SCIENTIFIC AND INFORMATION-ANALYTICAL MAGAZINE

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The Medical Radiology and Radiation Safety journal ISSN 1024-6177 was founded in January 1956 (before December 30, 1993 it was entitled Medical Radiology, ISSN 0025-8334). In 2018, the journal received Online ISSN: 2618-9615 and was registered as an electronic online publication in Roskomnadzor on March 29, 2018. It publishes original research articles which cover questions of radiobiology, radiation medicine, radiation safety, radiation therapy, nuclear medicine and scientific reviews. In general the journal has more than 30 headings and it is of interest for specialists working in thefields of medicine¸ radiation biology, epidemiology, medical physics and technology. Since July 01, 2008 the journal has been published by State Research Center - Burnasyan Federal Medical Biophysical Center of Federal Medical Biological Agency. The founder from 1956 to the present time is the Ministry of Health of the Russian Federation, and from 2008 to the present time is the Federal Medical Biological Agency.

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Medical Radiology and Radiation Safety. 2018. Vol. 63. No. 6. P. 71 –81

REVIEW

DOI: 10.12737/article_5c0eb50d2316f4.12478307

M.V. Vasin1, V.Yu. Solov’ev2, V.N. Mal’tsev2, I.E. Andrianova2, S.N. Luk’yanova2

Primary Radiation Stress, Inflammatory Reaction and the Mechanism of Early Postradiation Reparative Processes in Irradiated Tissues

1. Russian Medical Academy of Continuous Professional Education, Moscow, Russia. E-mail: This email address is being protected from spambots. You need JavaScript enabled to view it. ;
2. A.I. Burnasyan Federal Medical Biophysical Center, Moscow, Russia.

M.V. Vasin – Prof. of the Department, Dr. Sci. Med., Prof.; V.Yu. Soloviev – Head of Lab., Dr. Sci. Biol., PhD Tech.;
V.N. Mal’tsev – Leading Researcher, Dr. Sci. Med., Prof.; I.E. Andrianova – Leading Researcher, Dr. Sci. Med.;
S.N. Luk’yanova – Сhief Researcher, Dr. Sci. Biol., Prof.

Abstract

The products of radiolysis released from cellular compartment under the influence of ionizing radiation: highly mobile groups of proteins, damaged nuclear and mitochondrial DNA, extracellular ATP and oxidized low density lipoproteins, cause stress activation in irradiated tissues through a pattern of the receptors with start of the cascade r53 and NF-κB of pro-inflammatory ways conducting to an expression of pro-inflammatory genes stimulating synthesis of cytokines of the IL-1 family. Excessive activation of pro-inflammatory way under the influence of a radioactive stress is limited to synthesis, anti-inflammatory cytokines: IL-4, IL-10, IL-11, IL-13 and also antagonists of IL-1 receptor and TGF-β. G-CSF and MG-CSF induced by action of pro-inflammatory cytokines have anti-inflammatory and anti-apoptotic properties decreasing level of pro-inflammatory cytokines IL-6 and TNF. Glucocorticoids participate in regulation of primary radioactive stress, suppressing an excessive expression of genes of pro-inflammatory cytokines. Increased IL-1 level stimulates secretion of corticosteroids through mechanism of feedback. Adrenergic stimulation is capable to raise a gene IL-1β expression.

The mechanism of radiation apoptosis of stem cells is implemented through p53-Puma way which blocks interaction anti-apoptotic proteins of Bcl-2 with pro-apoptotic proteins of Bax and Bak. After release from mitochondrion of cytochrome C and apoptosis-inducing factor there is an activation of effector cаspаses: caspases 3, 6 and 7 through caspase 9, and final cell destruction.

Wnt way is crucial for post-radiation repair. Potential of the regenerative response of hemopoietic tissue to radiation injury depends on catenin and ability of Wnt way to stimulate post-radiation bone marrow reparation. Mesenchymal stem cells of bone marrow play a large role in post-radiation regeneration of hemopoietic tissue. Their main action is carried out through TLR2 and TLR4 receptors. Mobilization of hemopoietic stem cells is bound to release proteases from bone marrow, including neutrophil elastase and cathepsin G, and a matrix metalproteinase-9.

Radioprotective properties of exogenous IL-1 aren’t limited only by induction of raised G-CSF and GM-CSF production. The larger role in radiation protection is played by the reaction induced by IL-1 in the form of feedback with production anti-apoptotic and anti-inflammatory factors. Primary radioactive stress limits time of radiomitigable effect of IL-1 by 1–2 h after its application after radiation.

Key words: primary radiation stress, proinflammatory cytokines, interleukin-1β, anti-inflammatory cytokines, granulocyte-colony stimulating factor, postradiation blood reparation

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For citation: Vasin MV, Solov’ev VYu, Mal’tsev VN, Andrianova IE, Luk’yanova SN. Primary Radiation Stress, Inflammatory Reaction and Mechanism of Early Postradiation Reparative Processes in Irradiated Tissues. Medical Radiology and Radiation Safety. 2018;63(6):71-81. (Russian).

DOI: 10.12737/article_5c0eb50d2316f4.12478307

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