Perticone P, Palitti F, Cozzi R, D'Erme M, Bona R
Centro di Genetica Evoluzionistica del CNR, Università La Sapienza, Rome, Italy.
Mutat Res. 1990 Nov;245(3):211-5. doi: 10.1016/0165-7992(90)90052-l.
Many carcinogenic agents are able to affect the methylation level in mammalian cells cultivated in vitro. The capacity of azacytidine (AZA) to demethylate DNA can be used to examine the relationship between the genomic methylation level and cytogenetic end-points. Here we compared the sister-chromatid exchange (SCE) level with the genomic % methylcytosine in a Chinese hamster ovary cell line in vitro after giving a single 10-microM pulse of AZA. Both parameters were followed up to 16 cell cycles after the agent was removed. While the SCE level increased starting 2 cycles from the treatment and persisted for the entire 16 cycles, the methylcytosine level, after an initial 50% decrease, approached the control value, completely returning to it after 10 cell cycles. The possibility that the persistence in the SCE increase is an inherited phenomenon is discussed.
许多致癌剂能够影响体外培养的哺乳动物细胞中的甲基化水平。氮杂胞苷(AZA)使DNA去甲基化的能力可用于研究基因组甲基化水平与细胞遗传学终点之间的关系。在此,我们在给予单次10微摩尔的AZA脉冲后,比较了体外培养的中国仓鼠卵巢细胞系中姐妹染色单体交换(SCE)水平与基因组甲基胞嘧啶百分比。在去除该试剂后,对这两个参数进行了长达16个细胞周期的跟踪。虽然SCE水平从处理后第2个周期开始增加,并在整个16个周期中持续存在,但甲基胞嘧啶水平在最初下降50%后,接近对照值,在10个细胞周期后完全恢复到对照值。文中讨论了SCE增加持续存在是一种遗传现象的可能性。