The mechanism by which the weak tumor initiator dibenz[a,c]anthracene (DB[a,c]A) inhibits the skin-tumor-initiating activity of 7,12-dimethylbenz[a]anthracene (DMBA) was investigated. DB[a,c]A was found to be a potent inhibitor of DMBA initiation when given either 5 min, or 1, 12, or 36 hr before DMBA. Pretreatment of mice with unlabeled DB[a,c]A at either 1, 12, or 36 hr before killing increased the in vitro epidermally mediated covalent binding of [3H]DMBA to DNA more than pretreatment with unlabeled DMBA at comparable times. Only when the tumor experiments were mimicked did a decrease in DMBA covalent binding to DNA in vitro occur. The results suggest that some competition at the level of polycyclic hydrocarbon metabolism or at the genome level may exist between metabolites of the weak carcinogen and those of the strong carcinogen.
|Original language||English (US)|
|Number of pages||7|
|Journal||Research Communications in Chemical Pathology and Pharmacology|
|State||Published - Dec 1 1978|
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Pharmacology, Toxicology and Pharmaceutics(all)