Cherry L M, Hsu T C
Environ Mutagen. 1982;4(3):259-65. doi: 10.1002/em.2860040308.
Although actinomycin D (AMD) appears to cause chromatid breakage, it has been suggested that it merely weakens the chromosomal proteins, causing breaks to occur during the stress of fixation. To determine if this was true, we examined lymphocytes treated with AMD (3.5 micrograms/ml) for 90 min prior to harvesting for evidence of DNA repair. Besides single chromatid breaks, we observed a high frequency of chromatid exchange figures (translocations, inversions, rings) and closed isochromatid breaks, indicating that a type of DNA repair leading to chromosome aberration had occurred prior to cell fixation. Therefore, at least some of the breaks observed after AMD treatment in G2 represented true DNA damage and were not merely artifacts of fixation.
尽管放线菌素D（AMD）似乎会导致染色单体断裂，但有人提出它只是削弱了染色体蛋白，导致在固定应激过程中发生断裂。为了确定这是否属实，我们在收获细胞前检查了用AMD（3.5微克/毫升）处理90分钟的淋巴细胞，以寻找DNA修复的证据。除了单条染色单体断裂外，我们还观察到染色单体交换图形（易位、倒位、环状）和闭合等臂染色单体断裂的高频率出现，这表明在细胞固定之前就已经发生了一种导致染色体畸变的DNA修复类型。因此，在G2期AMD处理后观察到的至少一些断裂代表了真正的DNA损伤，而不仅仅是固定的假象。
