In vivo oxygen radical generation in the skin of the protoporphyria model mouse with visible light exposure:: An L-band ESR study
In vivo oxygen radical generation in the skin of the protoporphyria model mouse with visible light exposure:: An L-band ESR study
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DOI：
10.1111/j.0022-202x.2004.22601.x
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发表时间：
2004-06-01
影响因子：
6.5
通讯作者：
Utsumi, H
中科院分区：
文献类型：
--
作者：
Takeshita, K;Takajo, T;Utsumi, H
尽管氧自由基被认为在原卟啉引起的皮肤损伤中起着关键作用，但没有直接证据表明这些自由基在体内产生。这项研究使用了体内电子自旋共振光谱仪，配备了表面线圈式谐振器，可以检测皮肤表面约0.5 mm范围内的自由基，从而非侵入性地测量了灰黄霉素诱导的原卟啉模型小鼠皮肤中可见光引起的氧自由基的产生。静脉注射一种持久的氮氧自由基作为探针。光照射增加了灰黄霉素处理组小鼠的氮氧基信号的衰减，而光照射没有增强对照组小鼠的信号衰减。静脉注射羟基自由基清除剂、超氧化物歧化酶或过氧化氢酶，或腹腔注射去铁胺，可完全抑制增强的信号衰减。增强的信号随照明的衰减是可逆的，并对打开和关闭灯光做出快速反应。这些观察表明，羟基自由基是通过皮肤中铁催化的反应产生的。本文首次证明了原卟啉模型小鼠皮肤受光照射后产生的氧自由基的特异性。
Although oxygen radicals are thought to play a key role in the skin injury that is caused by protoporphyria, there is no direct evidence of generation of these radicals in vivo. This study measured the generation of oxygen radicals caused by visible light non-invasively in the skin of griseofulvin-induced protoporphyria model mice, using an in vivo electron spin resonance spectrometer equipped with a surface-coil-type resonator that could detect radicals within about 0.5 mm of the skin surface. A durable nitroxyl radical was administered intravenously as a probe. Light irradiation enhanced the decay of the nitroxyl signal in griseofulvin-treated mice, whereas light irradiation did not enhance the signal decay in control mice. The enhanced signal decay was completely suppressed by intravenous administration of hydroxyl radical scavengers, superoxide dismutase or catalase, or the intraperitoneal administration of desferrioxamine. The enhanced signal decay with illumination was reversible, and quickly responded to turning the light on and off. These observations suggest that the hydroxyl radical is generated via an iron-catalyzed reaction in the skin. This paper demonstrates, for the first time, the specific generation of oxygen radicals in response to light irradiation of the skin of protoporphyria model mice.