Dipple A, Tomaszewski J E, Moschel R C, Bigger C A, Nebzydoski J A, Egan M
Cancer Res. 1979 Apr;39(4):1154-8.
Comparison of the binding to DNA of 7-hydroxymethyl-12-methylbenza(a)anthracene and 7, 12-dimethylbenz(a)anthracene (DMBA) catalyzed by mouse embryo cells in culture or by rat liver microsomes indicates that the products formed are different for the two hydrocarbons. Thus, the hydroxy compound is not an intermediate in the binding of DMBA to DNA in these systems. Binding of the hydroxy compound to DNA in mouse embryo cells is less efficient than for DMBA and is inhibited by 1,1,1-trichloropropylene 2,3-oxide, an inhibitor of epoxide hydrase. This and the fluorescence spectra of the hydroxy compound-DNA adducts indicate that the hydroxy compound is activated for DNA binding through the formation of a diol-epoxide in the 1,2,3,4-ring. As previously found for DMBA, this is consistent with the activation of this compound through a bay-region diol-epoxide.
对培养的小鼠胚胎细胞或大鼠肝微粒体催化的7-羟甲基-12-甲基苯并(a)蒽与7,12-二甲基苯并(a)蒽（DMBA）与DNA结合的比较表明，两种碳氢化合物形成的产物不同。因此，在这些系统中，羟基化合物不是DMBA与DNA结合的中间体。羟基化合物在小鼠胚胎细胞中与DNA的结合效率低于DMBA，并且受到环氧水化酶抑制剂1,1,1-三氯丙烯2,3-氧化物的抑制。这以及羟基化合物-DNA加合物的荧光光谱表明，羟基化合物通过在1,2,3,4环中形成二醇环氧化物而被激活以与DNA结合。如先前对DMBA的发现，这与该化合物通过湾区二醇环氧化物的激活是一致的。
