Therapeutic Nuclear Medicine

Part of the series Medical Radiology pp 789-805


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

  • Ludwig E. FeinendegenAffiliated withHeinrich-Heine-UniversityBrookhaven National Laboratory Email author 
  • , Myron PollycoveAffiliated withSchool of Medicine, University of California San Francisco
  • , Ronald D. NeumannAffiliated withRadiology and Imaging Sciences, Clinical Center, The National Institutes of Health


Ionizing radiation primarily perturbs the basic molecular level proportional to dose, with potential damage propagation 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. Physical 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 differentiation-senescence, or by immune responses,—followed by replacement of lost elements. Another metabolic-dynamic defense arises delayed by up-regulating immediately operating defense mechanisms. Some of these adaptive protections may last beyond a year and all create temporary protection against renewed potentially 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.


Low-dose cancer risk Adaptive protections Hormesis