Abstract
The risks of exposure to low dose ionizing radiation (below 100 mSv) are estimated by extrapolating from data obtained after exposure to high dose radiation, using a linear no-threshold model (LNT model). However, the validity of using this dose-response model is controversial because evidence accumulated over the past decade has indicated that living organisms, including humans, respond differently to low dose/low dose-rate radiation than they do to high dose/high dose-rate radiation. In other words, there are accumulated findings which cannot be explained by the classical "target theory" of radiation biology. The radioadaptive response, radiation-induced bystander effects, low-dose radio-hypersensitivity, and genomic instability are specifically observed in response to low dose/low dose-rate radiation, and the mechanisms underlying these responses often involve biochemical/molecular signals that respond to targeted and non-targeted events.
Recently, correlations between the radioadaptive and bystander responses have been increasingly reported. We found that nitric oxide is an initiator for radiation-induced adaptive and bystander responses (Int. J. Radiat. Biol., 76: 1649-1657, 2000; Radiat. Res., 155: 387-396, 2001; Cancer Res., in press. 2007). This presentation focuses on the two phenomena, radioadaptive and bystander responses, by summarizing observations supporting their existence, and discussing the linkage between them from the aspect of production of reactive oxygen and nitrogen species.
