Miura Y, Anzai K, Urano S, Ozawa T
Department of Bioregulation Research, National Institute of Radiological Sciences, Inage-ku, Chiba-shi, Japan.
Free Radic Biol Med. 1997;23(4):533-40. doi: 10.1016/s0891-5849(97)00103-2.
The effect of x-irradiation on the reduction rates of nitroxyl radicals was examined in whole mice using in vivo EPR. One hour after irradiation, the reduction rates of nitroxyl increased up to 15 Gy irradiation, but decreased over this dose. The enhancement of the reduction rate of nitroxyl was suppressed by preadministration of a radioprotector, cysteamine, suggesting that the enhancement of nitroxyl reduction is related to the radiation damage. Thiobarbituric acid-reactive substances (TBARS) in liver homogenate were increased by x-irradiation, indicating that x-irradiation induced oxidative stress in mice. Endogenous antioxidant, alpha-tocopherol, and the activities of antioxidative enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase were not induced by x-irradiation under these experimental conditions. Eventually the nitroxyl reduction in whole mice should be enhanced by the oxidative stress due to x-irradiation. An in vivo EPR system probing the nitroxyl reduction should be applicable to the noninvasive study on the oxidative stress caused by radiation.
使用体内电子顺磁共振（EPR）技术，在整体小鼠中研究了X射线照射对硝酰自由基还原率的影响。照射后1小时，在高达15 Gy的照射剂量下，硝酰自由基的还原率升高，但超过此剂量后则下降。预先给予辐射防护剂半胱胺可抑制硝酰自由基还原率的升高，这表明硝酰自由基还原的增强与辐射损伤有关。X射线照射可使肝脏匀浆中的硫代巴比妥酸反应性物质（TBARS）增加，这表明X射线照射可诱导小鼠体内的氧化应激。在这些实验条件下，X射线照射并未诱导内源性抗氧化剂α-生育酚以及超氧化物歧化酶（SOD）、过氧化氢酶和谷胱甘肽过氧化物酶等抗氧化酶的活性。最终，由于X射线照射引起的氧化应激应会增强整体小鼠中硝酰自由基的还原。探测硝酰自由基还原的体内EPR系统应适用于对辐射引起的氧化应激进行无创研究。
