Jurkiewicz B A, Buettner G R
Free Radical Research Institute, University of Iowa, Iowa city 52242-1101, USA.
Photochem Photobiol. 1996 Dec;64(6):918-22. doi: 10.1111/j.1751-1097.1996.tb01856.x.
Ultraviolet radiation produces free radicals in Skh-1 mouse skin, contributing to photoaging and carcinogenesis. If a mouse model is a general indicator of free radical processes in human skin photobiology, then radical production observed in mouse and human skin should be directly comparative. In this work we show that UV radiation (lambda > 300 nm, 14 microW/cm2 UVB; 3.5 mW/cm2 UVA) increases the ascorbate free radical (Asc.-) electron paramagnetic resonance (EPR) signal in both Skh-1 mouse skin (45%) and human facial skin biopsies (340%). Visible light (lambda > 400 nm; 0.23 mW/cm2 UVA) also increased the Asc.- signal in human skin samples (45%) but did not increase baseline mouse Asc.-, indicating that human skin is more susceptible to free radical formation and that a chromophore for visible light may be present. Using EPR spin-trapping techniques, UV radiation produced spin adducts consistent with trapping lipid alkyl radicals in mouse skin (alpha-[4-pyridyl 1-oxide]-N-tert-butyl nitrone/alkyl radical adduct; aN = 15.56 G and aH = 2.70 G) and lipid alkoxyl radicals in human skin (5,5-dimethylpyrroline-1-oxide/alkoxyl radical adduct; aN = 14.54 G and aH = 16.0 G). Topical application of the iron chelator Desferal to human skin significantly decreases these radicals (approximately 50%), indicating a role for iron in lipid peroxidation; Desferal has previously been shown to decrease radical production in mouse skin. This work supports the use of the Skh-1 mouse as a predictive tool for free radical formation in human skin. These results provide the first direct evidence for UV radiation-induced free radical formation at near physiological temperatures in human skin and suggest that iron chelators may be useful as photoprotective agents.
紫外线辐射会在Skh-1小鼠皮肤中产生自由基，从而导致光老化和致癌作用。如果小鼠模型是人类皮肤光生物学中自由基过程的一般指标，那么在小鼠和人类皮肤中观察到的自由基产生情况应该可以直接比较。在这项研究中，我们发现紫外线辐射（波长>300nm，14μW/cm²UVB；3.5mW/cm²UVA）会使Skh-1小鼠皮肤（增加45%）和人类面部皮肤活检样本（增加340%）中的抗坏血酸自由基（Asc.-）电子顺磁共振（EPR）信号增强。可见光（波长>400nm；0.23mW/cm²UVA）也会使人类皮肤样本中的Asc.-信号增强（增加45%），但不会增加小鼠皮肤的基线Asc.-信号，这表明人类皮肤更容易形成自由基，并且可能存在可见光的发色团。使用EPR自旋捕获技术，紫外线辐射产生的自旋加合物与捕获小鼠皮肤中的脂质烷基自由基（α-[4-吡啶基1-氧化物]-N-叔丁基硝酮/烷基自由基加合物；aN = 15.56G，aH = 2.70G）以及人类皮肤中的脂质烷氧基自由基（5,5-二甲基吡咯啉-1-氧化物/烷氧基自由基加合物；aN = 14.54G，aH = 16.0G）一致。将铁螯合剂去铁胺局部应用于人类皮肤可显著减少这些自由基（约50%），表明铁在脂质过氧化中起作用；此前已证明去铁胺可减少小鼠皮肤中的自由基产生。这项研究支持将Skh-1小鼠用作预测人类皮肤中自由基形成的工具。这些结果首次提供了直接证据，证明紫外线辐射在接近生理温度下可诱导人类皮肤中自由基的形成，并表明铁螯合剂可能作为光保护剂有用。
