Repository of Research and Investigative Information

Repository of Research and Investigative Information

Kurdistan University of Medical Sciences

NADPH oxidase as a target for modulation of radiation response; implications to carcinogenesis and radiotherapy

(2019) NADPH oxidase as a target for modulation of radiation response; implications to carcinogenesis and radiotherapy. Current Molecular Pharmacology.

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Official URL: https://www.scopus.com/inward/record.uri?eid=2-s2....

Abstract

Background: Radiotherapy is a treatment modality for cancer. For better therapeutic efficiency, it could be used in combination with surgery, chemotherapy or immunotherapy. In addition to its beneficial therapeutic effects, exposure to radiation leads to several toxic effects on normal tissues. Also, it may induce some changes in genomic expression of tumor cells, thereby increasing the resistance of tumor cells. These changes lead to the appearance of some acute reactions in irradiated organs, increased risk of carcinogenesis, and reduction in the therapeutic effect of radiotherapy. Discussion: So far, several studies have proposed different targets such as cyclooxygenase-2 (COX-2), some toll-like receptors (TLRs), mitogen-activated protein kinases (MAPKs) etc., for the amelioration of radiation toxicity and enhancing tumor response. NADPH oxidase includes five NOX and two dual oxidases (DUOX1 and DUOX2) subfamilies that through the production of superoxide and hydrogen peroxide, play key roles in oxidative stress and several signaling pathways involved in early and late effects of ionizing radiation. Chronic ROS production by NOX enzymes can induce genomic instability, thereby increasing the risk of carcinogenesis. Also, these enzymes are able to induce cell death, especially through apoptosis and senescence that may affect tissue function. ROS-derived NADPH oxidase causes apoptosis in some organs such as intestine and tongue, which mediate inflammation. Furthermore, continuous ROS production stimulates fibrosis via stimulation of fibroblast differentiation and collagen deposition. Evidence has shown that in contrast to normal tissues, the NOX system induces tumor resistance to radiotherapy through some mechanisms such as induction of hypoxia, stimulation of proliferation, and activation of macrophages. However, there are some contradictory results. Inhibition of NADPH oxidase in experimental studies has shown promising results for both normal tissue protection and tumor sensitization to ionizing radiation. Conclusion: In this article, we aimed to review the role of different subfamilies of NADPH oxidase in radiation-induced early and late normal tissue toxicities in different organs. © 2019 Bentham Science Publishers.

Item Type: Article
Keywords: cyclooxygenase 2; dual oxidase; dual oxidase 1; dual oxidase 2; mitogen activated protein kinase; nitric oxide; reactive oxygen metabolite; reduced nicotinamide adenine dinucleotide phosphate oxidase; reduced nicotinamide adenine dinucleotide phosphate oxidase 1; reduced nicotinamide adenine dinucleotide phosphate oxidase 2; reduced nicotinamide adenine dinucleotide phosphate oxidase 4; reduced nicotinamide adenine dinucleotide phosphate oxidase 5; synaptophysin; toll like receptor; unclassified drug; reactive oxygen metabolite; reduced nicotinamide adenine dinucleotide phosphate oxidase, angiogenesis; apoptosis; cancer radiotherapy; carcinogenesis; cell aging; cell death; cell differentiation; cell proliferation; DNA damage; feedback system; fibroblast; genomic instability; human; hypoxia; in vitro study; in vivo study; inflammation; ionizing radiation; macrophage activation; oxidative stress; priority journal; protein expression; protein function; radiation protection; radiation response; radiosensitization; Review; risk factor; signal transduction; upregulation; bystander effect; carcinogenesis; chemistry; ionizing radiation; metabolism; neoplasm; radiation response, Bystander Effect; Carcinogenesis; Genomic Instability; Humans; NADPH Oxidases; Neoplasms; Oxidative Stress; Radiation, Ionizing; Reactive Oxygen Species
Page Range: pp. 50-60
Journal or Publication Title: Current Molecular Pharmacology
Volume: 12
Number: 1
Publisher: Bentham Science Publishers B.V.
Identification Number: 10.2174/1874467211666181010154709
ISSN: 18744672
Depositing User: مهندس جمال محمودپور
URI: http://eprints.muk.ac.ir/id/eprint/2110

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