Grimmond H E, Beerman T
Biochem Pharmacol. 1982 Nov 1;31(21):3379-86. doi: 10.1016/0006-2952(82)90615-3.
The results reported in this paper show the changes in chromatin structure caused by the binding of adriamycin (ADR), daunorubicin (DR) and ethidium bromide (EtdBr) to DNA in chromatin, either isolated or in nuclei or whole cells. Micrococcal nuclease was used as the structural probe of chromatin. The binding of the drugs to chromatin DNA induced two structural changes. First, it produced an unfolding of the overall chromatin structure as evidenced by the increased production of acid-soluble oligonucleotides for the drug-treated samples above the level of the control sample. Second, it caused a disruption of the core particle structure with increased production of DNA of subnucleosomal size and smearing of the nucleosome pattern. The effects were greatest for duanorubicin, followed by adriamycin and ethidium bromide.
本文报道的结果显示了阿霉素（ADR）、柔红霉素（DR）和溴化乙锭（EtdBr）与染色质中的DNA结合，无论是在分离的染色质、细胞核还是全细胞中，所引起的染色质结构变化。微球菌核酸酶被用作染色质的结构探针。药物与染色质DNA的结合诱导了两种结构变化。首先，它导致整体染色质结构展开，这可通过药物处理样品的酸溶性寡核苷酸产量高于对照样品水平来证明。其次，它导致核心颗粒结构破坏，亚核小体大小的DNA产量增加，核小体模式出现拖尾。柔红霉素的作用最大，其次是阿霉素和溴化乙锭。
