Can radiolytic oxygen depletion quantitatively explain FLASH sparing?
In plain words
One idea is that a very fast dose uses up the oxygen in tissue faster than blood can resupply it, and oxygen-starved tissue is harder to damage. The question is whether the numbers work.
Precise statement
Compute the transient oxygen tension during a 100 ms, 2000 rad exposure using measured radiolytic oxygen consumption of about 0.2 to 0.5 micromolar per 100 rad, tissue diffusion constants and capillary resupply, and test whether the resulting dip at physiological $pO2$ of about 5 to 40 mmHg produces the measured change in oxygen enhancement ratio. An answer is yes or no with an error budget on consumption yield, diffusion and perfusion.
What would settle it
Time-resolved in vivo oxygen measurements with sub-millisecond response during FLASH delivery, compared against the reaction-diffusion prediction.
Status in the literature
Unverified note: it names recent work and was partly written without a live literature search; it awaits a check by an editor.
Several 2020 to 2024 analyses conclude depletion is too small at normal tissue $p\mathrm{O}2$, while others retain it as a partial contribution.
Parent problems
- Special case of Physical mechanism of normal-tissue sparing at ultra-high dose rate · open · from revision 1
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