Abstract
As for low-LET radiation, we previously reported that challenge irradiation after pre-irradiation at a low dose or a low dose-rate resulted in lower levels of p53 accumulation and apoptosis incidence than those observed after the challenge irradiation alone in human cultured cells and mice spleen. In this study, to clarify the LET dependency in radioadaptive response, wild-type p53 cells (H1299/wtp53) were irradiated with X-rays (7.5 Gy) 0-18 h after pre-irradiation with X-rays or 70 KeV/µm Carbon-beams at low doses (0-0.50 Gy). On the other hand, p53 deficient cells (H1299/neo) were irradiated with 70 KeV/µm Carbon-beams (4 Gy) 0-18 h after pre-irradiation with X-rays or 70 KeV/µm Carbon-beams at low doses (0-0.50 Gy). The cells were fixed 48 h after the challenge irradiation. Apoptosis incidence was measured by Hoechst33342 staining. We found the suppression of apoptosis induced with X-rays 3-9 h after pre-irradiation with X-rays (0.01-0.05 Gy) to H1299/wtp53 cells but not Carbon-beams. In contrary, we did not find the suppression of apoptosis induced with Carbon-beams after pre-irradiation with X-rays or Carbon-beams in H1299/neo cells. >From these findings, we assume that high-LET radiation induces irreparable DNA damage, because we did not observe the radioadaptive response in the cells exposed to high-LET radiation.
