Abstract
Only few data are available on the carcinogenic potency of individual PCB congeners. In this study, we tested the ‘non-dioxinlike’ congeners PCB 28 and 101 for their potency as liver tumor promoters in female rats which received diethyl- N-nitrosamine as an initiator. After 8 or 16 weeks of PCB treatment (50 and 150 μmol/kg body weight per week), each congener was recovered in the liver according to the dose levels applied, with PCB 28, at the same dose level, showing nine- to 16-fold higher hepatic levels than PCB 101 (approximately, 44 μmol/kg versus 5 μmol/kg liver at low dose, 145 μmol/kg versus 9 μmol/kg liver at high dose). PCB 28 was found to mildly induce hepatic EROD activity, while both congeners induced PROD activity. With each congener, no significant increase in the number of ATPase-deficient or GSTP-positive preneoplastic foci was obtained, while a significant increase in the relative hepatic volume of ATPase-deficient foci was found in the livers of DEN pre-treated animals having received 50 μmol/kg body weight of PCB 101 per week over 16 weeks. Our results revealed that neither the accumulative PCB 28 nor the more readily metabolisable PCB 101 was an efficacious tumor promoter in the livers of female rats.
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