Abstract
Preneoplastic hepatocyte nodules (HN) generated in the rat liver by different experimental protocols display a common pattern in the xenobiotic metabolism, namely a decrease of the phase I components and an increase of the phase II ones1. If initiated hepatocytes share with HN these metabolic properties (which explain the observed increase of HN resistance to many liver toxins), then any mild but prolonged liver injury by chemicals needing bioactivation should cause, in addition to liver cirrhosis, also the appearance of HN and tumors, providing the liver has been exposed to initiating stimuli.
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