Comparison of two routes of chemical administration on the lung adenoma response in strain A/J mice.

This study was undertaken to determine the ability of a series of 19 compounds representing different chemical classes of carcinogens to induce lung tumors in strain A/J mice after either ip or po administration. Aflatoxin B1, dibutylnitrosamine, 1,2-dimethylhydrazine, and methylnitrosourea induced a significant increase in the lung tumor response in both sexes after ip and po administration. Azaserine was active in both sexes only after ip administration. Benzene, 1,2-dibromoethane, and epichlorohydrin, following ip administration, produced significant increases in the tumor response in at least one sex. Aflatoxin B1, azaserine, benzene, 1,2-dibromoethane, dibutylnitrosamine, and epichlorohydrin were more active when given ip than after po administration. In contrast, dimethylhydrazine and methylnitrosourea were more active (in females only) when given po. 2-Acetylaminofluorene, azobenzene, chloroform, 1,4-dioxane, FANFT (N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide), lead subacetate, methylmethanesulfonate, beta-naphthylamine, beta-propiolactone, safrole, and 2,4,6-tri-chlorophenol did not induce lung tumors in strain A/J mice. These data confirm previous observations on the importance of the route of chemical administration on the lung tumor response in strain A mice, and on the inability of the lung tumor bioassay to detect certain liver and bladder carcinogens and unstable alkylating agents.