The carcinogen benzo(e)pyrene is metabolized by DM15 cells without an uncoupling effect on their gap junctions.

Benzo(e)pyrene (B(e)P) promotes carcinogenesis in the skin. Unlike some other promoters however, B(e)P does not produce an uncoupling effect on gap junction permeability in DM15 transformed fibroblasts. This study demonstrates that DM15 cells exhibit a relatively high level of B(e)P metabolism. Moreover, although pretreatment of DM15 cells with benz(a)anthracene results in an 8-fold increase of arylhydrocarbon hydroxylase activity and a 2-fold increase in the rate of B(e)P metabolism, it did not enable B(e)P to affect Lucifer Yellow transfer between DM15 cells. We conclude that neither B(e)P nor its metabolites are capable of uncoupling gap junction permeability in DM15 cells.