Abstract
Incubation of cultured Chinese hamster cells [lung V79-B310H] in the presence of the DNA chain terminator 2'',3''-dideoxythymidine (ddThd) following .gamma. irradiation enhances cell killing. Maximum enhancement is obtained with 10 .mu.g/ml ddThd and incubation for 90 min. If the addition of ddThd is delayed for 1 h after irradiation, no enhancement is observed. Although the drug kills S-phase cells which are more radiation resistant, this is not the main reason for the observed enhancement of radiation response. The magnitude of the effect in cells synchronized at the G1-S interface is similar to that in asynchronous population. When ddThd treatment is combined with other treatments that enhance radiation response, i.e., BUdR substitution and hyperthermia, the effects are less than additive. Repair of radiation-induced DNA damage apparently is interfered with by ddThd either by incorporation into gaps formed during excision of damage and/or by inhibition of DNA polymerase .beta. which is involved with excision repair.