论文部分内容阅读
采用ＡＭ１方法计算了环境致癌物１，３－丁二烯（ＢＤ）的代谢产物１，２－环氧－３，４－丁烯（ＥＢ）和１，２，３，４－二环氧丁烷（ＤＥＢ）与ＤＮＡ腺嘌呤和胞嘧啶烷化反应过程速率控制步骤的活化能，以及ＤＥＢ在ＤＮＡ大沟侧与不同序列ＤＮＡ片断生成烷化股间横向交联产物的结构和能量．结论认为：用烷化反应的难易程度难以解释ＤＥＢ的致突性比ＥＢ约大１００倍的实验事实；强致突的ＤＥＢ可与碱基发生２次烷化反应，生成ＤＮＡ交联产物；而ＥＢ则不能交联，这可能为２者基因毒性差异巨大的分子机制；同时ＤＥＢ在ＤＮＡ大沟侧可与多种不同的ＤＮＡ序列发生股间横向交联，对比在小沟侧只与２种序列交联，此发生股间横交联几率的差异合理地解释了ＤＥＢ致突的碱基选择性
The metabolic products of 1,3-butadiene (BD), an environmental carcinogen, were calculated using the AM1 method. 1,2-epoxy-3,4-butylene (EB) (DEB) and DNA adenine and cytosine alkylation reactions, and the structure and energy of the cross-linked product between DEB and alkylated strands of DNA fragments with different DNA sequences. The conclusion is that it is difficult to explain the fact that the mutagenicity of DEB is about 100 times greater than that of EB by using the ease of alkylation reaction. The strongly mutagenized DEB can undergo two alkylation reactions with the base to form DNA cross-linked products. While EB can not be cross-linked, which may be a huge molecular mechanism of genotoxicity differences between the two; at the same time, DEB cross-strand cross-strands with a variety of different DNA sequences, The sequence cross-linking, the difference in the probability of cross-linking between strands reasonably explains the base selectivity of the DEB-striking