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用从头计算Hartree-Fork方法和密度泛函B3LYP方法在6-311G(d)水平上对β-甲基亚硝基哌嗪类化合物代谢活化后的邻基参与作用机理进行了研究.计算结果表明,哌嗪环上N′原子和N′-取代基上氧原子的邻基参与作用明显提高了β-甲基亚硝基哌嗪代谢物的亲电反应活性,促进了对DNA的烷化作用.解释了甲基取代的N-亚硝基哌嗪较其母体化合物的致癌性具有显著增强的现象,为N-亚硝基哌嗪在其γ-位形成第二亲电活性中心的致癌代谢途径提供了理论依据.
The mechanism of the orthologous participation of β-methylnitrosopiperazines after metabolic activation at the 6-311G(d) level was studied using the ab initio computation Hartree-Fork method and the density functional B3LYP method. The participation of the N′ atom on the piperazine ring and the ortho-group of the oxygen atom on the N′-substituent significantly improves the electrophilic reactivity of β-methylnitrosopiperazine metabolites and promotes the alkylation of DNA. Explains that the methyl-substituted N-nitrosopiperazine has a significantly enhanced carcinogenicity compared to its parent compound and is an oncogenic metabolism of N-nitrosopiperazine at its γ-position forming a second electrophilic active center. The route provides a theoretical basis.