The influence of oxygen on the induction of radiation damage in DNA in mammalian cells after sensitization by intracellular glutathione depletion.

Treatment of mammalian cells with buthionine sulphoximine (BSO) or diethyl maleate (DEM) results in a decrease in the intracellular GSH (glutathione) and non-protein-bound SH (NPSH) levels. The effect of depletion of GSH and NPSH on radiosensitivity was studied in relation to the concentration of oxygen during irradiation. Single- and double-strand breaks (ssb and dsb) and cell killing were used as criteria for radiation damage.

Reduction of intracellular glutathione content and radiosensitivity.

The intracellular glutathione (GSH) content of HeLa, CHO and V79 cells was reduced by incubating the cells in growth medium containing buthionine sulphoximine or diethyl maleate (DEM). Clonogenicity, single-strand DNA breaks (ssb) and double-strand DNA breaks (dsb) were used as criteria for radiation-induced damage after X- or gamma-irradiation. In survival experiments, DEM gave a slightly larger sensitization although it gave a smaller reduction of the intracellular GSH.

Induction of mutations in bacteriophage T7 by gamma-rays: no influence of the SOS repair pathway.

Under conditions where the reversion of an amber mutant of bacteriophage lambda by gamma-rays is enhanced by subjecting the irradiated phage to SOS repair, gamma-ray-induced reversion of two T7 ambers is not influenced by this error-prone bacterial repair system. The survival of T7 gamma-irradiated under anoxic conditions is somewhat enhanced by SOS repair, whereas the survival of phage irradiated under oxygen is not affected.

Influence of SOS repair on the specificity of radiation mutagenesis in bacteriophage phiX174.

The ochre mutant oc9 of bacteriophage phiX174 was irradiated with gamma-rays and the revertants were assayed on unirradiated and UV-irradiated host bacteria carrying an amber suppressor. The yield of revertants (amber + wild type) was higher on UV-irradiated than on unirradiated bacteria, showing that gamma-irradiated phiX174 was subjected to W-mutagenesis. For oc9 gamma-irradiated in the presence of oxygen the fraction of amber mutants among the revertants was lower when mutants were scored on UV-irradiated bacteria than when assayed on unirradiated indicator cells.

gamma-Ray mutagenesis in bacteriophage T4 is not enhanced by oxygen.

As in the induction of r mutants in bacteriophage T4 by gamma-rays, the radiation-induced reversion of T4 amber mutants to wild-type was found to depend on the product of the DNA-repair gene x of the phage. Neither the efficiency of induction of r mutants nor the efficiency of reversion of ambers was enhanced by the presence of oxygen during irradiation. T4 differed in this respect from phage T7, for which no indication has been found that gamma-ray mutagenesis results from error-prone repair of DNA damage.

Induction of mutations in bacteriophage T7 by gamma-rays: independence of host-repair mechanisms.

Amber mutants of bacteriophage T7 are reverted by gamma-rays to pseudo wild-type particles, i.e. particles able to propagate in a suppressorless host.