The oxygen enhancement ratio (OER) is defined as the ratio of the isoeffect dose to hypoxic cells to that to aerobic cells. OER generally ranges between 2 and 3 for low-LET radiation where the higher the dose the higher the OER.
Hyperbaric oxygen (HBO) serve as radiosensitizer (its use just prior to radiotherapy) and also as a treatment modality for radiation necrosis (e.g., osteoradionecrosis after radiotherapy).
The mechanistic underpinnings of the oxygen effects remain incompletely understood, but indirect effects to nuclear DNA are explained above by others. Here I wish to highlight two other potential mechanisms.
A recent study attributed the oxygen effect to radiation-induced effects in mitochondria, such that reactive oxygen species generated in mitochondria target nuclear DNA indirectly.
https://www.ncbi.nlm.nih.gov/pubmed/26894978
Targeted cyctoplasmic irradiation induces DNA damage, inactivates clonogenic potential and causes mitochondrial dysfunction leading to increased oxidative stress. These suggest extranuclear target for radiation effects.
The new study now shows, for the first time, linear energy transfer (LET) dependent changes in the oxygen enhancement ratio (OER) for DNA double strand breaks following X-ray or heavy ion irradiation. OER was calculated as the slope of phosphorylated histone H2AX foci/Gy formed at 1 h post irradiation of A549 human non-small cell lung cancer under an oxic condition divided by that under a hypoxic condition. Such OER was about 3 for X-rays and at 13 keV/µm, about 2 at 30 and 50 keV/µm, and about 1 at 65, 80 and 200 keV/µm.