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British Journal of Radiology (2005) Supplement_27, 185-195
© 2005 British Institute of Radiology
doi: 10.1259/bjr/64628752

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British Journal of Radiology Supplement_27 (2005),185-195 ©2005 The British Institute of Radiology

Full Paper

Significance of basic and clinical research in radiation medicine: challenges for the future

L E Feinendegen, MD

Heinrich-Heine-University Düsseldorf, Germany and Brookhaven National Laboratory, Upton, NY, USA

Correspondence: Ludwig E Feinendegen, MD, Wannental 45, 88131 Lindau, Germany. E-mail: feinendegen@gmx.net

Tissue effects are the consequences of cellular reactions and responses. This review deals with cellular responses to low absorbed doses of ionising radiation, which are not readily predictable by extrapolation of responses observed at high doses. One of the reasons for this unpredictability is the relationship between the relatively low density of particle tracks in tissue at low radiation doses with their generation of largely stochastic ionisations and excitation of constituent molecules, and moreover, bursts of reactive oxygen species (ROS). The other reason is the abundant and constant generation of ROS and other endogenous toxins, on top of which low dose radiation acts. At low doses, a dual effect on cellular DNA occurs: one concerns damage, whilst the other brings adaptive protection which develops within hours and may last for days to months. Radiation-induced apoptosis and immune responses add to protection by reducing genomic instability and eliminating pre-damaged cells from tissues. Protective responses express adaptive responses to suprabasal metabolic perturbations and also mimic oxygen stress responses. Analysis of the consequences of this low dose scenario, which also applies to background irradiation, predicts that the linear no-threshold hypothesis is scientifically unfounded. In cases of protracted or chronic irradiation, the time interval between repetitive particle tracks in a defined biological target at a given dose rate may determine to what degree damage or adaptive protection prevails. Tissue failure following chronic exposure at low dose rate appears to result from the rather sudden shift from a low to a high ratio of radiogenic damage to protection against endogenous damage, within the net response of largely still elusive signalling networks in cells and tissues.







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