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硒缺乏对小鼠X射线和碳离子束辐照生物学结果的影响。

Effects of selenium deficiency on biological results of X-ray and carbon-ion beam irradiation in mice.

作者信息

Ueno Megumi, Shibata Sayaka, Nakanishi Ikuo, Aoki Ichio, Yamada Ken-Ichi, Matsumoto Ken-Ichiro

机构信息

Quantitative RedOx Sensing Group, Department of Radiation Regulatory Science Research, National Institute of Radiological Sciences, Quantum Life and Medical Science Directorate, National Institutes for Quantum Science and Technology, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan.

Applied MRI Research Group, Department of Molecular Imaging and Theranostics, Institute for Quantum Medical Science, Quantum Life and Medical Science Directorate, National Institutes for Quantum Science and Technology, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan.

出版信息

J Clin Biochem Nutr. 2023 Mar;72(2):107-116. doi: 10.3164/jcbn.22-57. Epub 2022 Dec 8.

Abstract

The impact of radiation-induced hydrogen peroxide (HO) on the biological effects of X-rays and carbon-ion beams was investigated using a selenium-deficient (SeD) mouse model. Selenium is the active center of glutathione peroxidase (GSH-Px), and SeD mice lack the ability to degrade HO. Male and female SeD mice were prepared by feeding a torula yeast-based SeD diet and ultrapure water. Thirty-day survival rates after whole-body irradiation, radiation-induced leg contracture, and MRI-based redox imaging of the brain were assessed and compared between SeD and normal mice. Thirty-day lethality after whole-body 5.6 Gy irradiation with X-rays or carbon-ion beams was higher in the SeD mice than in the normal mice, while SeD did not give the notable difference between X-rays and carbon-ion beams. SeD also did not affect the maximum leg contracture level after irradiation with carbon-ion beams, but delayed the leg contraction rate. In addition, no marked effects of SeD were observed on variations in the redox status of the brain after irradiation. Collectively, the present results indicate that SeD slightly altered the biological effects of X-rays and/or carbon-ion beams. GSH-Px processes endogenous HO generated through mitochondrial respiration, but does not have the capacity to degrade HO produced by irradiation.

摘要

利用缺硒(SeD)小鼠模型研究了辐射诱导的过氧化氢(HO)对X射线和碳离子束生物学效应的影响。硒是谷胱甘肽过氧化物酶(GSH-Px)的活性中心,缺硒小鼠缺乏降解HO的能力。通过喂食以圆酵母为基础的缺硒饮食和超纯水制备雄性和雌性缺硒小鼠。评估并比较了缺硒小鼠和正常小鼠全身照射后的30天存活率、辐射诱导的腿部挛缩以及基于MRI的脑部氧化还原成像。用X射线或碳离子束全身照射5.6 Gy后,缺硒小鼠的30天致死率高于正常小鼠,而缺硒对X射线和碳离子束之间没有显著差异。缺硒也不影响碳离子束照射后的最大腿部挛缩水平,但延迟了腿部收缩率。此外,未观察到缺硒对照射后脑部氧化还原状态变化有明显影响。总体而言,目前的结果表明缺硒略微改变了X射线和/或碳离子束的生物学效应。GSH-Px处理通过线粒体呼吸产生的内源性HO,但没有能力降解由辐射产生的HO。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/219c/10017320/bc8145faf33b/jcbn22-57f01.jpg

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