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 micromol/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 micromol/kg versus 5 micromol/kg liver at low dose, 145 micromol/kg versus 9 micromol/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 micromol/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.