Regional Responses in Radiation-Induced Normal Tissue Damage

Normal tissue side effects remain a major concern in radiotherapy. The improved precision of radiation dose delivery of recent technological developments in radiotherapy has the potential to reduce the radiation dose to organ regions that contribute the most to the development of side effects. This review discusses the contribution of regional variation in radiation responses in several organs. In the brain, various regions were found to contribute to radiation-induced neurocognitive dysfunction. In the parotid gland, the region containing the major ducts was found to be critical in hyposalivation. The heart and lung were each found to exhibit regional responses while also mutually affecting each other’s response to radiation. Sub-structures critical for the development of side effects were identified in the pancreas and bladder. The presence of these regional responses is based on a non-uniform distribution of target cells or sub-structures critical for organ function. These characteristics are common to most organs in the body and we therefore hypothesize that regional responses in radiation-induced normal tissue damage may be a shared occurrence. Further investigations will offer new opportunities to reduce normal tissue side effects of radiotherapy using modern and high-precision technologies.

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Protective effect of ramipril, inhibitor of angiotensin converting enzyme on radiation-induced normal tissue damage without tumor protection

International Journal of Radiation Oncology*Biology*Physics ◽

10.1016/j.ijrobp.2004.07.165 ◽

2004 ◽

Vol 60 (1) ◽

pp. S340 ◽

Cited By ~ 1

Author(s):

R. Kohl ◽

S.L. Brown ◽

G. Zhu ◽

A. Kolozsvary ◽

J.H. Kim

Keyword(s):

Angiotensin Converting Enzyme ◽

Protective Effect ◽

Tissue Damage ◽

Normal Tissue ◽

Converting Enzyme ◽

Normal Tissue Damage ◽

Tumor Protection ◽

Radiation Induced

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

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/3010342 ◽

2019 ◽

Vol 2019 ◽

pp. 1-11 ◽

Cited By ~ 14

Author(s):

Jinlong Wei ◽

Bin Wang ◽

Huanhuan Wang ◽

Lingbin Meng ◽

Qin Zhao ◽

...

Keyword(s):

Oxidative Stress ◽

Tissue Damage ◽

Normal Tissue ◽

Noncoding Rna ◽

Nicotinamide Adenine Dinucleotide Phosphate ◽

Redox System ◽

Epigenetic Mechanisms ◽

Rna Regulation ◽

Normal Tissue Damage ◽

Radiation Induced

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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