McArdle F, Rhodes L E, Parslew R, Jack C I A, Friedmann P S, Jackson M J
Department of Medicine, University of Liverpool, Liverpool, UK.
Free Radic Biol Med. 2002 Nov 15;33(10):1355-62. doi: 10.1016/s0891-5849(02)01042-0.
Previous studies of cultured skin cells and murine skin in vivo have indicated that UVR-induced damage involves the generation of reactive oxygen species and depletion of endogenous antioxidant systems. In order to explore the relevance of this to UVR-induced damage to human skin, we have undertaken a detailed examination of the time-course of changes in markers of oxidative stress in human skin following exposure to physiological amounts of UVR in vivo. In addition, we have examined the skin bioavailability of a common nutritional antioxidant, vitamin C, and have assessed the effects of supplementation on markers of oxidative stress. Our hypothesis was that acute exposure of human skin to UVR in vivo would lead to oxidation of cellular biomolecules that could be prevented by prior vitamin C treatment. A UVR-challenge of 120 mJ/cm2 of broadband UVB (peak 310 nm, range 270-400 nm) was applied to buttock skin of 8 healthy volunteers. This caused a rapid and significant rise in activity of skin catalase at 1 h and an increase in the oxidized/total glutathione ratio at 6 h post-UVR. AP-1 DNA binding also peaked at 1-6 h post-UVR, then declined rapidly to baseline levels. No significant changes were seen in skin malonaldehyde content. Oral vitamin C supplements (500 mg/day) were taken by 12 volunteers for 8 weeks resulting in significant rises in plasma and skin vitamin C content. Supplementation had no effect on the UVR-induced erythemal response. The skin malonaldehyde content was reduced by vitamin C supplementation, but surprisingly, reductions in the skin content of total glutathione and protein thiols were also seen. We speculate that this apparently paradoxical effect could be due to regulation of total reductant capacity by skin cells, such that vitamin C may have been replacing other reductants in these cells. No evidence was obtained for an effect of the supplementary vitamin C on the mild oxidative stress seen in human skin following UVR exposure.
先前对培养的皮肤细胞和体内小鼠皮肤的研究表明，紫外线辐射（UVR）诱导的损伤涉及活性氧的产生和内源性抗氧化系统的消耗。为了探究这与UVR诱导的人类皮肤损伤的相关性，我们对人体皮肤在体内暴露于生理剂量的UVR后氧化应激标志物变化的时间进程进行了详细研究。此外，我们检测了一种常见的营养抗氧化剂维生素C在皮肤中的生物利用度，并评估了补充维生素C对氧化应激标志物的影响。我们的假设是，人体皮肤在体内急性暴露于UVR会导致细胞生物分子氧化，而预先进行维生素C处理可以预防这种氧化。对8名健康志愿者的臀部皮肤施加120 mJ/cm² 的宽带UVB（峰值310 nm，范围270 - 400 nm）的UVR刺激。这导致皮肤过氧化氢酶活性在1小时时迅速显著升高，并且在UVR照射后6小时氧化型/总谷胱甘肽比值增加。AP - 1 DNA结合在UVR照射后1 - 6小时也达到峰值，然后迅速下降至基线水平。皮肤丙二醛含量未见显著变化。12名志愿者口服维生素C补充剂（500毫克/天），持续8周，导致血浆和皮肤中维生素C含量显著升高。补充维生素C对UVR诱导的红斑反应没有影响。维生素C补充剂降低了皮肤丙二醛含量，但令人惊讶的是，总谷胱甘肽和蛋白质硫醇的皮肤含量也有所降低。我们推测这种明显矛盾的效应可能是由于皮肤细胞对总还原能力的调节，使得维生素C可能替代了这些细胞中的其他还原剂。没有获得补充维生素C对人类皮肤在UVR照射后出现的轻度氧化应激有影响的证据。
