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A new expression for the radial dose distribution, tested against available data, and yielding good agreement with enzyme and virus cross sections, is used to calculate cellular inactivation cross sections from track theory models and parameters. We use a cellular model and radiosensitivity parameters, fitted to HILAC data 15 years ago, to represent mammalian cells irradiated at the UNILAC. The observed branching with Z and the decline in cellular action cross sections with an increase in ion LET are attributed to thindown; that is, to the limits imposed by the maximum radial penetration of delta rays. Target size and structure (hence the model) also play a role. Similar effects are observed with nuclear emulsions, scintillation counters, and thermoluminescent crystals at ion speeds approaching the Bragg peak, where, in the track width regime, the cross sections depend more on the ion speed than on LET.