Warters R L, Barrows L R, Chen D J
Department of Radiology, University of Utah Health Sciences Center, Salt Lake City 84132.
Mutat Res. 1995 Jan;336(1):1-7.
The capacity of two radiation-sensitive clones (SX9 and SX10) of the mouse mammary carcinoma cell line SR1 to rejoin radiation-induced DNA double-strand breaks (DSBs) was determined by pulsed-field agarose gel electrophoresis. DSBs were produced with equivalent efficiency in all three cell lines. Both the SX9 and SX10 cell lines demonstrated a significantly diminished capacity to rejoin radiation-induced DSBs. The fraction of the original DNA DSB damage remaining in the DNA of 20 Gy-exposed SR1, SX9 and SX10 cells after 6 h of 37 degrees C incubation was estimated to be 14, 82 and 54%, respectively. In addition the SX10 cell line exhibited enhanced cytotoxicity when exposed to the DNA topoisomerase II poison mitoxantrone. The results indicate that both the SX9 and SX10 cell lines are DNA DSB repair mutants.
通过脉冲场琼脂糖凝胶电泳法测定了小鼠乳腺癌细胞系SR1的两个辐射敏感克隆（SX9和SX10）修复辐射诱导的DNA双链断裂（DSB）的能力。在所有这三种细胞系中，DSB的产生效率相当。SX9和SX10细胞系修复辐射诱导的DSB的能力均显著降低。在37℃孵育6小时后，20 Gy照射的SR1、SX9和SX10细胞的DNA中，残留的原始DNA DSB损伤比例分别估计为14%、82%和54%。此外，当暴露于DNA拓扑异构酶II毒药米托蒽醌时，SX10细胞系表现出增强的细胞毒性。结果表明，SX9和SX10细胞系均为DNA DSB修复突变体。
