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评价1,4-二-[[2-(二甲氨基-N-氧化物)乙醇]氨基]5,8-双羟基氧化蒽-9,10-二酮((1,4-bis-{[2-(dimethylamino-N-oxide)ethyl]amino}-5,8-dihydroxyanthracene-9,10dione),AQ4N)辐射增敏效果和乏氧选择性,分析一氧化氮合成酶(Induciblenitrogenmonoxidesynthase,iNOS)对AQ4N代谢活化的影响和作用特点。结果显示AQ4N是一种低毒性的化合物,仅在乏氧条件显示较弱的细胞毒性,可以引起肿瘤细胞凋亡。AQ4N对肿瘤细胞尤其是乏氧肿瘤细胞具有良好的辐射增敏作用。同亲本细胞相比,iNOS基因转染的细胞克隆,仅在乏氧条件下显示出对AQ4N化学敏感性的增强和细胞的G2/M期阻滞。提示iNOS仅在乏氧条件下参与AQ4N的代谢活化过程。
Synthesis of 1,4-bis- [[2- (dimethylamino- N-oxide) ethanol] amino] 5,8-bishydroxy anthracene-9,10-dione (Dimethylamino-N-oxide) ethyl] amino} -5,8-dihydroxyanthracene-9,10 dione), AQ4N) radiation sensitivity and hypoxia selective nitric oxide synthase (iNOS) Metabolic activation of the impact and role characteristics. The results show that AQ4N is a low toxicity compound that shows weak cytotoxicity only under hypoxic conditions and can cause tumor cell apoptosis. AQ4N on tumor cells, especially hypoxia tumor cells have a good radiosensitization. Cell clones transfected with iNOS genes showed enhanced chemosensitivity to AQ4N and G2 / M arrest in cells only under hypoxic conditions compared to parental cells. Suggesting that iNOS is involved in the metabolic activation of AQ4N only under hypoxic conditions.