radiationsensitivity

Radiation sensitivity refers to the relative susceptibility of cells, tissues, or organisms to damage from ionizing radiation. It influences the likelihood of cell death, tissue injury, mutagenesis, and cancer risk following exposure. Sensitivity varies among cell types and conditions and is shaped by intrinsic factors and the environment.

Determinants include DNA repair capacity, cell-cycle stage, and oxygenation. Cells with efficient DNA repair, or those in certain phases of the cell cycle, may be more resistant, while hypoxic conditions often reduce damage due to the lack of oxygen radicals. Apoptosis, senescence pathways, chromatin structure, and genetic status (such as p53) also affect sensitivity. Inheritable conditions like ataxia-telangiectasia confer higher sensitivity, whereas some tumors exhibit intrinsic radiosensitivity or radioresistance that influences treatment response.

Radiation sensitivity is commonly quantified with survival curves from clonogenic assays and described by radiobiological models such as the linear-quadratic model. Parameters like D0, Dq, and the alpha/beta ratio summarize the curve’s shape and help compare tissues or tumors. Clinically, differences in sensitivity guide radiotherapy planning (fractionation, dose delivery) to maximize tumor control while limiting normal-tissue injury, and inform radiation protection standards for workers and the public.

In practice, tissue and individual sensitivity reflect a complex mix of genetic, cellular, and microenvironmental factors. The concept encompasses stochastic late effects, such as cancer risk, and deterministic early effects, such as acute tissue damage, each with distinct dose–response behaviors. Understanding radiosensitivity supports safer imaging, occupational guidelines, and personalized cancer therapy.