Takeshita Keizo, Chi Cuiping, Hirata Hiroshi, Ono Mitsuhiro, Ozawa Toshihiko
Faculty of Pharmaceutical Sciences, Sojo University, Ikeda, Kumamoto, Japan.
Free Radic Biol Med. 2006 Mar 1;40(5):876-85. doi: 10.1016/j.freeradbiomed.2005.10.049. Epub 2005 Nov 2.
Although free radicals may be involved in various types of UV-induced injuries, only a few in vivo studies of the generation of free radicals, including oxygen radicals, during exposure to ultraviolet light (UV) have been reported. In this study, the nitroxyl probe 3-carbamoyl-2,2,5,5-tetramethylpyrrolidine-N-oxyl was intravenously injected into hairless mice, and its decay was monitored in the skin with an in vivo EPR spectrometer equipped with a surface-coil-type resonator. The rate of decay of the EPR signal increased during UV (UVA+B) irradiation. This increase in signal decay was suppressed by preadministration of a spin trap, N-tert-butyl-alpha-phenylnitrone (PBN). PBN did not change the rate of signal decay in nonirradiated mice. The correlation between signal decay rate and physiological parameters such as blood velocity, blood mass, or skin temperature was low. The decay rate responded rapidly and reversibly to starting and stopping the UV illumination. Hydroxyl and peroxyl radicals caused reduction of the probe signal in vitro, and PBN inhibited only the peroxyl radical-induced signal reduction. These observations suggest that peroxyl radicals are generated in the skin of live mice during UVA+B irradiation.
尽管自由基可能参与各种紫外线诱导的损伤，但关于暴露于紫外线（UV）期间包括氧自由基在内的自由基生成的体内研究报道较少。在本研究中，将硝酰基探针3-氨基甲酰基-2,2,5,5-四甲基吡咯烷-N-氧基静脉注射到无毛小鼠体内，并用配备表面线圈型谐振器的体内电子顺磁共振光谱仪监测其在皮肤中的衰减。在紫外线（UVA+B）照射期间，电子顺磁共振信号的衰减速率增加。自旋捕集剂N-叔丁基-α-苯基硝酮（PBN）预先给药可抑制信号衰减的这种增加。PBN不会改变未照射小鼠的信号衰减速率。信号衰减速率与诸如血流速度、血容量或皮肤温度等生理参数之间的相关性较低。衰减速率对开始和停止紫外线照射反应迅速且可逆。羟基自由基和过氧自由基在体外导致探针信号降低，而PBN仅抑制过氧自由基诱导的信号降低。这些观察结果表明，在UVA+B照射期间，活小鼠皮肤中会产生过氧自由基。
