Effect of hypoxia on sunburn cell formation and inflammation induced by ultraviolet radiation.

Photo-dermatology Pub Date : 1988-12-01
J I Youn, R W Gange, D Maytum, J A Parrish
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Abstract

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.

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缺氧对紫外线致晒伤细胞形成及炎症的影响。
氧中间体是造成许多紫外线辐射效应的原因。为了验证紫外线诱导的晒伤细胞和皮肤水肿(耳肿胀)的形成是由氧化损伤引起的假设,我们研究了小鼠耳中缺氧组织对紫外线的反应。在中波紫外线照射之前或之后,夹耳造成的血管闭塞导致缺氧,减少了晒伤细胞的形成。单独夹耳会引起明显的耳部肿胀,当与UVB接触时,这种肿胀会增强。使用外用8-甲氧基补骨脂素+ UVA (PUVA),在UVA暴露前夹耳10分钟观察到晒伤细胞增加,但在暴露后没有观察到。在暴露期间夹住耳朵时,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,UVB和PUVA诱导晒伤细胞形成的机制不同。
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