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.