Characterization of radiation-induced apoptosis in rodent cell lines

被引:36
作者
Guo, M
Chen, CH
Vidair, C
Marino, S
Dewey, WC
Ling, CC
机构
[1] MEM SLOAN KETTERING CANC CTR, DEPT MED PHYS, NEW YORK, NY 10021 USA
[2] MEM SLOAN KETTERING CANC CTR, RADIAT BIOPHYS LAB, NEW YORK, NY 10021 USA
[3] UNIV CALIF SAN FRANCISCO, DEPT RADIAT ONCOL, SAN FRANCISCO, CA 94143 USA
[4] COLUMBIA UNIV, NEVIS LAB, RARAF, CTR RADIOL RES, IRVINGTON, NY 10533 USA
关键词
D O I
10.2307/3579336
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
For REC:myc(chl), Rat1 and Rat1:myc, cells, we determined the events in the development of radiation-induced apoptosis to be in the following order: cell division followed by chromatin condensation, membrane blebbing, loss of adhesion and the uptake of vital dye. Experimental data which were obtained using He-4 ions of well-defined energies and which compared the dependence of apoptosis and clonogenic survival on He-4 range strongly suggested that in our cells both apoptosis and loss of clonogenic survival resulted from radiation damage to the cell nucleus. Corroboratory evidence was that BrdU incorporation sensitized these cells to radiation-induced apoptosis. Comparing the dose response for apoptosis and the clonogenic survival curves for Rat1 and Rat1:myc(b) cells, we concluded that radiation-induced apoptosis contributed to the overall radiation-induced cell inactivation as assayed by clonogenic survival, and that a modified linear-quadratic model, proposed previously, modeled such a contribution effectively. In the same context, the selective increase in radiation-induced apoptosis during late S and G(2) phases reduced the relative radioresistance observed for clonogenic survival during late S and G(2) phases. (C) 1997 by Radiation Research Society.
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页码:295 / 303
页数:9
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