Mechanisms of recovery from sublethal damage and potentially lethal damage induced by BrdUrd/313 nm light treatment: alkali-labile lesions.

BrdUrd pulse labelling of synchronous Chinese hamster cell cultures was used to correlate repair of sublethal damage with removal of alkali-labile lesions. Both processes were modified in a quantitatively similar manner by cysteamine. In addition, the age responses for repair of sublethal damage and for cysteamine reduction of repair agreed. Through the use of thymidine as an S-phase-blocking agent it was further demonstrated that progression past the S-phase of the cell cycle was required for the loss of resistance to UVB light in BrdUrd-substituted cells. Similarly, a thymidine block administered before synthesis upon the BrdUrd-substituted template prevented the cell from acquiring the sensitivity to UVB light normally associated with synthesis on a lesioned template. The UVB-light-sensitive mutant V79-UC was shown to have reduced capacities both for the accumulation of sublethal injury and for the removal of alkali-labile lesions. These data support the notion that alkali-labile lesions are responsible for sublethal damage in BrdUrd pulse-labelled Chinese hamster cells.