A DNA double-strand break repair-deficient mutant of CHO cells shows reduced radiosensitization after exposure to hyperthermic temperatures in the plateau phase of growth.
Heat response and heat-induced radiosensitization were studied in plateau-phase cultures of CHO cells and their radiation-sensitive counterpart, the xrs-5 cells. The xrs-5 cells were more sensitive to heat alone than were CHO cells. A large enhancement in radiation-induced killing was observed in CHO cells pre-exposed to heat (43 degrees C), expressed as a reduction in the values of Do and Dq. Contrary to the results obtained with CHO cells, pre-exposure to heat of xrs-5 cells affected radiation sensitivity to a much lesser extent. D1, the radiation dose required to reduce cell survival to 1%, decreased in CHO cells from 8.7 Gy to 2.5 Gy with increasing heat damage (cell survival after exposure to heat alone), whereas it decreased from 1.4 Gy to 0.9 Gy in xrs-5 cells. These results suggest that heat-induced radiosensitization is compromised in plateau-phase xrs-5 cells. Since xrs-5 cells are deficient in DNA dsb repair, it is hypothesized that DNA dsb repair proficiency is a prerequisite for heat radiosensitization and that heat-induced inhibition of DNA dsb repair is likely to contribute to the radiosensitization observed in repair-proficient cell lines after exposure to high temperatures.
Thomas Jefferson University, Department of Radiation Oncology, Philadelphia, PA.
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G
Iliakis
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R
Seaner
D000818:Animals; D002453:Cell Cycle; D002455:Cell Division; D002460:Cell Line; D002470:Cell Survival / Q000528:radiation effects; D004249:DNA Damage; D004260:DNA Repair / Q000235:genetics / Q000528:radiation effects*; D004307:Dose-Response Relationship, Radiation; D006358:Hot Temperature; D009154:Mutation; D011836:Radiation Tolerance