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甲基多环芳烃的代谢过程中,角环湾区的阳离子及亚甲基阳离子孰是“终致癌剂”的理论一直存在争论。本文以B[a]A为例,依据生物体内的代谢模型、应用量子化学从头计算方法和密度泛函理论(DFT),系统计算了苯并[a]蒽母体及其各个位置取代甲基衍生物代谢过程产物的总能量,发现碳正离子形成的难易程度是引起其致突和致癌活性差异的一个重要因素。计算结果表明,湾区阳离子与甲基阳离子两个亲电活性中心两种作用机制相比较,显然后者的相关性更为明显。
In the metabolism of methylpolycyclic aromatic hydrocarbons, the theory of the “terminal carcinogen” has been controversial for the cations and methylene cations in the area around the Bay Area. In this paper, B [a] A is taken as an example. Based on the in vivo metabolic model, ab initio calculations and density functional theory (DFT) were applied to calculate the benzo [a] The total energy of the metabolic process product, found that the ease of formation of carbon positive ions is caused by its sudden and carcinogenic activity difference is an important factor. The calculated results show that the Bay Area cation and methyl cation two electrophilic centers compared to the two mechanisms of action, it is clear that the latter is more obvious correlation.