The cells of a C3H mouse mammary carcinoma were examined for their ability to repair sublethal radiation injury using the split-dose technique and <tex-math>${\rm TCD}_{50}$</tex-math> as the end point (<tex-math>${\rm TCD}_{50}$</tex-math> = radiation dose that yields local control of half of the irradiated tumors). Radiation was administered either under conditions of local tissue hypoxia (application of a clamp across the root of the thigh bearing the tumor for 2 minutes prior to and during irradiation) or under "<tex-math>${\rm O}_{2}30\ {\rm psi}$</tex-math>" conditions (respiring pure oxygen at 3 atmospheres of pressure absolute for 15 minutes prior to and during irradiation). The <tex-math>${\rm TCD}_{50}$</tex-math> values were 5372 rads for v = 1 (single dose) and 6853 rads for v = 2 (<tex-math>$D_{1}=3000$</tex-math> rads, hypoxia; <tex-math>$t_{i}=6\ \text{hours}$</tex-math>; <tex-math>$D_{2}=\text{variable}$</tex-math>, hypoxia). Thus, these acutely hypoxic mammary carcinoma cells repaired radiation damage rapidly and extensively; results were consistent with an extrapolation number of approximately 50. To test for repair of radiation damage by chronically hypoxic cells, a first dose of 3000 rads was administered under <tex-math>${\rm O}_{2}30$</tex-math> psi conditions. Only chronically hypoxic cells would survive such a treatment. After 6 hours, a variable and second dose was administered under hypoxic conditions; <tex-math>${\rm TCD}_{50}$</tex-math> (v = 2) was 5330 rads. This compares with a <tex-math>${\rm TCD}_{50}$</tex-math> of 4860 rads for single-dose irradiation under <tex-math>${\rm O}_{2}30$</tex-math> psi conditions and suggests that the chronically hypoxic cells were less able to repair radiation damage than acutely hypoxic cells.

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