Radiation-hormesis phenotypes, the related mechanisms and implications for disease prevention and therapy

Abstract

Humans are continuously exposed to ionizing radiation throughout life from natural sources that include cosmic, solar, and terrestrial. Much harsher natural radiation and chemical environments existed during our planet’s early years. Mammals survived the harsher environments via evolutionarily‐conserved gifts ̶ a continuously evolving system of stress‐induced natural protective measures (i.e., activated natural protection [ANP]). The current protective system is differentially activated by stochastic (i.e., variable) low‐radiation‐dose thresholds and when optimally activated in mammals includes antioxidants, DNA damage repair, p53‐related apoptosis of severely‐damaged cells, reactive‐oxygen‐species (ROS)/reactive‐nitrogen‐species (RNS)‐ and cytokine‐regulated auxiliary apoptosis that selectively removes aberrant cells (e.g., precancerous cells), suppression of disease promoting inflammation, and immunity against cancer cells. The intercellular‐signaling‐based protective system is regulated at least in part via epigenetic reprogramming of adaptive‐response genes. When the system is optimally activated, it protects against cancer and some other diseases, thereby leading to hormetic phenotypes (e.g., reduced disease incidence to below the baseline level; reduced pain from inflammation‐related problems). Here, some expressed radiation hormesis phenotypes and related mechanisms are discussed along with their implications for disease prevention and therapy.

Sustained Lower Incidence of Thyroid Cancer in West Cumbria, UK

“…Epigenetic changes take place in response to (long-term) low dose radiation exposure, resulting in induction of a term coined activated natural protection by Scott [13]. In essence, a cluster of different cell defence mechanisms are activated to protect cells and DNA in particular -examples include increased antioxidants, activation of DNA repair genes, programmed cell death (apoptosis) of irreversibly damaged cells, and modulation of inflammatory pathways [13]. Taken together, these cellular processes have the potential to reduce the risk of cells becoming cancerous.…”

Estimation of occupational compensation based on a linear-quadratic methodology for the nuclear industry

“…The radiation hormesis model states that low dose radiation stimulates intrinsic cellular defence mechanisms that protect the organism against the development of cancer. This was initially proposed in the late 1950s and is gaining increasing support (Tubiana et al, 2009;Scott, 2014;Doss, 2013). The well-known effects of cell/tissue damage and cancer development are produced only by higher radiation doses.…”

“…Microhomology-mediated end joining, homologous recombination and non-homologous end joining mechanisms repair the damaged double strand breaks (DSB) of DNA (Scott, 2014).…”

The CGL1 (HeLa × Normal Skin Fibroblast) Human Hybrid Cell Line: A History of Ionizing Radiation Induced Effects on Neoplastic Transformation and Novel Future Directions in SNOLAB

“…The linear no threshold model proposes that cancer risk increases with radiation dose in a linear relationship while the threshold model infers that below a certain dose there is no increased risk (114). The hormetic model suggests that below a given dose, instead of increased risk, the health effects may be prophylactic (115). However, all of these models inherently include NBR exposure and consequently there is a deficit in our understanding of the biological effects of ionizing radiation exposure at levels sub-NBR.…”