>of</strong> aflatoxin M1 was roughly 25% that <strong>of</strong> the parent compound
(Sinnhuber et al, 1974). Using a sensitive trout embryo exposure
carcinogenesis assay, AFM 1 was nontumourogenic (Hendricks et al,1980). In
hepatocytes isolated from rainbow trout, AFM1 formed DNA adducts at a
level significantly less than that <strong>of</strong> AFB 1 (20% less), but interestingly, this
binding activity was much higher than would be predicted from III VIVO
carcinogenesis studies (Lovel<strong>and</strong> et al, 1988).
2.10. <strong>Biochemical</strong> <strong>Effects</strong>
<strong>Biochemical</strong>ly, aflatoxins can affect energy metabolism, carbohydrate
<strong>and</strong> lipid metabolism. <strong>Aflatoxin</strong>s may be considered as biosynthetic
inhibitors both in vivo <strong>and</strong> in vitro, with large doses causing total inhibition
<strong>of</strong> biological systems <strong>and</strong> lower doses affecting different metabolic systems
(Moreau <strong>and</strong> Moss, 1969).
2.10 3. Energy metabolism
It has been shown that aflatoxin Bj, G 1 <strong>and</strong> M 1 inhibit oxygen uptake
in whole tissues by acting on the electron transport chain system. They
inhibit the activity <strong>of</strong> the enzyme adenosine triphosphatase to varying
degrees, resulting in decreased production <strong>of</strong> adenosine triphosphate (Moss
<strong>and</strong> Smith, 1985).
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