Biological basis for radiation hormesis in mammalian cellular communities

It is now known that low doses and dose rates of certain agents (e.g., radiation and genotoxic chemicals) can induce protective processes that together lead to a reduction in mutations and neoplastic transformation below the spontaneous frequency in mammalian in vitro and in vivo cellular communities. However, after high doses, some of the protection is lost, leading to elevated risks relative to the background risk. The indicated pattern of induced protection is a form of radiation hormesis (low-dose stimulation and high-dose suppression of protective processes). In this paper, a modified existing dose-response model (NEOTRANS3) is summarised which provides a biological basis for radiation hormesis for specific stochastic radiobiological effects (mutations, neoplastic transformation and cancer). Implications for low-dose cancer risk assessment, cancer prevention, cancer therapy and lifespan lengthening are discussed.