The role of radiation induced oxidative stress as a regulator of radio-adaptive responses

2020 · Unclear · Insufficient evidence

← Research stream

UnclearInsufficient evidencePaper 1610

This review discusses how radiation-induced oxidative stress (RIOS) is implicated as a regulator of adaptive responses in radiation-exposed cells, including activation of p53-related signaling, intrinsic apoptosis pathways, MAPK and PI3K/Akt-associated prolif…

Study snapshot

Publicationmanual · 2020

Study typereview

Reported directionUnclear

Evidence ratingInsufficient

Abstract

The role of radiation induced oxidative stress as a regulator of radio-adaptive responses Sisakht M, Darabian M, Mahmoodzadeh A, Bazi A, Shafiee SM, Mokarram P, Khoshdel Z. The role of radiation induced oxidative stress as a regulator of radio-adaptive responses. Int J Radiat Biol. 2020 Jan 24:1-40. doi: 10.1080/09553002.2020.1721597. 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". Manuscript 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. ncbi.nlm.nih.gov

Machine Enhanced Logic

AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typereview

Effect directionunclear

PopulationNot supplied

Sample sizeNot supplied

ExposureNot supplied

Evidence strengthInsufficientConfidence: 74% · Peer reviewed: yes

Main findings

Outcomes measured

radiation-induced oxidative stress (RIOS)
radio-adaptive responses
molecular signaling pathways (e.g., p53, MAPKs, PI3K/Akt)
apoptosis (mitochondrial depolarization, caspase cascade)
proliferative responses
genetic instability (DNA structural/epigenetic alterations, DNA repair attenuation)
inflammation (MIF, NF-κB, STAT-3)

Limitations

Narrative synthesis; no quantitative effect estimates reported in the abstract.
Exposure types are broad (radiofrequency, microwave, ionizing radiation, low-dose X-radiation) without specific frequencies/doses detailed in the abstract.
No specific populations or study designs of included studies are described in the abstract.

View raw extracted JSON

{
  "study_type": "review",
  "exposure": {
    "band": null,
    "source": null,
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": null
  },
  "population": null,
  "sample_size": null,
  "outcomes": [
    "radiation-induced oxidative stress (RIOS)",
    "radio-adaptive responses",
    "molecular signaling pathways (e.g., p53, MAPKs, PI3K/Akt)",
    "apoptosis (mitochondrial depolarization, caspase cascade)",
    "proliferative responses",
    "genetic instability (DNA structural/epigenetic alterations, DNA repair attenuation)",
    "inflammation (MIF, NF-κB, STAT-3)"
  ],
  "main_findings": "This review discusses how radiation-induced oxidative stress (RIOS) is implicated as a regulator of adaptive responses in radiation-exposed cells, including activation of p53-related signaling, intrinsic apoptosis pathways, MAPK and PI3K/Akt-associated proliferative responses, genetic instability, and inflammatory transcription factors (e.g., MIF, NF-κB, STAT-3).",
  "effect_direction": "unclear",
  "limitations": [
    "Narrative synthesis; no quantitative effect estimates reported in the abstract.",
    "Exposure types are broad (radiofrequency, microwave, ionizing radiation, low-dose X-radiation) without specific frequencies/doses detailed in the abstract.",
    "No specific populations or study designs of included studies are described in the abstract."
  ],
  "evidence_strength": "insufficient",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "oxidative stress",
    "radiation-induced oxidative stress",
    "adaptive response",
    "radio-adaptive response",
    "electromagnetic radiation",
    "radiofrequency",
    "microwave",
    "ionizing radiation",
    "p53",
    "MAPK",
    "PI3K/Akt",
    "apoptosis",
    "genetic instability",
    "inflammation",
    "NF-κB",
    "STAT-3",
    "MIF"
  ],
  "suggested_hubs": []
}

AI can be wrong. Always verify against the paper.

AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.1080/09553002.2020.1721597
PubMed: Not supplied

Read the original paper →

Related papers

← Back to the Research Library