Effects of prototypic PCBs on benzo[a]pyrene mutagenic activity related to vitamin A intake

The effects of vitamin A dietary intake (2 and 20 IU */g of food) on the mutagenic activity of benzoa]pyrene (B(a)P) toward Salmonella typhimurium (TA98) were studied either in control rats or in animals treated by the PCB congeners 2,4,5,2',4',5'-hexachlorobiphenyl 2,4,5)2Cl) and 3,4,3',4'-tetrachlorobiphenyl 3,4)2Cl). (3,4)2Cl (a planar compound) strongly increased B(a)P monooxygenase (B(a)PMO) activity and glutathione transferase, (2,4,5)2Cl (a non-planar PCB) was a strong inducer of epoxide hydrolase and a weak inducer of B(a)PMO. Enzyme induction was not modified by changes in vitamin A dietary intake. A higher mutagenic effect was observed in the (3,4)2Cl group than in the (2,4,5)2Cl one. This could be related to the specific form of cytochrome P-450 induced by (3,4)2Cl. In the untreated animals, the activation of B(a)P was higher in the 2-IU group than in the 20-IU one. Conversely, in PCB-treated rats the mutagenic activity of B(a)P was higher in the 20-IU group than in the 2-IU one. PCB induction increased the liver content of vitamin C in both the 2-IU and the 20-IU groups but only increased the glutathione levels in the 2-IU groups. This suggests that glutathione content in cellular fractions may be one of the determining parameters for the mutagenic activity of B(a)P.