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Polychlorinated biphenyls (PCBs) are industrial chemicals which are highly persistent and widely distributed in the environment. We have previously shown that 3,4,5,3',4'-pentachlorobiphenyl (PCB 126) is a potent tumour promoter in two separate 20 week initiation-promotion studies. In the present study, rat livers from these two studies were further investigated for connexin expression. The results demonstrated that treatment with PCB 126 caused a decrease in the amount of the two major liver connexins, cx 26 and cx 32, in livers of treated animals. This reduction was also prominent after treatment at low doses, although gamma-glutamyl transpeptidase-positive foci had not developed in these livers. The quantity of cx 26 and cx 32 in immunostained liver sections was determined using a computerized fluorescence image analyzer. Western blot analysis of liver extracts confirmed these results. No changes in the RNA levels in the treated rats were seen, suggesting that the down-regulation of cx 26 and cx 32 is post-transcriptional.

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This study was undertaken to investigate tumour promoting interactions of 2,4,5,2',4',5'-hexachlorobiphenyl (PCB 153) and 3,4,5,3',4'-pentachlorobiphenyl (PCB 126) in female Sprague-Dawley rats. Five weeks before the promotion treatment, the rats were partially hepatectomized and initiated with nitrosodiethylamine. The test substances were administered by weekly, subcutaneous injections for 20 weeks. The results from this study suggest that treatment with a combination of these two congeners causes a more than additive effect on the formation of gamma-glutamyltranspeptidase-positive hepatic foci. Co-exposure to PCB 126 and PCB 153 caused a dose-dependent reduction of the PCB 153-induced CYP2B1/B2-activity in these livers.