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采用密度泛函理论B3LYP方法,在6-31G*基组水平下,以乙硫醇(C_2H_5SH)作为含还原性巯基的生物蛋白大分子(R-SH)的简单模型物,全优化计算了4-氟硝基苯、4-氯硝基苯和4-溴硝基苯在生物体内的代谢还原中间体即其亚硝基化合物与乙硫醇反应的过渡态,从电子微观层次上探讨了卤代硝基芳烃的致毒机理。结果表明,卤代硝基芳烃至少存在两种致毒反应:一是被还原代谢前,与卤素相连的苯环碳可能受到亲核试剂进攻,卤原子被取代;二是其亚硝基代谢中间体与含巯基的蛋白质大分子发生反应,形成共价加合物。若在同一位置以不同卤素取代的硝基芳烃,其致毒反应机理类似,反应活性受卤素基团种类的影响较小。
Density Functional Theory B3LYP method was used to calculate the content of 4 (R-SH), a simple model product of thiol-containing biomacromolecule (R-SH) with ethanethiol (C_2H_5SH) -fluoronitrobenzene, 4-chloronitrobenzene and 4-bromonitrobenzene in the body of the metabolic reduction intermediates that nitroso compounds and ethanethiol transition state, from the electronic micro-level to explore the halogen Generation of nitroaromatic poisoning mechanism. The results showed that there were at least two kinds of toxic reactions of halonitroaromatics. One is the benzene ring carbon attached to halogen may be attacked by nucleophile and the halogen atom is replaced before it is reduced and metabolized. The other is the nitroso metabolism intermediate The body reacts with sulfhydryl-containing protein macromolecules to form covalent adducts. If the nitroaromatics substituted with different halogens at the same position have similar toxicogenic mechanism, the reactivity is less affected by the type of halogen groups.