The oxygen fixation hypothesis (OFH), developed in the late 1950s, is widely regarded as the most satisfactory explanation of why oxygen is a radiation sensitizer. Central to this hypothesis is the explicit belief that DNA lesions (originally called "target lesions") that are produced by x-rays with the chemical participation of oxygen pose a special threat to cell survival because these lesions cannot be chemically restored to an undamaged state. According to this hypothesis, oxygen sensitizes because these "nonrestorable" lesions ultimately increase the amount of stable DNA damage--and thus the extent of lethality--from a give dose.
The oxygen fixation hypothesis for indirect action of photons and other low linear energy transfer radiations is that molecular oxygen permanently fixes the DNA damage produced by free radicals, leading to irreparable damage. This radiochemical rationale is useful to explain the oxygen effects from the radiochemical viewpoint, although it does not necessarily consider biological repair (e.g., enzymatic DNA damage repair) independent of chemical repair.
This effect by molecular oxygen permanently fixes the DNA damage produced by free radicals, leading to irreparable damage. Obviously, there are competing mechanisms involved. One quantification by von Sonntag (2006) describes the competition between between oxygen fixation and chemical repair in a kinetic representation. This may be defined as the probability a DNA radical is reduced by the cellular environment rather than fixed by O2.
The formula utilized is given as f as the fraction of DNA radicals that undergo chemical repair, whereas (1-f) is the fraction that are “fixed” by oxygen