Tumor promoters can often be differentiated by their effects in two model systems: polynuclear aromatic hydrocarbon (PAH)-initiated carcinogenesis in mouse skin and nitrosamine-initiated carcinogenesis in regenerating rat or mouse liver. Phorbol esters promote in both systems, some phthalate esters promote the latter and fail to affect the former, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) promotes the latter and is an antipromoter for the former, while polychlorinated biphenyls (PCBs) may promote or act as an antipromoter for both depending on the dosages tested. A comparison of these classes of environmental pollutants may provide mechanistic insights absent when any one is studied by itself. Initial studies indicate that one must expect the effects of these compounds on given model systems (such as lipid peroxidation) to be significantly different in vitro from in vivo.
