Potential Ways to Increase Body Resistance to Damaging Action of Ionizing Radiation with Radiomitigators

Biology Bulletin Reviews - Tập 9 - Trang 503-519 - 2020
M. V. Vasin1, I. B. Ushakov2,3
1Russian Medical Academy of Continuous Professional Education, Ministry of Health of Russia Federation, Moscow, Russia
2Burnasyan Federal Medical Biophysical Center, Federal Medical Biological Agency of Russia, Moscow, Russia
3Nikiforov All-Russia Center of Emergency and Radiation Medicine, Ministry of the Russian Federation for Civil Defense, Emergencies, and Elimination of Consequences of Natural Disasters, St. Petersburg, Russia

Tóm tắt

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.

Tài liệu tham khảo

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