Bresler S E, Noskin L A, Stepanova I M, Kuzovleva N A
Mol Gen Genet. 1978 Jul 6;163(1):75-85. doi: 10.1007/BF00268966.
The effect of radioprotection of indolylalkylamines (5-methoxytryptamine) and aminothiols (cysteamine) on E. coli cells is practically absent if the cells have genetic defects in the repair systems. This means that the explanation of radioprotection by scavenging of free radicals is invalid and that specific repair mechanisms may be involved. In order to explain the radioprotective mechanism it was suggested that the radioprotectors interact with the damaged sites in DNA so that they become partly screened from repairing endonucleases. Under these conditions the reduction of incision rate results in diminished enzymatic induction of lethal double-strand breaks in DNA, this being important only in wild type cells. To prove this hypothesis an experimental procedure was developed using bacterial cells carrying plasmids (ColE1). This procedure enabled to determine the in vivo rate of enzymatic incision of gamma-sites. It was found that the protectors did not change the total amount of gamma-damages in DNA but reduced the rate of enzymatic incision.
如果大肠杆菌细胞在修复系统中存在基因缺陷，吲哚烷基胺（5-甲氧基色胺）和氨基硫醇（半胱胺）对其细胞的辐射防护作用实际上就不存在。这意味着通过清除自由基来解释辐射防护是无效的，并且可能涉及特定的修复机制。为了解释辐射防护机制，有人提出辐射防护剂与DNA中的损伤位点相互作用，从而使它们部分地免受修复内切酶的作用。在这些条件下，切口速率的降低导致DNA中致死性双链断裂的酶促诱导减少，这仅在野生型细胞中很重要。为了证明这一假设，开发了一种使用携带质粒（ColE1）的细菌细胞的实验程序。该程序能够确定体内γ位点的酶切速率。结果发现，防护剂并没有改变DNA中γ损伤的总量，但降低了酶切速率。
