Physics must join with biology in better assessing risk from low-dose irradiation.
This review summarises the complex response of mammalian cells and tissues to low doses of ionising radiation. This thesis encompasses induction of DNA damage, and adaptive protection against both renewed damage and against propagation of damage from the basic level of biological organisation to the clinical expression of detriment. The induction of DNA damage at low radiation doses apparently is proportional to absorbed dose at the physical/chemical level. However, any propagation of such damage to higher levels of biological organisation inherently follows a sigmoid function. Moreover, low-dose-induced inhibition of damage propagation is not linear, but instead follows a dose-effect function typical for adaptive protection, after an initial rapid rise it disappears at doses higher than approximately 0.1-0.2 Gy to cells. The particular biological response duality at low radiation doses precludes the validity of the linear-no-threshold hypothesis in the attempt to relate absorbed dose to cancer. In fact, theory and observation support not only a lower cancer incidence than expected from the linear-no-threshold hypothesis, but also a reduction of spontaneously occurring cancer, a hormetic response, in the healthy individual.
Feinendegen
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LE
Heinrich-Heine-University Düsseldorf, Germany. feinendegen@gmx.net
Neumann
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RD
D000222:Adaptation, Physiological / Q000528:radiation effects; D000818:Animals; D024201:Bystander Effect; D002471:Cell Transformation, Neoplastic / Q000528:radiation effects; D004247:DNA / Q000528:radiation effects*; D004249:DNA Damage; D004307:Dose-Response Relationship, Radiation; D009381:Neoplasms, Radiation-Induced; D055585:Physical Phenomena; D010825:Physics; D011829:Radiation Dosage; D011830:Radiation Effects; D011836:Radiation Tolerance; D011853:Radiobiology; D018570:Risk Assessment
D004247:DNA