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Recent results from animal irradiation studies have rekindled interest in thepotential of ultra-high dose rate irradiation (also known as FLASH) forreducing normal tissue toxicity. However, despite mounting evidence of a "FLASHeffect", a mechanism has yet to be elucidated. This article hypothesizes thatthe radioprotecting effect of FLASH irradiation could be due to the specificsparing of hypoxic stem cell niches, which have been identified in severalorgans including the bone marrow and the brain. To explore this hypothesis, anew computational model is presented that frames transient radiolytic oxygendepletion (ROD) during FLASH irradiation in terms of its effect on the oxygenenhancement ratio (OER). The model takes into consideration oxygen diffusionthrough the tissue, its consumption by metabolic cells, and its radiolyticdepletion to estimate the relative decrease in radiosensitivity of cellsreceiving FLASH irradiation. Based on this model, several predictions are madethat could be tested in future experiments: (1) the FLASH effect shouldgradually disappear as the radiation pulse duration is increased from <1s to 10s; (2) dose should be deposited using the smallest number of radiation pulsesto achieve the greatest FLASH effect; (3) a FLASH effect should only beobserved in cells that are already hypoxic at the time of irradiation; and (4)changes in capillary oxygen tension (increase or decrease) should diminish theFLASH effect.

A computational model of radiolytic oxygen depletion during FLASH irradiation and its effect on the oxygen enhancement ratio