European Cancer and Environment Research-ECERI, 1000 Bruxelles, Belgium.
Euro Mediterranean Scientific Biomedical Institute-ISBEM Research Centre, 72023 Mesagne (Brindisi), Italy.
Int J Environ Res Public Health. 2018 Sep 10;15(9):1971. doi: 10.3390/ijerph15091971.
We reviewed available evidence in medical literature concerning experimental models of exposure to ionizing radiations (IR) and their mechanisms of producing damages on living organisms. The traditional model is based on the theory of "stochastic breakage" of one or both strands of the DNA double helix. According to this model, high doses may cause the breaks, potentially lethal to the cell by damaging both DNA strands, while low doses of IR would cause essentially single strands breaks, easily repairable, resulting in no permanent damages. The available evidence makes this classical model increasingly less acceptable, because the exposure to low doses of IR seems to have carcinogenic effects, even after years or decades, both in the exposed individuals and in subsequent generations. In addition, the cells that survived the exposure to low doses, despite being apparently normal, accumulate damages that become evident in their progeny, such as nonclonal chromosomal aberrations, which can be found even in cells not directly irradiated due to the exchange of molecular signals and complex tissue reactions involving neighboring or distant cells. For all these reasons, a paradigm shift is needed, based on evidence and epigenetics.
我们回顾了医学文献中有关暴露于电离辐射(IR)的实验模型及其在生物体中产生损伤的机制的现有证据。传统模型基于 DNA 双螺旋中一条或两条链“随机断裂”的理论。根据该模型,高剂量可能会导致断裂,通过破坏两条 DNA 链,对细胞造成潜在的致命伤害,而低剂量的 IR 则会导致基本上单链断裂,容易修复,不会造成永久性损伤。现有的证据使得这个经典模型越来越不可接受,因为暴露于低剂量的 IR 似乎具有致癌作用,即使在暴露个体和随后的几代中也是如此。此外,尽管暴露于低剂量的细胞表面上看起来正常,但它们会积累在其后代中变得明显的损伤,例如非克隆性染色体异常,即使由于分子信号的交换和涉及邻近或远处细胞的复杂组织反应,也可以在未直接照射的细胞中发现这些损伤。基于证据和表观遗传学,我们需要进行范式转变。