Comparison of two routes of chemical administration on the lung adenoma response in strain A/J mice. Toxicol Appl Pharmacol 1986 Jan;82(1):19-31
Date
01/01/1986Pubmed ID
3945940DOI
10.1016/0041-008x(86)90433-3Scopus ID
2-s2.0-0022626612 (requires institutional sign-in at Scopus site) 33 CitationsAbstract
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.
Author List
Stoner GD, Conran PB, Greisiger EA, Stober J, Morgan M, Pereira MAMESH terms used to index this publication - Major topics in bold
AdenomaAdministration, Oral
Animals
Caprylates
Carcinogens
Dimethyl Sulfoxide
Female
Injections, Intraperitoneal
Lung Neoplasms
Male
Mice
Mice, Inbred A
Triglycerides
