Forster R, Green M H, Priestley A, Gorrod J W
Mutat Res. 1981 Aug;85(4):187-94. doi: 10.1016/0165-1161(81)90035-2.
The results presented here confirm that 2-acetylaminofluorene (AAF) can be activated to a mutagen by S105 rat liver post-microsomal fraction. The activity is Aroclor-inducible. It appears partly NADPH-independent, but on repeated centrifugation the NADPH independence is lost though the NADPH-dependent activation is retained. S105 activation is obtained whether the fraction is prepared with 0.15 M KCl or 0.25 M sucrose. Increasing amounts of S105 give increasing activation, with no evidence of an optimum. Activation by S105 is reduced in the presence of excess S9 and is inhibited by norharman. Under the same conditions, S105 produces mutagenic metabolites of 2-aminofluorene and 2-aminoanthracene but not ethidium bromide, dimethylaminoazobenzene or benzo(alpha)pyrene.
此处呈现的结果证实，2-乙酰氨基芴（AAF）可被S105大鼠肝脏微粒体后组分激活成为诱变剂。该活性可被多氯联苯诱导。它部分不依赖于NADPH，但反复离心后，尽管保留了依赖NADPH的激活作用，但NADPH非依赖性却丧失了。无论该组分是用0.15M氯化钾还是0.25M蔗糖制备，均可获得S105激活作用。S105量的增加会导致激活作用增强，且没有最佳值的证据。在过量S9存在的情况下，S105的激活作用会降低，且会被去甲哈尔满抑制。在相同条件下，S105可产生2-氨基芴和2-氨基蒽的诱变代谢产物，但不会产生溴化乙锭、二甲基氨基偶氮苯或苯并(α)芘的诱变代谢产物。
