A comparison of the initiating and promoting actions of 9,10-dimethyl-1,2-benzanthracene and 1,2,5,6-di-benzanthracene in skin tumorigenesis.

The skin of Swiss albino mice was exposed once to 0.16 #g. of 9,10-dimethyl-l ,~benzanthracene (DMBA) or 1,2,5,6-dibenzanthracene (DBA), followed by continuous t rea tment with croton oil. Other mice were exposed to 0.0~ ug. of the same carcinogens. Control mice were t reated once with acetone followed by continuous t r ea tmen t with croton oil. A higher incidence of skin tumors was observed for all the carcinogen-treated groups as compared with the controls. However, the increase was statistically significant only for the mice exposed to 0.16 #g. DBA. A significantly greater number of skin tumors per mouse was obtained among the mice t reated with 0.16 ug. D M B A (P < 0.05), 0.16 ug. DBA (P < 0.005), and 0.0~ #g. DBA (P < 0.05), as compared with the acetonetreated controls. I t is apparent tha t the carcinogen DBA contributes a greater initiating stimulus in skin tumorigenesis than D M B A at the low dosages employed. Strain DBA mice were exposed once on the skin to an init iat ing dose of D M B A followed 1 month later by month ly applications of 0.15 per cent D M B A or 0.3 per cent DBA. Fif ty per cent of the mice given month ly t rea tments of D M B A developed visible skin tumors after a la tent period Of ~ 6 days. On the other hand, a latent period of 339 days was observed in the case of the mice t reated with DBA, despite the higher concentration employed. This indicates tha t D M B A is more potent than DBA in the promotion of skin tumors.