H Tanooka1. 1. Genetics Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan. htanooka@ncc.go.jp
Abstract
PURPOSE: 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. CONCLUSIONS: 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.
PURPOSE: To discuss the threshold dose problem in radiation carcinogenesis after a review of the present author's experimental data on mousetumour induction by chronic beta-irradiation and other relevant data. CONCLUSIONS: 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.
Authors: Yehoshua Socol; Ludwik Dobrzyński; Mohan Doss; Ludwig E Feinendegen; Marek K Janiak; Mark L Miller; Charles L Sanders; Bobby R Scott; Brant Ulsh; Alexander Vaiserman Journal: Dose Response Date: 2013-11-07 Impact factor: 2.658