Active oxygen mechanisms of UV inflammation.
Active oxygen radicals are important in the pathogenesis of UV irradiation injury. The initiating mechanisms involve the generation of hydroxyl radicals, superoxide, and organic hydroperoxides due to photochemical reactions. These active oxygen species lead to DNA strand breakage, mutation and the generation of inflammatory mediators such as cytokines and arachidonic acid metabolites which amplify the irradiation-induced inflammation. Several compounds have recently been utilized to successfully decrease these effects. Improved understanding of the mechanisms by which active oxygen species induce injury in skin now promises improved treatment.
Pentland
A P
AP
Division of Dermatology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D015777:Eicosanoids / Q000378:metabolism; D066246:ErbB Receptors / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000503:physiopathology*; D010741:Phospholipases A / Q000378:metabolism; D011832:Radiation Injuries / Q000378:metabolism / Q000503:physiopathology*; D017382:Reactive Oxygen Species; D012867:Skin / Q000378:metabolism / Q000528:radiation effects; D013472:Sunlight / Q000009:adverse effects*; D014466:Ultraviolet Rays / Q000009:adverse effects*
D000975:Antioxidants; D015777:Eicosanoids; D017382:Reactive Oxygen Species; D066246:ErbB Receptors; D010741:Phospholipases A