Abstract

The magnitude of biological response varies with different radiation types. Using Linear Energy Transfer (LET) to differentiate types of incident radiation beam, the Relative Biologic Effectiveness (RBE) as a function of LET (RBE-LET) was found to have a characteristic shape with a peak around LET values 100 - 200 eV/nm. This general feature is believed to be a property of the incident beam. Our systems engineering model, however, suggests that the shape of the RBE-LET curve is a cell trait, a property of the cell. Like any other trait, phenotypic variations result from interactions of the genes and their context. State-space block diagram of the differential equation model suggests the genes are those in the DNA double strand break (dsb) repair pathway; and the context is cellular stress responsing to DNA damage by both external stimuli and internal redox state. At a deeper level, the block diagram suggests cell using mathematical calculations in its decision-making when facing a stress signal. The MRN protein complex, in particular, may perform addition to count the degree of DNA twisting for the homeostatic regulation of DNA supercoiling. The ATM protein may act as a feedback amplifier.

Highlights

  • Textbook of radiation biology such as [1] explains the Relative Biologic Effectiveness (RBE)-Linear Energy Transfer (LET) curve in terms of the spacing of energy deposition near DNA diameter

  • Attempts to measure DNA dsb as a function of LET, failed to show an optimal LET value [2]. Another model based on microdosimetry explains the RBE-LET curve in relation to the “clustered damage site”

  • The result here indicates that the RBE-LET curve is a property of the cell and not a property of the incident beam, as suggested by the name, Relative Biologic Effectiveness itself

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Summary

Introduction

Textbook of radiation biology such as [1] explains the RBE-LET curve in terms of the spacing of energy deposition near DNA diameter. Another model based on microdosimetry explains the RBE-LET curve in relation to the “clustered damage site”. This model sees cells as system, different types of radiation as input, and cellular response as output (Figure 1). An incident particle interacts with the detector, in this case, a living cell, at discrete transfer points.

Results
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