Feinendegen L E
Heinrich-Heine-University Düsseldorf, Germany.
Radiat Prot Dosimetry. 2003;104(4):337-46. doi: 10.1093/oxfordjournals.rpd.a006197.
In reviewing the tissue effects of low-dose radiation (1) absorbed dose to tissue is replaced by the sum of energy deposited with track events in cell-equivalent tissue micromasses, i.e. with microdose hits, in the number of exposed micromasses and (2) induced cell damage and adaptive protection are related to microdose hits in exposed micromasses for a given radiation quality. DNA damage increases with the number of microdose hits. They also can induce adaptive protection, mainly against endogenous DNA damage. This protection involves cellular defences, DNA repair and damage removal. With increasing numbers of low linear energy transfer (LET) microdose hits in exposed micromasses, adaptive protection first tends to outweigh damage and then (above 200 mGy) fails and largely disappears. These experimental data predict that cancer risk coefficients derived by epidemiology at high-dose irradiation decline at low doses and dose rates when adaptive protection outdoes DNA damage. The dose-risk function should include both linear and non-linear terms at low doses.
在回顾低剂量辐射的组织效应时,(1)组织吸收剂量被细胞等效组织微团中径迹事件沉积的能量总和所取代,即微剂量击中,以暴露微团的数量来计算,并且(2)对于给定的辐射质量,诱导的细胞损伤和适应性保护与暴露微团中的微剂量击中有关。DNA损伤随微剂量击中次数增加。它们还可诱导适应性保护,主要针对内源性DNA损伤。这种保护涉及细胞防御、DNA修复和损伤清除。随着暴露微团中低传能线密度(LET)微剂量击中次数的增加,适应性保护首先倾向于超过损伤,然后(超过200 mGy)失效并基本消失。这些实验数据预测,当适应性保护超过DNA损伤时,高剂量辐射流行病学得出的癌症风险系数在低剂量和低剂量率下会下降。低剂量时的剂量-风险函数应同时包括线性和非线性项。