OER is calculated by the ratio

OER = Dose (without oxygen)/Dose(with oxgen) for the same biological effect.

This relationship is defined mainly for low LET radition, because there the interaction with the water in the cell plasma is dominant. OER describes the impact of radicals like OH, H etc in cell water, which interact in a second step with DNA. This is called indirect radiation effect.

Hypoxic cells are more resistant to radiotherapy than normal cells. I think this book will aid you to understand the answer for your question.

Adv Exp Med Biol. 2017;977:91-99. doi: 10.1007/978-3-319-55231-6_13.

Tumor Oxygenation Status: Facts and Fallacies.

Vaupel P1, Mayer A2.

The pathogenesis of ionizing radiation damage starts at with the physicochemical processes. These processes give origin to reactive compounds that act on molecular level and cause radiation cellular changes. This causes cells to losing their specific properties. At the subcellular level there are irregularities happening to the biochemical processes:

The activity of enzymes changes

phosphorylation mechanisms are disrupted

the synthesis of nucleic acid

specific proteins do no longer work.

The cellular level of damage first manifests itself with a decrease in the number of proliferating cellular populations. The loss of specialized cells causes the biochemical changes to intensify. The changes starts to interfere with the functions of vitally important organs such as hematopoietic tissues, intestinal epithelium etc. The resulting organ and systemic changes to the whole organism initiates the development of radiation sickness. There are also latent somatic and genetic damages, which can be seen on a population level.

Biological effects of the same doses of ionizing radiation can differ greatly. These effects depend on the linear energy transfer and on the spatial distribution of a given dose. DNA molecules are the most critical cellular structures that can be affected by ionizing radiation. Ionizing radiation can induce a number of changes in the size, structure and shape of these molecules.

The oxygen effect was first observed in 1912 by Swartz in Germany, but the first quantitative data were reported by Thomlinson and Gray in 1955 (Gray is the origin for the unit of the absorbed dose Gy). In 1956, Gray published a paper "Oxygen tension as a factor in radiotherapy".

https://www.researchgate.net/publication/307578608_The_Life_of_Louis_Harold_Gray

Article The Life of Louis Harold Gray

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).

https://www.ncbi.nlm.nih.gov/pubmed/28613568

https://www.ncbi.nlm.nih.gov/pubmed/28126298

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. 

https://www.ncbi.nlm.nih.gov/pubmed/24080278

https://www.ncbi.nlm.nih.gov/pubmed/17575156

https://www.ncbi.nlm.nih.gov/pubmed/10220401

The oxygen enhancement ratio (OER) is the ratio of doses under hypoxica to aerated conditions that produce the same biologic effect.

The presence or absence of molecular oxygen dramatically influences the biologic effect of x-rays.

Oxygen presence (aerated cells) increases radiation effectiveness for cell killing.

Lack of oxygen (hypoxic cells) results in more radio resistant cells.

The maximum OER depends mainly on the ionizing density or LET of the radiation. Radiation with higher LET and higher relative biological effectiveness (RBE) have a lower OER in mammalian cell tissues . The value of the maximum OER varies from about 1-4. The maximum OER ranges from about 2-4 for low-LET radiations such as X-rays, beta particles and gamma rays, whereas the OER is unity for high-LET radiations such as low energy alpha particles.

Can any please provide me OER values in different phases (M, G1, G2 and S) of cell cycles. Such as CHO, V79 and other cell lines. 5 or 6 cell lines would be enough. My assessment of radiation sensitivity is different. Please see my paper

Oxygen in S phase of a cell cycle JRP 2015. Thanks in advance.

Radiat Res. 1991 Sep;127(3):297-307.

Oxygen enhancement ratio as a function of dose and cell cycle phase for radiation-resistant and sensitive CHO cells.

Freyer JP1, Jarrett K, Carpenter S, Raju MR.

