The role of radiation induced oxidative stress as a regulator of radio-adaptive responses. (3rd May 2020)

• Record Type: Journal Article
• Authors: Sisakht, Mohsen; Darabian, Maryam; Mahmoodzadeh, Amir; Bazi, Ali; Shafiee, Sayed Mohammad; Mokarram, Pooneh; Khoshdel, Zahra
• Is Part Of: International journal of radiation biology. Volume 96:Number 5(2020)
• Page Start: 561
• Page End: 576
• Publication Date: 2020-05-03
• Subjects: Radiation-induced oxidative stress -- adaptive response -- molecular response; Radiation -- Physiological effect -- Periodicals; Radiobiology -- Periodicals; 571.45
• DOI: 10.1080/09553002.2020.1721597
• Languages: English
• ISSNs: 0955-3002

Abstract

Abstract: Purpose: Various sources of radiation including radiofrequency, electromagnetic radiation (EMR), low- dose X-radiation, low-level microwave radiation and ionizing radiation (IR) are indispensable parts of modern life. In the current review, we discussed the adaptive responses of biological systems to radiation with a focus on the impacts of radiation-induced oxidative stress (RIOS) and its molecular downstream signaling pathways. Materials and methods: A comprehensive search was conducted in Web of Sciences, PubMed, Scopus, Google Scholar, Embase, and Cochrane Library. Keywords included Mesh terms of "radiation, " "electromagnetic radiation, " "adaptive immunity, " "oxidative stress, " and "immune checkpoints." Manuscripts published up until December 2019 were included. Results: RIOS induces various molecular adaptors connected with adaptive responses in radiation exposed cells. One of these adaptors includes p53 which promotes various cellular signaling pathways. RIOS also activates the intrinsic apoptotic pathway by depolarization of the mitochondrial membrane potential and activating the caspase apoptotic cascade. RIOS is also involved in radiation-induced proliferative responses through interaction with mitogen-activated protein kinases (MAPks) including p38 MAPK, ERK, and c-Jun N-terminal kinase (JNK). Protein kinase B (Akt)/phosphoinositide 3-kinase (PI3K) signaling pathway has also been reported to be involved in RIOS-induced proliferative responses. Furthermore, RIOS promotes genetic instability by introducing DNA structural and epigenetic alterations, as well as attenuating DNA repair mechanisms. Inflammatory transcription factors including macrophage migration inhibitory factor (MIF), nuclear factor κB (NF-κB), and signal transducer and activator of transcription-3 (STAT-3) paly major role in RIOS-induced inflammation. Conclusion: In conclusion, RIOS considerably contributes to radiation induced adaptive responses. Other possible molecular adaptors modulating RIOS-induced responses are yet to be divulged in future studies.