The advances of research on hyperradiation sensitivity and induced radioresistance

Low dose hyperradiation sensitivity (HRS) and induced radioresistance (IRR) are two important phenoma in radiobiology. Illustrating the mechanism of HRS/IRR is important to radiation protection, tumor control and creation new functional materials. Radiation-induced DNA double-strand breaks (DSBs) is primer lesions in radiation-induced inactivation, and failure repair of (or misrepair of) DSBs is a prime cause of cell death. Low-dose hyperradiation sensitivity is more prominent in G2 phase cells compared with cells in G1 or S phase. The mechanism regulating the transition between HRS and IRR is likely to be due to an active process occurring in a small fraction of G2-phase cells. DNA repair plays an important role during HRS/IRR. When the radiation dose was lower than 20 cGy, radiation led to less efficient damage response (HRS). When the dose was higher than 20 cGy, DNA double strands broke. ATM and G2 phase specific checkpoint were activated. Cell cycle was arrested. DNA repair and cell survival were promoted, IRR appeared at this time. Although lots of results had been got, many problems were still remained. For example, why some cell lines had HRS/IRR, while others not; whether there was mutated HRS/IRR corresponding to single dose or not. These problems are likely to be the future research directions. (authors)