Mammalian cell survival and radiation quality: analysis with allowance for delta tracks

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Abstract
The RBE for mammalian cell survival is analysed in relation to the distribution of LET. Complex target theory is described, together with a procedure for applying LET distributions to experimental findings in order to estimate the modes of cellular inactivation. Track segment theory is shown to have previously unrecognised limitations. The stepwise method is adopted to calculate the LET distributions for the radiations ( alpha -particles, deuterons and X-rays) used by Barendsen et al. (1966) in their study of the survival of T1 cells of human origin. Satisfactory fits of theory to experiment are obtained. Three distinctive modes of cellular inactivation, with independent energy transfers (direct and indirect) to complex targets comprising 2, 4 and 6 elements respectively, appear to be involved overall. At 'low dose', no contribution from the 2-transfer-mode can be discerned; only this mode is reparable. Saturation cross-sections (at high LET) for the 2- and 4-transfer-, but not the 6-transfer-mode, are oxygen-dependent. All three modes of inactivation might entail unrepaired double strand breaks and/or some form of mutation in DNA, at 1, 2 and 3 vulnerable sections, respectively.

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