Dörr W
Department of Radiation Oncology and Christian Doppler Laboratory for Medical Radiation Research for Radiooncology, Comprehensive Cancer Centre, Medical University Vienna/Vienna General Hospital, Waehringer Guertel 18-20, A-1090 Vienna, Austria
Ann ICRP. 2015 Jun;44(1 Suppl):58-68. doi: 10.1177/0146645314560686. Epub 2015 Mar 5.
Tissue effects of radiation exposure are observed in virtually all normal tissues, with interactions when several organs are involved. Early reactions occur in turnover tissues, where proliferative impairment results in hypoplasia; late reactions, based on combined parenchymal, vascular, and connective tissue changes, result in loss of function within the exposed volume; consequential late effects develop through interactions between early and late effects in the same organ; and very late effects are dominated by vascular sequelae. Invariably, involvement of the immune system is observed. Importantly, latent times of late effects are inversely dependent on the biologically equieffective dose. Each tissue component and--importantly--each individual symptom/endpoint displays a specific dose-effect relationship. Equieffective doses are modulated by exposure conditions: in particular, dose-rate reduction--down to chronic levels--and dose fractionation impact on late responding tissues, while overall exposure time predominantly affects early (and consequential late) reactions. Consequences of partial organ exposure are related to tissue architecture. In 'tubular' organs (gastrointestinal tract, but also vasculature), punctual exposure affects function in downstream compartments. In 'parallel' organs, such as liver or lungs, only exposure of a significant (organ-dependent) fraction of the total volume results in clinical consequences. Forthcoming studies must address biomarkers of the individual risk for tissue reactions, and strategies to prevent/mitigate tissue effects after exposure.
几乎在所有正常组织中都能观察到辐射暴露的组织效应，当多个器官受到影响时会产生相互作用。早期反应发生在更新组织中，增殖受损导致发育不全；晚期反应基于实质、血管和结缔组织的综合变化，导致暴露区域内功能丧失；后续晚期效应通过同一器官中早期和晚期效应的相互作用而产生；而非常晚期效应则以血管后遗症为主。无一例外，都会观察到免疫系统受到影响。重要的是，晚期效应的潜伏期与生物等效剂量成反比。每个组织成分，以及重要的是，每个个体症状/终点都呈现出特定的剂量效应关系。等效剂量受暴露条件调节：特别是剂量率降低至慢性水平以及剂量分割对晚期反应组织有影响，而总暴露时间主要影响早期（以及后续晚期）反应。部分器官暴露的后果与组织结构有关。在“管状”器官（胃肠道以及血管系统）中，点状暴露会影响下游区域的功能。在“并行”器官，如肝脏或肺部，只有当总容积的相当一部分（取决于器官）受到暴露时才会产生临床后果。未来的研究必须关注个体组织反应风险的生物标志物，以及暴露后预防/减轻组织效应的策略。
