Youn J I, Gange R W, Maytum D, Parrish J A
Department of Dermatology, Harvard Medical School, Massachusetts General Hospital, Boston.
Photodermatol. 1988 Dec;5(6):252-6.
Oxygen intermediates are responsible for a number of ultraviolet (UV) radiation effects. To test the hypothesis that UV-induced formation of sunburn cells and skin edema (ear swelling) result from oxidative damage, we examined the effect of hypoxia tissue responses to UV in the mouse ear. Hypoxia resulting from vascular occlusion by ear clamping, either before or after UVB exposure, decreased formation of sunburn cells. Ear clamping alone caused significant ear swelling, which was enhanced when combined with UVB exposure. Using topical 8-methoxypsoralen + UVA (PUVA), increased sunburn cells were observed when ears were clamped for 10 min prior to UVA exposure, but not following exposure. Ear swelling caused by PUVA was also enhanced when ears were clamped during exposure. These results suggest that induction of sunburn cells by UVB is dependent on oxygen, and that UVB and PUVA induce sunburn cell formation by distinct mechanisms.
氧中间体与多种紫外线(UV)辐射效应有关。为了验证紫外线诱导晒伤细胞形成和皮肤水肿(耳部肿胀)是由氧化损伤所致这一假说,我们研究了缺氧对小鼠耳部紫外线组织反应的影响。在紫外线B(UVB)照射之前或之后,通过夹耳造成血管阻塞导致的缺氧,减少了晒伤细胞的形成。单独夹耳会导致明显的耳部肿胀,当与UVB照射相结合时肿胀会加剧。使用外用8-甲氧基补骨脂素+紫外线A(PUVA),在紫外线A照射前夹耳10分钟时观察到晒伤细胞增多,但照射后则不然。在照射期间夹耳时,PUVA引起的耳部肿胀也会加剧。这些结果表明,UVB诱导晒伤细胞的形成依赖于氧气,并且UVB和PUVA通过不同机制诱导晒伤细胞形成。