Okuno S, Takeishi K, Seno T
Cancer Lett. 1979 Jan;6(1):1-5. doi: 10.1016/s0304-3835(79)80012-9.
The effect of paraoxon, a microsomal deacetylase inhibitor, on the mutant genicity of 2-acetylaminofluorene (AAF) by liver homogenates was compared between the AAF carcinogenesis-resistant guinea pigs and the susceptible mice and rats. The mutagenicity of AAF was mostly abolished by paraoxon, not only in the 3 kinds of untreated animals but also in guinea pigs treated with a combination of phenobarbital and 5,6-benzoflavone, whereas about 50% of the mutagenicity was resistant to paraoxon in treated mice and rats. We suggest that microsomal deacetylase activity is crucially involved in the mutagenic activation of AAF by guinea pig liver homogenates, while the enzyme activity other than the deacetylase activity is also important in the activation by liver homogenates from treated mice or rats.
比较了微粒体脱乙酰酶抑制剂对氧磷对2-乙酰氨基芴（AAF）在抗AAF致癌豚鼠以及易感小鼠和大鼠肝脏匀浆中致突变性的影响。对氧磷不仅在3种未处理的动物中，而且在接受苯巴比妥和5,6-苯并黄酮联合处理的豚鼠中，都能基本消除AAF的致突变性，而在处理过的小鼠和大鼠中，约50%的致突变性对氧磷具有抗性。我们认为，微粒体脱乙酰酶活性在豚鼠肝脏匀浆对AAF的诱变激活中起关键作用，而除脱乙酰酶活性外的其他酶活性在处理过的小鼠或大鼠肝脏匀浆的激活中也很重要。
