苯并咪唑和苯并咪唑醌的氮丙啶取代基对正常细胞和范可尼贫血细胞毒性的影响。
The influence of the aziridinyl substituent of benzimidazoles and benzimidazolequinones on toxicity towards normal and Fanconi anaemia cells.
机构信息
School of Chemistry, National University of Ireland, Galway, Ireland.
出版信息
Eur J Med Chem. 2010 May;45(5):1873-9. doi: 10.1016/j.ejmech.2010.01.026. Epub 2010 Jan 20.
Aziridinyl substituted benzimidazolequinones are more toxic than methoxy analogues towards normal human fibroblast cells (GM00637). The aziridinyl substituent is required for hypersensitive killing of Fanconi anaemia (FA) cells (PD20i) deficient in FANCD2. Despite lacking quinone functionality, 4,7-dimethoxy-N-[(aziridin-2-yl)methyl]benzimidazole also induces hypersensitivity from FA cells, similar to their response towards mitomycin C. Expression of FANCD2 (in PD20:RV) corrects FA cell hypersensitivity supporting cellular response via the FANC pathway.
氮丙啶取代的苯并咪唑醌比甲氧基类似物对正常人成纤维细胞（GM00637）更具毒性。氮丙啶取代基是导致 Fanconi 贫血（FA）细胞（PD20i）中 FANCD2 缺陷细胞超敏杀伤所必需的。尽管缺乏醌功能，但 4,7-二甲氧基-N-[(氮丙啶-2-基)甲基]苯并咪唑也会引起 FA 细胞的超敏反应，类似于它们对丝裂霉素 C 的反应。FANCD2 的表达（在 PD20：RV 中）纠正了 FA 细胞的超敏反应，通过 FANC 途径支持细胞反应。
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