抄録
Low doses in vitro and in vivo induce an adaptive response that reduces both radiation-induced and spontaneous risks. A single low dose of low LET radiation increased the latency (with no change in frequency) of radiation-induced or spontaneous cancer in both normal and cancer prone (Trp53 heterozygous) mice. A prior low dose given during the time of fetal organ development lowered the risk of radiation-induced birth defects, and a low dose prior to a high dose protected the offspring of male mice from heritable mutations produced by a subsequent large dose. Chronic exposures protected against age related ulcerative dermatitis in Trp53 normal (but not Trp53 heterozygous) mice. These observations challenge the Linear No Threshold Hypotheses and other principles and practices used for radiation protection. Dose thresholds for increased risk of cancer are apparent. Below those dose thresholds overall risk is reduced below that of the unexposed controls, indicating that dose rate reduction factors (DDREF) approach infinity. Different tissues have different thresholds for detriment, indicating that individual tissue weighting factors (WT) are also not constant. Because risk from low LET radiation is not constant with dose, and dose responses from high LET are non-linear due to detrimental bystander effects, radiation-weighting factors (WR) for high LET radiation cannot be constant at low dose.
