Low-dose radiation triggers a strategic purge where tissues sacrifice their most damaged cells to keep the rest of the organ healthy.
Exposure to small amounts of radiation was long viewed as a series of random cellular accidents. Tissues actually employ an evolved defense mechanism that identifies and eliminates cells with high mutational loads. This hyper-radiosensitivity ensures that genetic errors do not accumulate and lead to cancer later in life. By killing off the weak links, the body maintains the long-term genetic integrity of the entire organ. This discovery changes how we view the risks of medical imaging and environmental radiation exposure.
Minimising mutation load as a mechanism for low-dose hyper-radiosensitivity and induced radioresistance
research_square · rs-6674497
Abstract Low-dose hyper-radiosensitivity (HRS) and induced radioresistance (IRR) are unexpected features of cellular survival curves that challenge classical radiobiological models. While often interpreted phenomenologically, their underlying biological purpose remains unclear. Here we propose that these effects reflect an evolved strategy by which tissues minimise mutational burden through context-dependent cell elimination. We introduce the Minimum Mutation Load (MML) model, a mechanistic fram