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In previous work we found that weekly injections of the polynuclear aromatic hydrocarbon (PAH) carcinogen 7,12-dimethylbenzaanthracene (DMBA) induced spontaneous aortic plaques in cockerels to grow to a larger size and at a faster rate than plaques in control animals. To determine whether plaque-stimulating ability is related to carcinogenic potency or mutagenicity we have now tested a variety of agents, including PAH carcinogens, non-PAH carcinogens and weakly carcinogenic PAHs. Cockerels were injected weekly (from 4-20 weeks of age) with one of the following compounds: benzoapyrene (BaP), benzoepyrene (BeP), dibenza,hanthracene (AH), dibenza,canthracene (AC), 3-methylcholanthrene (MCA), acetylaminofluorene (AAF), N-methyl-N,N'-nitro-nitrosoguanidine (MNNG) or anthracene (ANT). Plaques were present in the abdominal aortas of all animals. Plaque volumes were 8-14 times greater in AC-, BaP-, BeP-, MCA- and AH-treated cockerels than in controls. Plaques were slightly larger in the AAF-treated group than in control animals, and in the ANT- and MNNG-treated groups were indistinguishable in size from plaques in control animals. The largest plaque volumes were in AH-treated cockerels and were comparable in size to those elicited by DMBA treatment. The accelerated development of plaques is consistent with a 'promotional' role for these agents. There was a poor correlation between mutagenicity or carcinogenicity and plaque 'promotion', which may reflect a role for different metabolites in these processes.
Penn et al. (Fri,) studied this question.