Ionizing Radiation, DNA Double Strand Break and Mutation

Abstract

Ionizing radiation has been proved a major stress that can induce carcinogenesis. Nuclear DNA is the main target of ionizing radiation, exposure of which is followed by many types of DNA damages. DNA double-strand breaks (DSBs) induced by ionizing radiation are considered the most relevant lesion for mutations and carcinogenesis, and unrepaired or misrepaired DSBs are a serious threat to genomic integrity. The increased mutation induced by radiation has been proved to be tightly associated with carcinogenesis. Radiation-induced bystander effect (RIBE), which was found in the 1990s, challenged the conventional dogma that no effects were expected in the cell population that had not been exposed to radiation. With the RIBE, the irradiated cells could secret some signal factor(s) to affect the nearby non-irradiated cells or cells that had received the transferred conditioned medium, and then to induce DSBs, mutation and cell death etc. in the non-irradiated cells. As such, RIBE “enlarges” the area or the target of bio-effect of radiation from the directly irradiated cells to non-irradiated cells surrounding or even away from the irradiated cells, with the effect particularly significant in the low radiation-dose regime. The existence of RIBE led to a non-linear relationship between the cancer risk and the radiation dose (in the low-dose regime). Studies on the mechanism underlying RIBE have also enlightened us on directions to radiation protection against low-dose environmental radiation as well as during radiotherapy.