The role of repair in the survival of mammalian cells from heavy ion irradiation: approximation to the ideal case of target theory.
Theories of cellular radiation sensitivity that preclude a significant role for cellular repair processes in the final biological expression of cellular damage induced by ionizing radiation are unsound.  Experiments are discussed here in which the cell-cycle dependency of the repair deficiency of the S/S variant, of the L5178Y murine leukemic lymphoblast was examined by treatment with the heavy ions, 20Ne, 28Si, 40Ar, 56Fe and 93Nb.  Evidence from those studies, which will be described in detail elsewhere, provide support for the notion that as the linear energy transfer (LET infinity) of the incident radiation increases the ability of the S/S cell to repair radiation damage decreases until effectively it is eliminated around 500 keV/micrometer.  In the region of the latter LET infinity value, the behavior of the S/S cell approximates the ideal case of target theory where post-irradiation metabolism (repair) does not influence cell survival.  The expression of this phenomenon among different cell types and tissues will depend upon the actual repair systems involved and other considerations.
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Department of Radiology and Radiation Biology, Colorado State University, Fort Collins 80523.
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D000818:Animals; D001973:Bromodeoxyuridine; D001976:Bromouracil; D002453:Cell Cycle / Q000528:radiation effects; D002470:Cell Survival / Q000528:radiation effects*; D004260:DNA Repair; D007477:Ions; D007945:Leukemia, Lymphoid / Q000378:metabolism / Q000473:pathology*; D018499:Linear Energy Transfer; D051379:Mice; D014407:Tumor Cells, Cultured
D007477:Ions; D001976:Bromouracil; D001973:Bromodeoxyuridine