Kligman L H, Zheng P, Kligman A M
Department of Dermatology, University of Pennsylvania School of Medicine, Philadelphia 19104-6142, USA.
Acta Derm Venereol. 1995 May;75(3):205-11. doi: 10.2340/0001555575205211.
While assessing the protective effect of broad-spectrum sunscreens against chronic UVA radiation, we observed a paradoxical worsening of skin damage with one product. To further examine this finding, five proprietory broad-spectrum sunscreens were applied to albino hairless mice irradiated thrice weekly for 32 weeks with a UVASUN lamp (> 340 nm). Appropriate age-matched controls were included. After approximately 12 weeks, two sunscreens induced a marked dermatitis. Biopsies showed damage greatly exceeding that found in UVA-irradiated, unprotected controls. Histologically, elastic fibers were hyperplastic, coalescing into elastotic clumps. Glycosaminoglycans also increased. Collagen damage was notable since UVA alone does not induce a histologic change. Electron microscopy confirmed these findings. Two other sunscreens provided nearly complete protection. Against chronic UVB radiation, the two UVA photoirritating sunscreens provided substantial protection. Since the UVA sunfilter, oxybenzone, was the same in all sunscreens, we postulate that an irritating component of the vehicle was responsible for the UVA-induced photoirritation. The fifth sunscreen produced severe damage with UVB and UVA.
在评估广谱防晒霜对慢性紫外线A辐射的防护效果时，我们发现有一种产品出现了矛盾的情况，即皮肤损伤反而加剧。为了进一步研究这一发现，我们将五种专利广谱防晒霜涂抹在白化无毛小鼠身上，每周用UVASUN灯（> 340纳米）照射三次，持续32周。同时设置了年龄匹配的适当对照组。大约12周后，两种防晒霜引发了明显的皮炎。活检显示，损伤程度大大超过了未涂抹防晒霜而仅接受紫外线A照射的对照组。从组织学上看，弹性纤维增生，聚集成弹性组织团块。糖胺聚糖也增加了。值得注意的是，仅紫外线A照射不会引起组织学变化，而此处出现了胶原蛋白损伤。电子显微镜检查证实了这些发现。另外两种防晒霜提供了几乎完全的防护。对于慢性紫外线B辐射，这两种具有紫外线A光刺激性的防晒霜提供了实质性的防护。由于所有防晒霜中的紫外线A滤光剂二苯甲酰甲烷是相同的，我们推测载体中的一种刺激性成分是导致紫外线A诱导的光刺激的原因。第五种防晒霜对紫外线B和紫外线A都造成了严重损伤。
