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Implications for human and environmental health of low doses of ionising radiation

兴奋 放射生物学 旁观者效应 适应性反应 电离辐射 低剂量辐射 表观遗传学 DNA损伤 辐射暴露 生物 生物效应 毒理 物理 计算生物学 生物物理学 医学 剂量-反应关系 遗传学 放射治疗 辐照 DNA 核医学 氧化应激 药理学 免疫学 内科学 基因 核物理学
作者
Carmel Mothersill,Colin Seymour
出处
期刊:Journal of Environmental Radioactivity [Elsevier BV]
卷期号:133: 5-9 被引量:36
标识
DOI:10.1016/j.jenvrad.2013.04.002
摘要

The last 20 years have seen a major paradigm shift in radiation biology. Several discoveries challenge the DNA centric view which holds that DNA damage is the critical effect of radiation irrespective of dose. This theory leads to the assumption that dose and effect are simply linked – the more energy deposition, the more DNA damage and the greater the biological effect. This is embodied in radiation protection (RP) regulations as the linear-non-threshold (LNT) model. However the science underlying the LNT model is being challenged particularly in relation to the environment because it is now clear that at low doses of concern in RP, cells, tissues and organisms respond to radiation by inducing responses which are not readily predictable by dose. These include adaptive responses, bystander effects, genomic instability and low dose hypersensitivity, and are commonly described as stress responses, while recognizing that “stress” can be good as well as bad. The phenomena contribute to observed radiation responses and appear to be influenced by genetic, epigenetic and environmental factors, meaning that dose and response are not simply related. The question is whether our discovery of these phenomena means that we need to re-evaluate RP approaches. The so-called “non-targeted” mechanisms mean that low dose radiobiology is very complex and supra linear or sub-linear (even hormetic) responses are possible but their occurrence is unpredictable for any given system level. Issues which may need consideration are synergistic or antagonistic effects of other pollutants. RP, at present, only looks at radiation dose but the new (NTE) radiobiology means that chemical or physical agents, which interfere with tissue responses to low doses of radiation, could critically modulate the predicted risk. Similarly, the “health” of the organism could determine the effect of a given low dose by enabling or disabling a critical response. These issues will be discussed.

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