生物系统对低剂量电离辐射的反应。

Ludwig E Feinendegen, Myron Pollycove, Charles A Sondhaus
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引用次数: 0

摘要

生物组织通过在信号网络中共同行动的细胞来运作。这些信号网络确保细胞在不断暴露于一系列潜在毒性物质的情况下,仍能协调运作,这些毒性物质既有来自外部环境的,也有来自新陈代谢的。生命组织确实是一个复杂的适应系统。为了研究低剂量辐射的特定组织效应,(1) 组织中的吸收剂量由细胞等效组织微量(1 毫微克)在所有受照微量中每个轨迹事件或命中沉积的能量总和来代替,即由受照微量中所有微剂量命中的平均能量来代替,细胞剂量表示来自多个微剂量的每个微量的总能量;(2) 组织效应与细胞损伤和细胞保护反应有关,即在特定辐射质量下,受照射微质量中的所有微剂量照射的平均细胞损伤和细胞保护反应。每次低线性能量转移(LET)平均微剂量照射造成 DNA 直接损伤的概率极小,在一定剂量范围内与照射次数成比例增加。延迟的临时适应性保护(AP)包括:(a) 诱导活性氧解毒;(b) DNA 修复率提高;(c) 诱导受损细胞凋亡,随后正常细胞替代和细胞分化;(d) 刺激免疫反应,所有这些都会引起基因表达的相应变化。这些 AP 类别可能持续不到一天,也可能持续数周,并通过细胞对再次辐照的反应来检验。它们在生理学上是针对非辐射性的、主要是内源性的 DNA 损伤起作用的,这种损伤大量且持续存在。每个微质量的罕见微剂量照射造成的本底辐射损伤要少得多。除细胞凋亡外,AP 在超过约 200 mGy 的低辐射(相当于每个受照射微质量约 200 微剂量照射)时会逐渐失效。在长期暴露的情况下,这一比率似乎每天超过 1。损伤和保护之间的平衡有利于低剂量细胞的保护和高剂量细胞的损伤。高剂量细胞对未受辐照邻近细胞的旁观效应似乎包括损伤和保护。关于肿瘤发生,基于上述低剂量和剂量率的双重反应模式的模型与非线性反应数据一致,并与辐射诱发癌症的线性无阈剂量风险假说相矛盾。事实上,剂量-癌症风险函数应包括线性和非线性项。
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Responses to low doses of ionizing radiation in biological systems.

Biological tissues operate through cells that act together within signaling networks. These assure coordinated cell function in the face of constant exposure to an array of potentially toxic agents, externally from the environment and endogenously from metabolism. Living tissues are indeed complex adaptive systems.To examine tissue effects specific for low-dose radiation, (1) absorbed dose in tissue is replaced by the sum of the energies deposited by each track event, or hit, in a cell-equivalent tissue micromass (1 ng) in all micromasses exposed, that is, by the mean energy delivered by all microdose hits in the exposed micromasses, with cell dose expressing the total energy per micromass from multiple microdoses; and (2) tissue effects are related to cell damage and protective cellular responses per average microdose hit from a given radiation quality for all such hits in the exposed micromasses.The probability of immediate DNA damage per low-linear-energy-transfer (LET) average micro-dose hit is extremely small, increasing over a certain dose range in proportion to the number of hits. Delayed temporary adaptive protection (AP) involves (a) induced detoxification of reactive oxygen species, (b) enhanced rate of DNA repair, (c) induced removal of damaged cells by apoptosis followed by normal cell replacement and by cell differentiation, and (d) stimulated immune response, all with corresponding changes in gene expression. These AP categories may last from less than a day to weeks and be tested by cell responses against renewed irradiation. They operate physiologically against nonradiogenic, largely endogenous DNA damage, which occurs abundantly and continually. Background radiation damage caused by rare microdose hits per micromass is many orders of magnitude less frequent. Except for apoptosis, AP increasingly fails above about 200 mGy of low-LET radiation, corresponding to about 200 microdose hits per exposed micromass. This ratio appears to exceed approximately 1 per day for protracted exposure. The balance between damage and protection favors protection at low cell doses and damage at high cell doses. Bystander effects from high-dosed cells to nonirradiated neighboring cells appear to include both damage and protection.Regarding oncogenesis, a model based on the aforementioned dual response pattern at low doses and dose rates is consistant with the nonlinear reponse data and contradicts the linear no-threshold dose-risk hypothesis for radiation-induced cancer. Indeed, a dose-cancer risk function should include both linear and nonlinear terms.

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