Abstract
Summary
Previous studies have shown that dietary phenobarbital reduces 2-acetyl-aminofluorene (AAF)-induced hepatic tumorigenesis when fed simultaneously with the carcinogen, but enhances tumorigenesis when fed after the cessation of AAF feeding. Since DNA may be a primary target of chemical carcinogens, the effects of phenobarbital on the binding in vivo of AAF metabolites to hepatic nuclear DNA were investigated. The results show that the prolonged feeding of phenobarbital prior to the injection of AAF-9-14C reduced the binding of label to DNA, but the binding of label was not reduced if phenobarbital feeding was begun after the injection of AAF.
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