For REC:myc(chl), Rat1 and Rat1:myc, cells, we determined the events i
n the development of radiation-induced apoptosis to be in the followin
g order: cell division followed by chromatin condensation, membrane bl
ebbing, loss of adhesion and the uptake of vital dye. Experimental dat
a which were obtained using He-4 ions of well-defined energies and whi
ch compared the dependence of apoptosis and clonogenic survival on He-
4 range strongly suggested that in our cells both apoptosis and loss o
f clonogenic survival resulted from radiation damage to the cell nucle
us. Corroboratory evidence was that BrdU incorporation sensitized thes
e cells to radiation-induced apoptosis. Comparing the dose response fo
r 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 clonogen
ic survival, and that a modified linear-quadratic model, proposed prev
iously, modeled such a contribution effectively. In the same context,
the selective increase in radiation-induced apoptosis during late S an
d G(2) phases reduced the relative radioresistance observed for clonog
enic survival during late S and G(2) phases. (C) 1997 by Radiation Res
earch Society.