{"title":"Mitochondrial reactive oxygen species-mediated fibroblast activation has a role in tumor microenvironment formation in radiation carcinogenesis.","authors":"Tsutomu Shimura, Akira Ushiyama","doi":"10.1093/rpd/ncae027","DOIUrl":null,"url":null,"abstract":"<p><p>Cancer risks attributable to low-dose and low-dose-rate radiation are a serious concern for public health. Radiation risk assessment is based on lifespan studies among Hiroshima-Nagasaki A-bomb survivors; however, there are statistical limitations due to a small sample size for low-dose radiation. Therefore, basic biological studies are helpful in understanding the mechanism of radiation carcinogenesis. The detrimental effects of ionising radiation (IR) are caused by reactive oxygen species (ROS)-mediated oxidative DNA damage. IR-induced delayed ROS are produced in the electron transport chain reaction of the mitochondrial complex. Thus, mitochondria are a source of ROS and a primary target for ROS attacks. Consequently, mitochondrial dysfunction is thought to be a key event in the metabolic changes of cancer cells and is important in radiation-induced carcinogenesis. In this paper, we present recent findings on radiation carcinogenesis effect assessment, focusing on mitochondrial function as stress sensors.</p>","PeriodicalId":20795,"journal":{"name":"Radiation protection dosimetry","volume":null,"pages":null},"PeriodicalIF":0.8000,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Radiation protection dosimetry","FirstCategoryId":"93","ListUrlMain":"https://doi.org/10.1093/rpd/ncae027","RegionNum":4,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Cancer risks attributable to low-dose and low-dose-rate radiation are a serious concern for public health. Radiation risk assessment is based on lifespan studies among Hiroshima-Nagasaki A-bomb survivors; however, there are statistical limitations due to a small sample size for low-dose radiation. Therefore, basic biological studies are helpful in understanding the mechanism of radiation carcinogenesis. The detrimental effects of ionising radiation (IR) are caused by reactive oxygen species (ROS)-mediated oxidative DNA damage. IR-induced delayed ROS are produced in the electron transport chain reaction of the mitochondrial complex. Thus, mitochondria are a source of ROS and a primary target for ROS attacks. Consequently, mitochondrial dysfunction is thought to be a key event in the metabolic changes of cancer cells and is important in radiation-induced carcinogenesis. In this paper, we present recent findings on radiation carcinogenesis effect assessment, focusing on mitochondrial function as stress sensors.
期刊介绍：
Radiation Protection Dosimetry covers all aspects of personal and environmental dosimetry and monitoring, for both ionising and non-ionising radiations. This includes biological aspects, physical concepts, biophysical dosimetry, external and internal personal dosimetry and monitoring, environmental and workplace monitoring, accident dosimetry, and dosimetry related to the protection of patients. Particular emphasis is placed on papers covering the fundamentals of dosimetry; units, radiation quantities and conversion factors. Papers covering archaeological dating are included only if the fundamental measurement method or technique, such as thermoluminescence, has direct application to personal dosimetry measurements. Papers covering the dosimetric aspects of radon or other naturally occurring radioactive materials and low level radiation are included. Animal experiments and ecological sample measurements are not included unless there is a significant relevant content reason.
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