Tanooka H
Genetics Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
Int J Radiat Biol. 2001 May;77(5):541-51. doi: 10.1080/09553000110034612.
To discuss the threshold dose problem in radiation carcinogenesis after a review of the present author's experimental data on mouse tumour induction by chronic beta-irradiation and other relevant data.
A threshold dose-response in radiation carcinogenesis appears in certain tissues and under certain conditions. The optimum condition for demonstrating an apparent threshold is with partial-body chronic or repeated radiation rather than with acute whole-body radiation. Its possible mechanism is host tolerance, involving DNA repair, apoptosis and an immune response activated by low radiation doses. This tolerance level was examined by a survey in the literature of non-tumour-inducing doses, D(nt), the highest dose at which no significant increase of tumours was observed above the control level.