Yahyapour, R. and Motevaseli, E. and Rezaeyan, A. and Abdollahi, H. and Farhood, B. and Cheki, M. and Rezapoor, S. and Shabeeb, D. and Musa, A.E. and Najafi, M. and Villa, V. (2018) Reduction�oxidation (redox) system in radiation-induced normal tissue injury: molecular mechanisms and implications in radiation therapeutics. Clinical and Translational Oncology, 20 (8). pp. 975-988.
Full text not available from this repository.Abstract
Every year, millions of cancer patients undergo radiation therapy for treating and destroying abnormal cell growths within normal cell environmental conditions. Thus, ionizing radiation can have positive therapeutic effects on cancer cells as well as post-detrimental effects on surrounding normal tissues. Previous studies in the past years have proposed that the reduction and oxidation metabolism in cells changes in response to ionizing radiation and has a key role in radiation toxicity to normal tissue. Free radicals generated from ionizing radiation result in upregulation of cyclooxygenases (COXs), nitric oxide synthase (NOSs), lipoxygenases (LOXs) as well as nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase), and their effected changes in mitochondrial functions are markedly noticeable. Each of these enzymes is diversely expressed in multiple cells, tissues and organs in a specific manner. Overproduction of reactive oxygen radicals (ROS), reactive hydroxyl radical (ROH) and reactive nitrogen radicals (RNS) in multiple cellular environments in the affected nucleus, cell membranes, cytosol and mitochondria, and other organelles, can specifically affect the sensitive and modifying enzymes of the redox system and repair proteins that play a pivotal role in both early and late effects of radiation. In recent years, ionizing radiation has been known to affect the redox functions and metabolism of NADPH oxidases (NOXs) as well as having destabilizing and detrimental effects on directly and indirectly affected cells, tissues and organs. More noteworthy, chronic free radical production may continue for years, increasing the risk of carcinogenesis and other oxidative stress-driven degenerative diseases as well as pathologies, in addition to late effect complications of organ fibrosis. Hence, knowledge about the mechanisms of chronic oxidative damage and injury in affected cells, tissues and organs following exposure to ionizing radiation may help in the development of treatment and management strategies of complications associated with radiotherapy (RT) or radiation accident victims. Thus, this medically relevant phenomenon may lead to the discovery of potential antioxidants and inhibitors with promising results in targeting and modulating the ROS/NO-sensitive enzymes in irradiated tissues and organ injury systems. © 2018, Federación de Sociedades Españolas de OncologÃa (FESEO).
| Item Type: | Article |
|---|---|
| Additional Information: | cited By 12 |
| Uncontrolled Keywords: | calvasculin; lipoxygenase; matrix metalloproteinase; myeloid differentiation factor 88; nitric oxide; nitric oxide synthase; prostaglandin synthase; 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; STAT6 protein; toll like receptor 4, blood vessel injury; bystander effect; cell communication; cell damage; cell death; cytokine release; deoxygenation; DNA damage; DNA repair; enzymology; epigenetics; gap junction; gene expression; genomic instability; hypoxia; inflammation; ionizing radiation; mismatch repair; mitochondrial respiration; necrosis; oxidation reduction reaction; oxidative phosphorylation; oxidative stress; protein expression; respiratory chain; Review; tissue injury |
| Subjects: | QS Human Anatomy WN Radiology. Diagnostic Imaging |
| Depositing User: | eprints admin |
| Date Deposited: | 29 Dec 2018 08:01 |
| Last Modified: | 21 Aug 2019 07:47 |
| URI: | http://eprints.iums.ac.ir/id/eprint/5860 |
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