Preston R J
Mutat Res. 1980 Jan;69(1):71-9. doi: 10.1016/0027-5107(80)90177-3.
The yield of X-ray-induced chromosome aberrations in unstimulated human lymphocytes is greatly enhanced when the cells are incubated with cytosine arabinoside (ara-C) after irradiation. There is an increase in aberration yield with increasing time of incubation in ara-C (1, 2 or 3 h). When G2 cells are X-irradiated and incubated with ara-C until fixation, the deletion yields are considerably increased, but no interchanges are observed. In the absence of ara-C, 0.29 interchanges per cell were observed. The G2 results suggest that ara-C inhibits the repair of damage that leads to the formation of exchange aberrations. The increase in yield in unstimulated lymphocytes is interpreted to be due to an accumulation of strand breaks caused by ara-C inhibition of repair; when the inhibition is reversed with deoxycytidine, these breaks can interact to form aberrations. A possible mechanism for the induction of chromosome aberrations by X-rays is offered on the basis of these results.
当未受刺激的人类淋巴细胞在照射后与阿糖胞苷（ara-C）一起孵育时，X射线诱导的染色体畸变率会大大提高。随着在ara-C中孵育时间（1、2或3小时）的增加，畸变率会升高。当G2期细胞受到X射线照射并与ara-C一起孵育直至固定时，缺失率会显著增加，但未观察到互换。在没有ara-C的情况下，每个细胞观察到0.29次互换。G2期的结果表明，ara-C抑制了导致交换畸变形成的损伤修复。未受刺激的淋巴细胞中畸变率的增加被解释为是由于ara-C对修复的抑制导致链断裂的积累；当用脱氧胞苷逆转这种抑制时，这些断裂可以相互作用形成畸变。基于这些结果，提出了一种X射线诱导染色体畸变的可能机制。
