Slaga T J, Viaje A, Buty S G, Bracken W M
Res Commun Chem Pathol Pharmacol. 1978 Mar;19(3):477-83.
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 hours before DMBA. Pretreatment of mice with unlabeled DB[a,c]A at either 1, 12, or 36 hours 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 suggests 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.
对弱致癌起始剂二苯并[a,c]蒽（DB[a,c]A）抑制7,12-二甲基苯并[a]蒽（DMBA）皮肤致癌起始活性的机制进行了研究。发现当在DMBA之前5分钟、1小时、12小时或36小时给予DB[a,c]A时，它是DMBA起始的有效抑制剂。在处死前1小时、12小时或36小时用未标记的DB[a,c]A预处理小鼠，比在相同时间用未标记的DMBA预处理更能增加[3H]DMBA在体外表皮介导下与DNA的共价结合。只有在模拟肿瘤实验时，体外DMBA与DNA的共价结合才会减少。结果表明，弱致癌物和强致癌物的代谢产物之间可能在多环烃代谢水平或基因组水平存在某种竞争。
