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Review
. 2019 Nov 12:2019:3010342.
doi: 10.1155/2019/3010342. eCollection 2019.

Radiation-Induced Normal Tissue Damage: Oxidative Stress and Epigenetic Mechanisms

Jinlong Wei  1 , Bin Wang  1 , Huanhuan Wang  1 , Lingbin Meng  2 , Qin Zhao  1 , Xinyu Li  1 , Ying Xin  3 , Xin Jiang  1
Affiliations
Review

Radiation-Induced Normal Tissue Damage: Oxidative Stress and Epigenetic Mechanisms

Jinlong Wei et al. Oxid Med Cell Longev. .

Abstract

Radiotherapy (RT) is currently one of the leading treatments for various cancers; however, it may cause damage to healthy tissue, with both short-term and long-term side effects. Severe radiation-induced normal tissue damage (RINTD) frequently has a significant influence on the progress of RT and the survival and prognosis of patients. The redox system has been shown to play an important role in the early and late effects of RINTD. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are the main sources of RINTD. The free radicals produced by irradiation can upregulate several enzymes including nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase), lipoxygenases (LOXs), nitric oxide synthase (NOS), and cyclooxygenases (COXs). These enzymes are expressed in distinct ways in various cells, tissues, and organs and participate in the RINTD process through different regulatory mechanisms. In recent years, several studies have demonstrated that epigenetic modulators play an important role in the RINTD process. Epigenetic modifications primarily contain noncoding RNA regulation, histone modifications, and DNA methylation. In this article, we will review the role of oxidative stress and epigenetic mechanisms in radiation damage, and explore possible prophylactic and therapeutic strategies for RINTD.

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Conflict of interest statement

The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
The mechanisms of redox system activation, inflammation response, and epigenetic regulation following exposure to radiation.
See this image and copyright information in PMC

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