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.
Highlights
Cancer is one of the most challenging diseases in modern times
The redox system and various oxidases upregulated by free radicals and generated by radiation, including NADPH oxidase, LOXs, nitric oxide synthase (NOS), and COXs, participated in radiationinduced normal tissue damage (RINTD) through different regulatory mechanisms
reactive oxygen species (ROS) and NOS produced by inflammatory cells and mitochondria are involved in oxidative damage to bystander cells and untargeted tissues
Summary
Cancer is one of the most challenging diseases in modern times. In 2015, China reported about 4.2 million new cancer cases and 2.8 million cancer-related deaths [1]. The redox system is related to epigenetic regulation and can regulate the expression of microRNAs (miRNAs) and other molecules, playing a role in sustained oxidative damage after radiation [3]. The generation of ROS induces molecular changes and causes oxidative damage to proteins, lipids, and DNA. It can activate signal transduction pathways and early-response transcription factors [5]. Several studies have demonstrated that epigenetic modulators play an important role in normal tissue damage, after redox-induced ionizing radiation.
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