Abstract
Overall rates of tissue protein degradation in vivo during chemical hepatocarcinogenesis were estimated by a double-isotope method as well as from the accumulation of peptide intermediates in protein degradation induced by bestatin. Several parameters estimating rates of cell proliferation and cell loss have been measured in parallel. The two procedures adopted consistently indicated that protein turnover was significantly slowed down through the whole observation period (12 months after the initiating administration of DENA) in both 'preneoplastic' nodules and hepatomas as compared with control livers or perinodular tissue. Such a difference may confer a selective growth advantage to 'preneoplastic' and tumoral cells. Since protein degradation rates did not appreciably differ between nodules and hepatomas, either such advantage originated from some early step in the carcinogenetic process or it merely reflected the proliferative events in the two cell populations. Yet neither liver nodules nor hepatomas were characterized by very high rates of cell proliferation, however much increased with respect to control liver.
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