Open AccessIntercellular communications‐redox interactions in radiation toxicity; potential targets for radiation mitigation
Author(s) -
Farhood Bagher,
Goradel Nasser Hashemi,
Mortezaee Keywan,
Khanlarkhani Neda,
Salehi Ensieh,
Nashtaei Maryam Shabani,
Shabeeb Dheyauldeen,
Musa Ahmed Eleojo,
Fallah Hengameh,
Najafi Masoud
Publication year - 2018
Publication title -
journal of cell communication and signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 44
eISSN - 1873-961X
pISSN - 1873-9601
DOI - 10.1007/s12079-018-0473-3
Subject(s) - intracellular , microbiology and biotechnology , nitric oxide , ionizing radiation , toxicity , nitric oxide synthase , oxidative stress , chemistry , inflammation , dna damage , biology , immunology , biochemistry , irradiation , dna , physics , organic chemistry , nuclear physics
Abstract 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.