In vivo ESR imaging of redox status in mice after X-ray irradiation, measured by acyl-protected hydroxylamine probe, ACP
In vivo ESR imaging of redox status in mice after X-ray irradiation, measured by acyl-protected hydroxylamine probe, ACP
复制标题
X 射线照射后小鼠氧化还原状态的体内 ESR 成像，通过酰基保护羟胺探针 ACP 测量
DOI：
10.1016/j.freeradbiomed.2020.08.028
复制
发表时间：
2020
影响因子：
7.4
通讯作者：
Takeshita Keizo
中科院分区：
文献类型：
--
作者：
Saito Keita;Okazaki Shoko;Tachibana Yoko;Anzai Kazunori;Ozawa Toshihiko;Takeshita Keizo
需要对体内氧化还原状态进行更详细的研究，以阐明电离辐射引起损伤的机制。本研究以1-乙酰氧基-3-氨甲酰基-2，2，5，5-四甲基吡咯烷（ACP）为探针，腹腔注射后，用在体电子自旋共振（ESR）成像技术检测小鼠体内氧化还原状态。ACP在小鼠体内容易水解成羟胺形式，羟胺与相应的硝酰基自由基之间的相互转化反映了生物氧化还原状态。在7.5戈伊的X射线照射后4天，根据肝脏重量和血浆天冬氨酸转氨酶水平的变化检测小鼠的肝损伤。ESR成像显示，ACP给药后，受损和健康小鼠的肝脏区域的硝酰基自由基信号强度均较高。而对于健康小鼠，信号在肝脏区域衰减，而在受损小鼠中衰减可忽略不计。与健康小鼠不同，受损小鼠胸部的信号随时间增加。损伤和健康小鼠的羟胺和硝酰基自由基的总和的分布相似。X射线照射轻微降低了肝微粒体组分的硝酰基自由基的还原活性。受损小鼠肝脏中的硫代巴比妥酸反应物质高于健康小鼠;然而，还原型谷胱甘肽无显著差异。本研究结果表明，小鼠暴露于X射线照射后的氧化还原状态比健康小鼠更氧化。
More detailed investigations on thein vivoredox status are needed to elucidate the mechanisms contributing to damage caused by ionizing radiation. In the present study, thein vivoredox status of mice was examined usingin vivoelectron spin resonance (ESR) imaging after an intraperitoneal injection of 1-acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine (ACP) as a probe. ACP is easily hydrolyzed to its hydroxylamine form in the mouse body, and the interconversion between hydroxylamine and the corresponding nitroxyl radical reflects the biological redox status. Liver damage, based on changes in liver weight and plasma aspartate aminotransferase levels, was detected in mice 4 days after X-ray irradiation at 7.5 Gy. ESR imaging showed that the signal intensity of the nitroxyl radical was high at the liver area in both damaged and healthy mice after administration of ACP. Whereas the signal decayed at the liver area for healthy mouse, the decay was negligible in damaged mice. Unlike healthy mouse, signal in the chest for damaged mouse increased with time. The distribution of the sum of hydroxylamine and the nitroxyl radical was similar in damaged and healthy mice. X-ray irradiation slightly lowered the reduction activity of the liver microsomal fraction for the nitroxyl radical. Thiobarbituric acid reactive substances in the liver were higher in damaged mice than in healthy mice; however, no significant differences were noted in reduced glutathione. The present results indicate that the redox status of mice exposed to X-ray irradiation is more oxidative than that in healthy mice.