PMID- 31976798
OWN - NLM
STAT- MEDLINE
DCOM- 20201130
LR  - 20201130
IS  - 1362-3095 (Electronic)
IS  - 0955-3002 (Linking)
VI  - 96
IP  - 5
DP  - 2020 May
TI  - The role of radiation induced oxidative stress as a regulator of radio-adaptive 
      responses.
PG  - 561-576
LID - 10.1080/09553002.2020.1721597 [doi]
AB  - 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 kappaB (NF-kappaB), 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.
FAU - Sisakht, Mohsen
AU  - Sisakht M
AUID- ORCID: 0000-0002-9882-7211
AD  - Department of Medical Biochemistry, School of Medicine, Shiraz University of 
      Medical Sciences, Shiraz, Iran.
FAU - Darabian, Maryam
AU  - Darabian M
AUID- ORCID: 0000-0003-4033-1798
AD  - Department of Radiology, Faculty of Paramedical Sciences, Shiraz University of 
      Medical Sciences, Shiraz, Iran.
FAU - Mahmoodzadeh, Amir
AU  - Mahmoodzadeh A
AUID- ORCID: 0000-0002-0523-8152
AD  - Department of Medical Biochemistry, School of Medicine, Shiraz University of 
      Medical Sciences, Shiraz, Iran.
AD  - Medical Biology Research Center, Health Technology Institute, Kermanshah 
      University of Medical Sciences, Kermanshah, Iran.
FAU - Bazi, Ali
AU  - Bazi A
AUID- ORCID: 0000-0003-4872-1352
AD  - Faculty of Allied Medical Sciences, Zabol University of Medical Sciences, Zabol, 
      Iran.
FAU - Shafiee, Sayed Mohammad
AU  - Shafiee SM
AUID- ORCID: 0000-0002-9221-2267
AD  - Department of Medical Biochemistry, School of Medicine, Shiraz University of 
      Medical Sciences, Shiraz, Iran.
FAU - Mokarram, Pooneh
AU  - Mokarram P
AUID- ORCID: 0000-0002-9717-0473
AD  - Department of Medical Biochemistry, School of Medicine, Shiraz University of 
      Medical Sciences, Shiraz, Iran.
FAU - Khoshdel, Zahra
AU  - Khoshdel Z
AUID- ORCID: 0000-0003-2539-9997
AD  - Department of Medical Biochemistry, School of Medicine, Shiraz University of 
      Medical Sciences, Shiraz, Iran.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20200207
PL  - England
TA  - Int J Radiat Biol
JT  - International journal of radiation biology
JID - 8809243
RN  - 0 (Autophagy-Related Proteins)
RN  - 0 (Beclin-1)
RN  - 0 (Kelch-Like ECH-Associated Protein 1)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NF-kappa B)
RN  - 0 (NFE2L2 protein, human)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - EC 3.4.22.- (ATG4A protein, human)
RN  - EC 3.4.22.- (Cysteine Endopeptidases)
SB  - IM
MH  - AMP-Activated Protein Kinases/physiology
MH  - Adaptation, Biological/*radiation effects
MH  - Animals
MH  - Autophagy/physiology
MH  - Autophagy-Related Proteins/physiology
MH  - Beclin-1/physiology
MH  - Cysteine Endopeptidases/physiology
MH  - Humans
MH  - Kelch-Like ECH-Associated Protein 1/physiology
MH  - NF-E2-Related Factor 2/physiology
MH  - NF-kappa B/physiology
MH  - Oxidative Stress/physiology/*radiation effects
MH  - Signal Transduction/physiology
OTO - NOTNLM
OT  - Radiation-induced oxidative stress
OT  - adaptive response
OT  - molecular response
EDAT- 2020/01/25 06:00
MHDA- 2020/12/01 06:00
CRDT- 2020/01/25 06:00
PHST- 2020/01/25 06:00 [pubmed]
PHST- 2020/12/01 06:00 [medline]
PHST- 2020/01/25 06:00 [entrez]
AID - 10.1080/09553002.2020.1721597 [doi]
PST - ppublish
SO  - Int J Radiat Biol. 2020 May;96(5):561-576. doi: 10.1080/09553002.2020.1721597. 
      Epub 2020 Feb 7.