紫外线引起皮肤氧化性损伤的进展  

Ultraviolet-induced oxidative damage to skin

作　　者：黄淳韵[1] 严淑贤[1] 项蕾红[1] 

机构地区：[1]复旦大学附属华山医院,上海200040

出　　处：《国际皮肤性病学杂志》2009年第1期51-53,共3页International Journal of Dermatology and Venereology

摘　　要：皮肤中各种光敏物质或色基吸收紫外线能量后，通过电子传递产生氧自由基，氧自由基参与许多皮肤病理过程。尽管氧自由基可被皮肤自身存在的酶及非酶的抗氧化剂清除，然而过多的氧自由基会导致氧化航氧化不均衡从而产生氧化压力，使皮肤色素改变，DNA等分子氧化破坏，一些酶如基质金属蛋白酶、环氧化酶、一氧化氮合酶、血红素氧化酶等的表达上升。Ultraviolet photons can be absorbed by various photosensitizers （endogenous and exogenous） and chromophores in skin, thereafter stimulate the formation of reactive oxygen species （ROS） through electronic transfer, which are involved in many pathological processes in skin. Although ROS are partly removed by nonenzymic and enzymic antioxidants, residual ROS can cause a pro-oxidantJantioxidant disequilibrium defined as oxidative stress that subsequently leads to a change in skin pigmentation, damage to such molecules as DNA, as well as an increment in the expression of matrix metalloproteinases, cyclooxygenases, nitric oxide synthase, heine oxygenase, and so on.

关 键 词：紫外线 活性氧 损伤 

分 类 号：R751[医药卫生—皮肤病学与性病学]