Heat effects on the repair of DNA double-strand breaks in CHO cells

Heat effects on the repair of DNA double-strand breaks in CHO cells
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DOI:
10.1080/095530097143392
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发表时间:
1997-08-01
影响因子:
2.6
通讯作者:
Dikomey, E
Dikomey, E
中科院分区:
医学3区
文献类型:
--
作者:
DahmDaphi, J;Brammer, I;Dikomey, E

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采用恒场凝胶电泳法研究了60戈伊X射线照射CHO细胞后,热(43-45 ℃)对DNA双链断裂(dsb)诱导和修复的影响。在辐照前加热,辐照后立即测量,发现不改变dsb的数量。在非加热的细胞中,约80%的所有dsb迅速修复的半衰期为4分钟,而20%的修复更慢,T-1/2=160分钟。这些动力学被热严重改变。快速和缓慢的过程都被推迟了。然而,热的主要影响是缓慢重新加入的dsb的数量增加。这种增加被证明是由于在修复过程中早期额外形成的dsb(高达初始数量的1.4倍)。这表明,额外的dsb引起的基础损伤,修复是不平衡的热。没有发现凋亡参与这一过程的证据。额外的dsb的动力学被发现与热辐射增敏。
The effect of heat (43-45 degrees C) on the induction and the repair of DNA double-strand breaks (dsb) was studied in CHO cells after 60 Gy of X-rays using constant-field gel electrophoresis. Heat given prior to irradiation was found not to alter the number of dsb when measured immediately after irradiation. In non-heated cells, about 80% of all dsb were rapidly repaired with a half-time of 4 min, while 20% were repaired more slowly with T-1/2=160 min. These kinetics were grossly altered by heat. Both the fast and the slow process were retarded. However, the main effect of heat was an increase in the number of slowly rejoined dsb. This increase was shown to result from the additional formation (up to 1.4-fold the initial number) of dsb early during the repair course. It is suggested that the additional dsb arose from base damage, the repair of which was unbalanced by heat. No evidence was found for apoptosis being involved in this process. The kinetics of the additional dsb was found to correlate with thermal radiosensitization.