Purpose: It is proposed that the development and progression of radiation‐induced late effects are driven, in part, by chronic oxidative stress. This mini‐review presents data to support this hypothesis and provides the foundation for antioxidant‐based interventional approaches directed at modulating late normal tissue injury.

Conclusions: Although a causal link between chronic oxidative stress and radiation‐induced late normal tissue injury remains to be established, a growing body of evidence appears to support the hypothesis that chronic oxidative stress might serve to drive the progression of radiation‐induced late effects. The similarity between chronic tissue injury, chronic inflammation and fibrosis observed in a variety of disease states, including radiation late effects, is provocative and offers the opportunity to apply antioxidant‐based therapies to mitigate and/or treat late radiation‐induced normal tissue injury.