abstract
- The response of wild-type CHO-KI, radiation-sensitive XRS-5 and radiation-resistant XRS-5 revertant populations was examined following single and fractionated doses of cobalt-60 gamma-radiation. The results show that it is possible to induce a shoulder on the fractionated dose-survival curve of XRS-5 radio-sensitive cells, which is the same size as the wild-type CHO-KI shoulder. This shoulder persists as does the wild-type CHO-KI shoulder even after correction of the curve for lethal damage occurring in the progeny. Since this mechanism involves induction of repair, CHO-KI cells, XRS-5 cells and revertant XRS-5 cells, which are repair-proficient, were exposed to 8-azacytidine--an agent which demethylates DNA and has been shown to recover repair proficiency in sensitive XRS-5 cells. The results confirmed that azacytidine had no effect on repair-proficient CHO-KI cells but it removed the shoulder and prevented split-dose repair in XRS-5 revertant populations. The absence of heritable, lethal defects in XRS-revertant cells exposed to single doses of radiation contrasts with the situation in the wild-type CHO-KI line where these defects occur in high numbers. These results suggest that the XRS revertant is not the same as the wild-type. They also suggest that the mechanisms involved in repair of damage and production of the survival-curve shoulder following single doses of radiation are different to those which occur following split doses of radiation.