Hormesis by Low Dose Radiation Effects: Low-Dose Cancer Risk Modeling Must Recognize Up-Regulation of Protection

Abstract

Ionizing radiation primarily perturbs the basic molecular level proportional to dose, with potential damage prop- agation to higher levels: cells, tissues, organs, and whole body. There are three types of defenses against damage propagation. These operate deterministically and below a certain impact threshold there is no propagation. Phys- ical static defenses precede metabolic-dynamic defenses acting immediately: scavenging of toxins;—molecular repair, especially of DNA;—removal of damaged cells either by apoptosis, necrosis, phagocytosis, cell differ- entiation-senescence, or by immune responses,—fol- lowed by replacement of lost elements. Another metabolic-dynamic defense arises delayed by up-regu- lating immediately operating defense mechanisms. Some of these adaptive protections may last beyond a year and all create temporary protection against renewed poten- tially toxic impacts also from nonradiogenic endogenous sources. Adaptive protections have a maximum after single tissue absorbed doses around 100–200 mSv and disappear with higher doses. Low dose-rates initiate maximum protection likely at lower cell doses delivered repetitively at certain time intervals. Adaptive protection preventing only about 2–3 % of endogenous lifetime cancer risk would fully balance a calculated-induced cancer risk at about 100 mSv, in agreement with epidemiological data and concordant with an hormetic effect. Low-dose-risk modeling must recognize up-regulation of protection.