In an attempt to elucidate the pathologic and histochemical changes of aflatoxin B₁-induced hepatie lesions, the present study in male Sprague-Dawley rats was undertaken to evalute the relation between pathologic change of the liver and histochemical changes of several enzymes：alkaline phosphatase, acid phosphatase and succinic dehydrogenase at 3, 9, 24, 48, 72, and 144 hours after single administration of aflatoxin B₁ by gastric tube. The aflatoxin B₁ was dissolved in peanut oil(0.5mg aflatoxin B₁ to 0.5ml peanut oil)
Groups of male rats received aflatoxin B₁ 1mg and 4mg per kg of body weight, respectively.
Control animals were given a similar volume of peanut oil alone.
The results on morphologic and histochemical changes were as follows：
1. The necrotic change of liver was mainly periportal, and it became most severe at 24 hours and was more prominent in the large dose group than the small dose group.
2. Biliary ductular cell proliferation started to appear within 72 hours and after became regressed later in the small dose group, but it remained approximately 144 hours after exposure in the large dose group.
3. Electron microscopically, all three groups showed irregular nuclear membrane and nucleolar change characterized by segregation of granular and fibrillar elements.
All the groups showed cytoplasmie changes such as dilatation of rough endoplasmic reticulum with detached ribosome, hyperplasia of smooth endoplasmic reticulum, increased numbers of lipid droplets and mitochondrial alteration.
The above changes in the large dose group was more severe than those of the small dose group
4. In the histochemical study of experimental animals, there was a decrease in the intensity of the staining reaction of alkaline phosphatase and succinic dehydrogenase within 24 hours and a progressive decrease in staining intensity was noted at 144 hours.
And then the staining intensity of the acid phosphatase was similar to that shown by the control animal.
In summary, the data obtained by present experiments indicate aflatoxin B₁ exerts periportal necrosis of hepatic lobules accmpanied by bile ductular cell proliferation, and inhibition of protein synthesis, as judged by elertron microscopic and histochemical changes.
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