Sequential histological and histochemical study of the rat liver after single-dose aflatoxin B1 intoxication

Rats were given a single dose of aflatoxin B1 lethal to 50% of the animals (7.20 mg/kg). Their livers were examined histochemically in correlation with sequential histological lesions. Early periportal liver cell necrosis and marked biliary cell proliferation were observed. Periportal cytoplasmic gl...

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Published inCancer research (Chicago, Ill.) Vol. 35; no. 10; p. 2836
Main Authors Kalengayi, M M, Desmet, V J
Format Journal Article
LanguageEnglish
Published United States 01.10.1975
Subjects
Adenosine Triphosphatases - metabolism
Aflatoxins - poisoning
Alkaline Phosphatase - metabolism
Animals
Bile Ducts, Intrahepatic - pathology
Cell Division
Chemical and Drug Induced Liver Injury - metabolism
Chemical and Drug Induced Liver Injury - pathology
Glycogen - metabolism
Liver - drug effects
Liver - metabolism
Liver Regeneration
Male
Rats
RNA - metabolism
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Summary:Rats were given a single dose of aflatoxin B1 lethal to 50% of the animals (7.20 mg/kg). Their livers were examined histochemically in correlation with sequential histological lesions. Early periportal liver cell necrosis and marked biliary cell proliferation were observed. Periportal cytoplasmic glycogen and RNA depletion occurred during this early period and subsequently extended to the whole lobule. The enzymes investigated decreased or disappeared in the periportal area; but alkaline phosphatase increased strikingly in the centrolobular area, whereas canalicular adenosinetriphosphatase completely disappeared throughout the liver lobule. The histochemical changes reverted to normal after cessation of the necrosis. Histochemical techniques were more sensitive in detecting the vulnerability of the periportal parenchyma to aflatoxin. After the necrosis, regenerative foci appeared. They showed a variable content in glycogen and RNA and were characteristically enzyme deficient. This reflects the immaturity of regenerating hepatocytes. These early foci subsequently disappeared and are thus considered irrelevant to hepatomagenesis.
ISSN:0008-5472