Purpose: To investigate the effect of cycling hypoxia on low dose hyper-radiosensitivity (HRS).
Materials and methods: Human breast tumor T-47D cells were grown in a hypoxia workstation operated at 4% O(2) for 3-6 weeks and the pericellular oxygen concentration was recorded every 20 minutes. The presence of HRS in response to subsequent challenge irradiation was measured by clonogenic survival.
Results: T-47D cells adapted to growing with 4% O(2) in the gas phase but showed no HRS. However, HRS was recovered after between 48 h and two weeks of reoxygenation at 20% O(2). Medium transferred from the hypoxic T-47D cells removed HRS in recipient cells grown in ambient air. Cells irradiated with X-rays showed a shallower HRS-'dip' and a lower d(c)-value (dose where the change from the hypersensitive to the induced repair response is 63% complete) compared to cells irradiated with (60)Co γ-rays.
Conclusions: Cycling hypoxia transiently eliminates HRS in T-47D cells in vitro. This may partly explain the diverging results of in vivo studies of HRS. The effect of cycling hypoxia on HRS is comparable to our previous findings for T-47D cells receiving medium transfer from cells irradiated with 0.3 Gy at 0.3 Gy/h.