Krisch R E, Krasin F, Sauri C J
Curr Top Radiat Res Q. 1978 Jan;12(1-4):355-68.
Effects of 125I decay in DNA were investigated by measurements of strand breaks and lethal efficiencies of the decays. In bacteriophages T1 and T4, local decay effects were compared with effects of the emitted electrons by induction of both single (ssb) and double strand breaks (dsb) in the intact phage head and in extended free state DNA. Most dsbs were found to result from local decay effects whereas most real ssbs are caused by the electrons. A simple one-to-one relationship seems to exist in the phages between the decays of 125I, numbers of dsbs and lethal effects. In E. coli rec+ and recA repair of dsbs was studied in addition to lethal decay efficiencies. In rec+ more than 70% of the dsbs were repaired within 1 h at 37 degrees C. No repair was observed in recA. The probability of lethality per 125I decay per completed genome was found to be 0.37 for rec+ and 0.93 for recA cells. The number of lethal events per unrepaired dsb was found to be practically equal to unity. Unrepaired dsbs thus seem to be the primary mechanism of lethality caused by 125I decay, and all unrepaired dsbs seem to be lethal.
通过测量链断裂和衰变的致死效率，研究了125I在DNA中的衰变效应。在噬菌体T1和T4中，通过在完整噬菌体头部和延伸的游离状态DNA中诱导单链断裂（ssb）和双链断裂（dsb），比较了局部衰变效应与发射电子的效应。发现大多数dsb是由局部衰变效应导致的，而大多数真正的ssb是由电子引起的。在噬菌体中，125I的衰变、dsb的数量和致死效应之间似乎存在简单的一一对应关系。除了致死衰变效率外，还研究了大肠杆菌rec+和recA中dsb的修复情况。在rec+中，超过70%的dsb在37℃下1小时内得到修复。在recA中未观察到修复。发现rec+细胞每完成一个基因组的125I衰变致死概率为0.37，recA细胞为0.93。发现每个未修复的dsb的致死事件数实际上等于1。因此，未修复的dsb似乎是125I衰变导致致死的主要机制，并且所有未修复的dsb似乎都是致死的。
