Ikebuchi M, Kimura H
Department of Experimental Radiology, Shiga University of Medical Science, Otsu, Japan.
Radiat Res. 1998 Oct;150(4):416-22.
We previously showed that 0.23 M NaCl was able to fix slowly repairing potentially lethal damage (PLD), and that this slowly repairing PLD is distinct from rapidly repairing PLD that is sensitive to 0.5 M NaCl (Ikebuchi et al., Radiat. Res. 141, 19-27, 1995). In the present study, the effect of 0.23 M NaCl on repair of sublethal damage (SLD) was examined in cells of three rodent cell lines with normal radiosensitivity (Chinese hamster V79, BALB/c 3T3, RD13B2) and two radiosensitive lines derived from severe combined immunodeficient (scid) mice. Repair of SLD was detected as an increase in survival when the radiation dose was fractionated with an interval of incubation between the two doses. Repair of SLD occurred in V79 and BALB/c 3T3 cells but did not occur in the two scid cell lines which were defective in repair of double-strand breaks (DSBs), demonstrating that repair of DSBs is involved in repair of SLD. This was confirmed by the observation that repair of SLD occurred in RD13B2 cells, the scid line which had regained the ability to repair DSBs. When the V79 and BALB/c 3T3 cells were treated with 0.23 M NaCl during the interval between the split doses, repair of SLD was completely inhibited. On the other hand, repair of SLD occurred when the cells were incubated in culture medium between the treatment with 0.23 M NaCl and the second dose. From these observations, it is concluded that the inhibition of repair of SLD by 0.23 M NaCl is reversible, which is in contrast to the irreversible inhibition of repair of PLD by 0.23 M NaCl found previously. In addition, the fact that scid cells that were shown to have the ability to repair PLD that is sensitive to 0.23 M NaCl had little capacity to repair SLD suggests that there may be different processes involved in the two types of cellular repair.
我们之前的研究表明，0.23M的NaCl能够修复缓慢修复的潜在致死性损伤（PLD），并且这种缓慢修复的PLD与对0.5M NaCl敏感的快速修复的PLD不同（池内等人，《辐射研究》141卷，第19 - 27页，1995年）。在本研究中，我们检测了0.23M NaCl对三种具有正常放射敏感性的啮齿动物细胞系（中国仓鼠V79、BALB/c 3T3、RD13B2）以及两种源自严重联合免疫缺陷（scid）小鼠的放射敏感细胞系亚致死性损伤（SLD）修复的影响。当辐射剂量进行分割且两次剂量之间有孵育间隔时，SLD的修复表现为存活率增加。V79和BALB/c 3T3细胞中发生了SLD的修复，但在双链断裂（DSB）修复存在缺陷的两种scid细胞系中未发生，这表明DSB的修复参与了SLD的修复。这一点在RD13B2细胞（已恢复DSB修复能力的scid细胞系）中SLD修复的观察结果中得到了证实。当V79和BALB/c 3T3细胞在分割剂量之间的间隔期用0.23M NaCl处理时，SLD的修复被完全抑制。另一方面，当细胞在0.23M NaCl处理和第二次剂量之间在培养基中孵育时，SLD的修复发生了。从这些观察结果可以得出结论，0.23M NaCl对SLD修复的抑制是可逆的，这与之前发现的0.23M NaCl对PLD修复的不可逆抑制形成对比。此外，已证明对0.23M NaCl敏感的PLD具有修复能力的scid细胞几乎没有SLD修复能力这一事实表明，两种类型的细胞修复可能涉及不同的过程。
