Comparative radiobiology and protection the environment from the effects of ionizing radiation

摘要

The last few years has seen what people are now referring to as a “shifting paradigm” in our way of thinking about radiation effects on biological systems. The concept of the central role of DNA damage due to double strand breaks induced by a radiation “hit” has been itself hit by many studies showing persistent effects in the distant progeny of radiation exposed cells. This phenomenon is known as radiation induced genomic instability. More recently evidence has been accumulating that not even the parent cell need be exposed to radiation (the bystander effect), and that the bystander cells can demonstrate genomic instability and effects at low doses which are inconsistent with a mechanism based on DNA hits as important targets at low doses. The new paradigm suggests that cellular stress responses or damage signalling through a range of signal transduction pathways are involved. Cell-cell contact or secretion of damage signalling molecules can induce responses in undamaged and unirradiated cells. Are these new effects relevant to risk assessment, or does it matter how radiation affects cells if we have good epidemiological evidence on which to base our risk estimates? If DNA based dose responses are not so important at environmentally relevant doses, then it is not logical to base our environmental protection system on consideration of radiation dose as if this is in some way unique and not affected by the presence of other environmental stressors. The aim of this paper is to review the new concepts and to consider reasons why they might alter our methods of risk estimation. In particular the paper considers the impact of the new concepts on environmental protection and discusses the need for research in the field of comparative radiobiology if we are to develop policies which can adequately protect biodiversity.