Heinrich-Heine-University Düsseldorf. Germany; and Brookhaven National Laboratory, Upton, NY, USA.
Dose Response. 2009 Dec 10;8(2):227-52. doi: 10.2203/dose-response.09-035.Feinendegen.
IONIZING RADIATION PRIMARILY PERTURBS THE BASIC MOLECULAR LEVEL PROPORTIONAL TO DOSE, WITH POTENTIAL DAMAGE PROPAGATION TO HIGHER LEVELS: cells, tissues, organs, and whole body. There are three types of defenses against damage propagation. These operate deterministically and below a certain impact threshold there is no propagation. Physical-static defenses precede metabolic-dynamic defenses acting immediately: scavenging of toxins; - molecular repair, especially of DNA; - removal of damaged cells either by apoptosis, necrosis, phagocytosis, cell differentiation-senescence, or by immune responses, - followed by replacement of lost elements. Another metabolic-dynamic defense arises delayed by up-regulating immediately operating defense mechanisms. Some of these adaptive protections may last beyond a year and all create temporary protection against renewed potentially toxic impacts also from non-radiogenic endogenous sources. Adaptive protections have a maximum after single tissue absorbed doses around 100 to 200 mSv and disappear with higher doses. Low dose rates initiate maximum protection likely at lower cell doses delivered repetitively at certain time intervals. Adaptive protection preventing only about 2 - 3 % of endogenous life-time cancer risk would fully balance a calculated induced cancer risk at about 100 mSv, in agreement with epidemiological data and concordant with an hormetic effect. Low-dose-risk modeling must recognize up-regulation of protection.
电离辐射主要在与剂量成比例的基本分子水平上扰乱,潜在的损害可能会传播到更高的水平:细胞、组织、器官和整个身体。有三种防御机制可以对抗损害的传播。这些机制是确定性的,在一定的冲击阈值以下,就不会发生传播。物理-静态防御先于代谢-动态防御立即发挥作用:清除毒素;- 分子修复,尤其是 DNA;- 通过细胞凋亡、坏死、吞噬作用、细胞分化衰老或免疫反应去除受损细胞,- 然后替换丢失的元素。另一种代谢-动态防御是通过上调立即作用的防御机制而延迟发生的。这些适应性保护措施中的一些可能会持续一年以上,并且都能提供暂时的保护,防止新的潜在有毒影响,也包括非放射性内源性来源的影响。适应性保护在单次组织吸收剂量约为 100 至 200 毫希沃特时达到最大值,并在更高剂量下消失。低剂量率可能在较低的细胞剂量下启动最大保护,这些剂量在特定时间间隔内重复给予。适应性保护只能预防约 2-3%的内源性终生癌症风险,如果与流行病学数据一致,并与毒物兴奋效应一致,那么 100 毫希沃特的计算诱导癌症风险就可以完全平衡。低剂量风险建模必须认识到保护的上调。