Repair of Radiation-induced Chromatid Aberrations: Relationship to G₂ Arrest in CHO Cells

Summary

The literature suggests that the function of radiation-induced G₂ arrest is to allow repair of potentially lethal damage before cell-entry into, and damage expression in, mitosis. The nature of the damage repaired is not known, but chromosome aberrations have been considered. To examine this possibility in G₂ cells, the rate of repair of chromatid aberrations in CHO cells progressing to or arrested in G₂ was compared with the rate of repair of the damage which gives rise to G₂ arrest. To measure aberration repair rates, exponentially growing CHO cells arrested in G₂ with 1·5, 2·5 or 3·5 Gy of X-rays were released into mitosis by treatment with 5 mm caffeine immediately or 1, 2 or 3 h after irradiation. Aberration frequencies in these cells were then related to the caffeine-free (repair) interval. To measure the rate of repair of arrest-causing damage a split-dose procedure was used. The half-times for aberration repair were approximately 1 h for achromatic gaps and 1·5 h for breaks, intrachanges and interchanges. The half-time for arrest damage repair varied with radiation dose. This result suggests that chromatid aberrations are not a primary cause of radiation-induced G₂ arrest.