Bryant P E
Int J Radiat Biol Relat Stud Phys Chem Med. 1983 Apr;43(4):459-64. doi: 10.1080/09553008314550521.
Treatment of X-irradiated stationary Ehrlich ascites tumour cells with the DNA synthesis inhibitor beta-ara A (120 mumol/l, 30 min before and for 7 hours after irradiation) is shown to lead to a large increase in the incidence of anaphase chromosome abnormalities (anaphase bridges and fragments) at the first mitosis following irradiation. This increase is similar to the increase in cell killing observed for this cell line when treated with beta-ara A under the same conditions (Iliakis 1980). The results suggest that the increased frequency of chromosome abnormalities caused by beta-ara A may result not only from the inhibition of DNA double strand break repair, leading to additional unrepaired d.s.b. (Bryant and Blöcher 1982) and chromosome deletions, but also from an increase in the frequency of misrepair of d.s.b. leading to exchange aberrations.
用DNA合成抑制剂β-阿拉伯糖腺苷（120微摩尔/升，在照射前30分钟及照射后7小时）处理经X射线照射的静止期艾氏腹水瘤细胞，结果显示在照射后的第一次有丝分裂中，后期染色体异常（后期桥和片段）的发生率大幅增加。这种增加类似于在相同条件下用β-阿拉伯糖腺苷处理该细胞系时观察到的细胞杀伤增加情况（伊利亚基斯，1980年）。结果表明，β-阿拉伯糖腺苷导致的染色体异常频率增加，可能不仅源于对DNA双链断裂修复的抑制，从而导致额外的未修复双链断裂（布莱恩特和布洛彻，1982年）以及染色体缺失，还源于双链断裂错配修复频率的增加，进而导致交换畸变。