Author information

Abstract

There is still controversy over whether the oxygen enhancement ratio (OER) varies as a function of dose and cell cycle phase. In the present study, the OER has been measured as a function of survival level and cell cycle phase using volume flow cell sorting. This method allows both the separation of cells in different stages of the cycle from an asynchronously growing population, and the precise plating of cells for accurate measurements at high survival levels. We have developed a cell suspension gassing and sampling system which maintained an oxygen tension less than 20 ppm throughout a series of sequential radiation doses. For both radiation-resistant cells (CHO-K1) and a radiation-sensitive clone (CHO-xrs6), we could separate relatively pure populations of G1-phase, G1/S-boundary, S-, and G2-phase cells. Each cell line showed a typical age response, with cells at the G1/S-phase boundary being 4 (CHO-K1) to 12 (CHO-xrs6) times more sensitive than cells in the late S phase. For both cell lines, G1-phase cells had an OER of 2.3-2.4, compared to an OER of 2.8-2.9 for S-phase and 2.6-2.7 for G2-phase cells. None of these age fractions showed a dependence of OER on survival level. Asynchronously growing cells or cells at the G1/S-phase boundary had an OER similar to that of G1-phase cells at high survival levels, but the OER increased with decreasing survival level to a value near that of S-phase cells. These results suggest that the decrease in OER at high survival levels for asynchronous cells may be due to differences in the OERs of the inherent cell age subpopulations. For cells in one cell cycle stage, oxygen appears to have a purely dose-modifying effect.

Dear Eman, Thank you for the paper. I know Freyer paper of 1973. This is of great help. Is there a handbook where these values are given? If you have other cell lines OER values in different phases of the cell cycles, I would very much like to know. Thanks a million for your kindness.

Regards Akber

Oncol Rep. 2012 Mar;27(3):769-74. doi: 10.3892/or.2011.1604. Epub 2011 Dec 21.

Relative biological effectiveness of high linear energy transfer α-particles for the induction of DNA-double-strand breaks, chromosome aberrations and reproductive cell death in SW-1573 lung tumour cells.

Franken NA1, Hovingh S, Ten Cate R, Krawczyk P, Stap J, Hoebe R, Aten J, Barendsen GW.

Author information

Abstract

Ionizing radiation-induced foci (IRIF) of DNA repair-related proteins accumulated at DNA double-strand break (DSB) sites have been suggested to be a powerful biodosimetric tool. However, the relationship between IRIF induction and biologically relevant endpoints, such as cell death and formation of chromosome rearrangements is less clear, especially for high linear energy transfer (LET) radiation. It is thus not sufficiently established whether IRIF are valid indicators of biological effectiveness of the various radiation types. This question is more significant in light of the recent advancements in light ion-beam and radionuclide therapy. Dose-effect relationships were determined for the induction of DNA-DSBs, chromosome aberrations and reproductive cell death in cultured SW-1573 cells irradiated with γ-rays from a Cs-137 source or with α-particles from an Am-241 source. Values of relative biological effectiveness (RBE) of the high LET α-particles were derived for these effects. DNA-DSB were detected by scoring of γ-H2AX foci, chromosome aberrations by fragments and translocations using premature chromosome condensation and cell survival by colony formation. Analysis of dose-effect relations was based on the linear-quadratic model. Except for the survival curves, for other effects no significant contribution was derived of the quadratic term in the range of doses up to 2 Gy of γ-rays. Calculated RBE values derived for the linear component of dose-effect relations for γ-H2AX foci, cell reproductive death, chromosome fragments and colour junctions are 1.0±0.3, 14.7±5.1, 15.3±5.9 and 13.3±6.0, respectively. RBE values calculated at a certain biological effect level are 1, 4, 13 and 13, respectively. The RBE values derived from the LQ model are preferred as they are based on clinically relevant doses. The results show that with low LET radiation only a small fraction of the numerous DNA-DSBs yield chromosome damage and reproductive cell death. It is concluded that many of the chromosomal aberrations detected by premature chromosome condensation do not cause reproductive cell death. Furthermore, RBE values for DNA-DSB detectable by γ-H2AX foci shortly after irradiation, provide no information relevant to applications of high LET radiation in radiotherapy. The RBE values of chromosome aberrations assessed by premature chromosome condensation are close to the value for reproductive cell death. This suggests possible relevance to assess RBE values for radiotherapy with high LET ions.

PMID: 22200791 DOI: 10.3892/or.2011.1604[Indexed for MEDLINE]

Thanks for your help. Akber

I am looking for OER values in different phases of cell cycles in cell lines like CHO etc. Please read my paper on OXYGEN IN S PHASE OF CELL CYCLES.

Thanks