Intercellular communications-redox interactions in radiation toxicity; potential targets for radiation mitigation

Journal of Cell Communication and Signaling

article

Farhood, Bagher¹  Najafi, Masoud²  Goradel, Nasser Hashemi³  Mortezaee, Keywan⁴  Khanlarkhani, Neda⁵  Salehi, Ensieh⁵  Nashtaei, Maryam Shabani⁵  Shabeeb, Dheyauldeen⁷  Musa, Ahmed Eleojo⁷  Fallah, Hengameh^1,10 

[1] Department of Medical Physics and Radiology, Faculty of Paramedical Sciences, Kashan University of Medical Sciences;Radiology and Nuclear Medicine Department, School of Paramedical Sciences, Kermanshah University of Medical Sciences;Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences;Department of Anatomy, School of Medicine, Kurdistan University of Medical Sciences;Department of Anatomy, School of Medicine, Tehran University of Medical Sciences;Infertility Department, Shariati Hospital, Tehran University of Medical Sciences;Department of Medical Physics & Biomedical Engineering, School of Medicine, Tehran University of Medical Sciences;Department of Physiology, College of Medicine, University of Misan;Research Center for Molecular and Cellular Imaging, Tehran University of Medical Sciences;Department of Chemistry, Faculty of Science, Islamic Azad University

关键词: Radiation;    Cohort effect;    Bystander effect;    Non-targeted effect;    Radiation toxicity;    Radiation disaster;    Radiotherapy;    Intracellular communication;    Cytokines;    Redox system;    Mitigation;    Carcinogenesis;   

DOI  :  10.1007/s12079-018-0473-3

学科分类：分子生物学，细胞生物学和基因

来源: Springer

【 摘 要 】

Nowadays, using ionizing radiation (IR) is necessary for clinical, agricultural, nuclear energy or industrial applications. Accidental exposure to IR after a radiation terror or disaster poses a threat to human. In contrast to the old dogma of radiation toxicity, several experiments during the last two recent decades have revealed that intercellular signaling and communications play a key role in this procedure. Elevated level of cytokines and other intercellular signals increase oxidative damage and inflammatory responses via reduction/oxidation interactions (redox system). Intercellular signals induce production of free radicals and inflammatory mediators by some intermediate enzymes such as cyclooxygenase-2 (COX-2), nitric oxide synthase (NOS), NADPH oxidase, and also via triggering mitochondrial ROS. Furthermore, these signals facilitate cell to cell contact and increasing cell toxicity via cohort effect. Nitric oxide is a free radical with ability to act as an intercellular signal that induce DNA damage and changes in some signaling pathways in irradiated as well as non-irradiated adjacent cells. Targeting of these mediators by some anti-inflammatory agents or via antioxidants such as mitochondrial ROS scavengers opens a window to mitigate radiation toxicity after an accidental exposure. Experiments which have been done so far suggests that some cytokines such as IL-1β, TNF-α, TGF-β, IL-4 and IL-13 are some interesting targets that depend on irradiated organs and may help mitigate radiation toxicity. Moreover, animal experiments in recent years indicated that targeting of toll like receptors (TLRs) may be more useful for radioprotection and mitigation. In this review, we aimed to describe the role of intercellular interactions in oxidative injury, inflammation, cell death and killing effects of IR. Moreover, we described evidence on potential mitigation of radiation injury via targeting of these mediators.

【 授权许可】

CC BY