Repair of potentially lethal radiation damage in human squamous carcinoma cells after chronic hypoxia
Purpose : To examine the repair of radiation induced potentially lethal damage in A431 and CaSki cells after chronic hypoxia. Methods and Materials : Cells in exponential phase are subjected to hypoxia (< 10 ppm oxygen) for up to 12 h and then are allowed to reoxygenate in air for up to 4 h. Cell...
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Veröffentlicht in: | International journal of radiation oncology, biology, physics biology, physics, 1994-05, Vol.29 (2), p.255-258 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Purpose
: To examine the repair of radiation induced potentially lethal damage in A431 and CaSki cells after chronic hypoxia.
Methods and Materials
: Cells in exponential phase are subjected to hypoxia (< 10 ppm oxygen) for up to 12 h and then are allowed to reoxygenate in air for up to 4 h. Cells are then irradiated with γ rays. Cell survivals are measured by clonogenic assay immediately and at different times after irradiation.
Results
: Compared to aerobic controls, an increase in the level of potentially lethal damage repair (PLDR) is demonstrated in A431 cells reoxygenated for 10 min after > 4 h of hypoxia. The repair returned to aerobic control level by 3 h of reoxygenation. PLDR of A431 cells reached maximum at about 9 h after irradiation in cells reoxygenated for 10 min after hypoxia. However, the repair is maximum at 6 h in cells reoxygenated for 3 h after hypoxia and in aerobic cells not previously exposed to hypoxia. Reoxygenation after chronic hypoxia did not affect the PLDR capacity and repair kinetics of CaSki cells.
Conclusion
: The results suggest that radiosensitization by reoxygenation after chronic hypoxia is not related to inhibition of PLDR. |
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ISSN: | 0360-3016 1879-355X |
DOI: | 10.1016/0360-3016(94)90271-2 |