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Radiation‐induced apoptosis in human tumor cell lines: Adaptive response and split‐dose effect

Irradiation of human ovarian carcinoma cells (OVCAR 3) and myeloma cells (RPMI 8226) with graded doses of 137Cs‐γ‐rays led to a 35–40% increase in time‐dependent apoptosis 72 hr after 6–8 Gy irradiation. Large individual variations in sensitivity to radiation‐induced apoptosis were noted in human lymphocytes obtained from 5 donors. Pretreatment of OVCAR 3 and RPMI 8226 cells with 0.01 Gy increased their resistance to apoptosis after subsequent 6 Gy irradiation several hours or 48 and 72 hr later. A dose of 4 or 8 Gy given in 2 equal fractions at an interval of a few hours produced a low level of apoptosis compared to that resulting from a single administration of the same total dose. Adaptive response was demonstrated in 2 out of 3 samples of human lymphocytes isolated from different donors, and no split‐dose effect for apoptosis was noted in 2 other donors. In split‐dose experiments, there was no correlation between the sensitivity of cells to apoptosis and their position in the cell cycle, after the first half‐dose. No G1 block was observed in irradiated cell lines. Adaptive response and split‐dose effect were prevented by 3‐aminobenzamide and okadaic acid which inhibit poly(ADP‐ribose)polymerase and protein phosphatase, respectively. These results imply a common mechanism for acquired resistance to radiation‐induced apoptosis in adaptive response and the split‐dose effect. Int. J. Cancer 77:76–81, 1998.© 1998 Wiley‐Liss, Inc.