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Hepatocyte nodules produced by cyclic feeding of the rat liver carcinogen 2-acetylaminofluorene to male rats have been shown to exhibit specific metabolic characteristics. None of the characteristics of nodular tissue so far investigated has provided any explanation why initiated cells, such as in the "resistant hepatocyte model," were resistant to the mitoinhibitory effects of 2-acetylaminofluorene. In the present study, hepatocyte nodules are produced by cyclic feeding of 0.05% 2-AAF in the diet to male Wistar rats. N-hydroxy-2-acetylaminofluorene sulfotransferase levels were determined in the postmicrosomal supernatant prepared from nodules and from control rat liver. The average sulfotransferase activities were 0.29 and 4.75 nmol p-nitrophenol formed/min X mg protein, respectively. We suggest that the low sulfotransferase activity in preparations from nodular tissue might be an important part of the explanation for the resistance of focal and nodular tissue to the mitoinhibitory effects of 2-acetylaminofluorene.
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