Abstract

This review considers the potential mechanisms of radiomitigative effect of radioprotective drugs in interaction with pathophysiological processes accompanying radiation injury to tissues at the earliest stages of its development. Radiomitigators affect bodily systems throughout the development of primary radiation stress and inflammatory process upon the realization of radiation injury during the primary radiation reaction. Inflammation as a protective body reaction to pathogens represents a self-organized system that commits support and limits the intensity of its manifestation. For this reason, the implementation of the radioprotective effect of radiomitigators, including immunogens, proinflammatory cytokines, steroid hormones, biogenic amines, and purine nucleosides and their synthetic and natural analogs, which stimulate native immunity, depends on its initial state and the severity of radiation injury of the body. The inverse negative relation in response to the action of proinflammatory cytokines, which is manifested as induction of the synthesis of anti-inflammatory cytokines and hematopoietic growth factors (primarily, granulocyte colony–stimulating factor), promotes the activation of myelopoiesis and their antiapoptotic action. The interaction of the immunogen effect and radiation stress depends on pharmacodynamics and features of the realization of the radioprotective properties of drugs. The implementation of the action of radiomitigators depends on the functioning of the antioxidant system of the body, because it can be exhausted under the influence of inflammation. In this case, postradiation oxidative toxemia induces injuries to vital parenchymatous organs. This is observed under the influence of proinflammatory cytokines at combined radiation injuries. All of the listed groups of radiomitigators have identical radioprotective activity (DRF = 1.2–1.3). The absence of expressed side effects, good tolerance of radiomitigators by humans, and the duration of their possible effective application after irradiation are the key indices for assessment of their prospects in radiation accidents.

中文翻译：

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增强人体对放射性减轻剂对电离辐射的破坏作用的抵抗力的潜在方法

摘要

这篇综述考虑了辐射防护药物在其发展的最早阶段与放射损伤对组织的病理生理过程相互作用的潜在放射减轻作用机理。在初次放射反应期间实现放射损伤后，放射减轻剂会在整个初次放射应力和炎症过程的发展过程中影响人体系统。炎症是对病原体的一种保护性身体反应，它代表着一个自组织的系统，可以提供支持并限制其表现的强度。出于这个原因，包括免疫原，促炎性细胞因子，类固醇激素，生物胺和嘌呤核苷以及它们的合成和天然类似物在内的放射性减轻剂的辐射防护作用得以实现，这些物质能够刺激天然免疫力，取决于其初始状态和对人体的放射损伤的严重程度。响应促炎性细胞因子作用的负相关关系，表现为诱导抗炎性细胞因子和造血生长因子（主要是粒细胞集落刺激因子）的合成，促进了骨髓生成的激活及其抗凋亡作用。免疫原效应和放射应力的相互作用取决于药效学和药物放射防护特性的实现特征。放射线抑制器作用的实现取决于人体抗氧化剂系统的功能，因为它可以在炎症的影响下耗尽。在这种情况下，放射后氧化毒血症会导致对实质实质器官的伤害。这是在合并放射损伤的促炎细胞因子的影响下观察到的。列出的所有放射缓解组均具有相同的放射防护活性（DRF = 1.2–1.3）。没有明确的副作用，人体对放射线缓解剂的良好耐受性以及放射后可能有效应用的持续时间是评估其在放射事故中前景的关键指标。