Modification of radiation sensitivity: The oxygen effect

The relationships between cell killing, mutation induction and DNA double (dsb) and single (ssb) strand breaks have been studied in V79 cells irradiated with X-rays under oxic and anoxic conditions in the presence and in the absence of dimethylsulphoxide (DMSO). Curvilinear relationships were found between all pairs of endpoints, except for dsb versus ssb. Statistical analysis of experimental data has shown that in the absence of DMSO there is evidence of good correlations between cell killing, mutation induction and dsb in oxic and anoxic conditions. However, when DMSO was present, no significant correlation was found. In the presence of oxygen DMSO always exerts a protective effect while in anoxia it is generally much less protective and induces a strong sensitization with respect to mutation induction. Possibly DMSO acts not only as a radical scavenger but also as an agent inducing chromatin relaxation and/or under anoxia, forming highly mutagenic short-term radicals. The present data suggest that lethal and mutational events are at least partially independent and not proportional to the initial number of DNA breaks. This may imply that either other kinds of lesions are involved in cell lethality and mutability, or dose-dependent repair mechanisms of dsb have to be considered.

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“…1975b, Quintiliani 1979, Millar et al . 1981) while very few data are available on mutation induction .…”

Section: 1 Dose-response Relationshipsmentioning

confidence: 96%

Relationships Between Cell Killing, Mutation Induction and DNA Damage in X-irradiated V79 Cells: The Influence of Oxygen and DMSO

Sapora

Barone

Belli

et al. 1991

International Journal of Radiation Biology

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“…The same type of survival curve is also typical for sparsely ionizing radiations (X-rays, g-rays, electrons), which kill cells primarily by generation of free radicals that damage biological macromolecules, for example, DNA [Hall, 2000]. A well-known and extensively studied characteristic of this mechanism is reduction of killing efficiency if cells are exposed under hypoxic conditions [Howard-Flanders, 1960;Quintiliani, 1979;Nias, 1998;Hall, 2000]. One can reasonably hypothesize that nsEP, due to their extreme voltage, might be able to cause water ionization and/ or dissociation, leading to free radical formation and cell death.…”

Section: Introductionmentioning

confidence: 99%

Oxygen enhances lethal effect of high‐intensity, ultrashort electrical pulses

Walker¹,

Pakhomova

Kolb

et al. 2006

Bioelectromagnetics

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The study explored the effect of ambient oxygen on mammalian cell survival after exposure to 10 ns duration, high voltage electrical pulses (nsEP, 80-90 or 120-130 kV/cm; 200-400 pulses per exposure). Cell samples were equilibrated with pure nitrogen, atmospheric air, or pure oxygen prior to the nsEP treatment and were returned to the incubator (air + 5% CO2) shortly after the exposure. The experiments established that survival of hypoxic Jurkat and U937 cells exceeded that of air-equilibrated controls about twofold (P < .01). Conversely, saturation of the medium with oxygen prior to exposure decreased Jurkat cell survival about 1.5 times, P < .01. Attenuation of the cytotoxic effect under hypoxic conditions resembled a well-known effect of oxygen on cell killing by sparsely ionizing radiations and may be indicative of the similarity of underlying cell damage mechanisms.

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“…Although this O2-effect was discovered long ago [15,22], it has not been possible to satisfactorily explain the mechanism [17,18,20,26]. The most widely accepted hypothesis assumes: O2 is a dose-modifying agent, and does so by changing the amount of radiation-induced primary events.…”

Section: Discussionmentioning

confidence: 98%

Oxygen-effect as an inhibition of repair: Radiation studies on excision repair deficient mei-9L1-embryos of drosophila

Fritz-Niggli

Büchi

Schweizer

1981

Radiat Environ Biophys

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The excision repair deficient mei-9L1-embryos of Drosophila melanogaster are up to four times more radiosensitive than normal +/+ embryos. The lack of oxygen-effect in the repair deficient 4-h-embryos and the reduced O2-effect in the 13/4-h embryos suggest an interpretation of the oxygen effect as a modification of the ability to repair. The conversion of the early death (heavy damage) to late death (slight damage) by irradiation of normal embryos in N2 supports this interpretation. This theory can also explain the dependence of O2-effect on LET. The spontaneous lethality and the increase in radiosensitivity depend in heterozygous mei-9L1-embryos strictly upon the genotype of the mother, thus representing a maternal effect.

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Modification of radiation sensitivity: The oxygen effect

Cited by 27 publications

References 37 publications

Relationships Between Cell Killing, Mutation Induction and DNA Damage in X-irradiated V79 Cells: The Influence of Oxygen and DMSO

Relationships Between Cell Killing, Mutation Induction and DNA Damage in X-irradiated V79 Cells: The Influence of Oxygen and DMSO

Oxygen enhances lethal effect of high‐intensity, ultrashort electrical pulses

Oxygen-effect as an inhibition of repair: Radiation studies on excision repair deficient mei-9L1-embryos of drosophila

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