Mass M J
Respiratory Carcinogenesis Group, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711.
Anticancer Res. 1990 Jan-Feb;10(1):241-5.
Five retinoids were evaluated for their ability to inhibit N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced transformation of primary rat tracheal epithelial (RTE) cells in culture. Two retinoidal benzoic acids (arotenoids), Ro 13-6298 and Ro 13-7410, suppressed the transformation frequency by 80-90% at 330 pM; 330 pM retinoic acid (RA) suppressed the transformation frequency by 50%. Retinol and retinyl acetate were tested at 33 nM and found to be much less effective than RA at this concentration. In studies with all retinoids, the amount of inhibition of spontaneously occurring transformed epithelial foci was greater than the amount of inhibition of foci that arose in response to carcinogen treatment. A biological difference between carcinogen-induced and spontaneously arising foci is suggested by this result.