The skin is the largest human organ and permanently exposed to a variety of stresses. Among those, oxidative insults such as ultraviolet radiation and ozone exposure account for the cause of many skin disorders. However, oxidative damage are not responsible for all biological effects engendered by these stressors in the skin. Indeed, ultraviolet radiation (UVR) causes changes in the expression of genes encoding, e.g., proinflammatory cyto-kines, growth factors, stress response proteins, oncoproteins, and matrix metalloprotei-nases . Although the immediate target(s) of UVR is/are still unknown, certain kinases and transcription factors can be activated by UVR thereby increasing gene transcription . One transcription factor, NF-kB, appears of particular interest for the skin since the lack of its inhibitory protein, IKBa, is associated with the development of a widespread dermititis in knockout mice [81,82]. Furthermore, reactive oxygen species, such as the ones produced after UVR, are suspected to play an important role in the activation of NF-kB . Consequently, antioxidants have been found to be among the most potent NF-kB inhibitors. However, clinical studies are required in order to assess the effectiveness of these antioxidants, including the flavonoid silymarin, a-lipoic acid and the glutathione precursor N-acetyl-L-cysteine, on skin inflammatory disorders. Using high-throughput procedures such as the cDNA arrays, for instance , the evaluation of the antioxidants on the whole genome is henceforth possible. These studies will only confirm the hypothesis that antioxidants are responsible for a much broader action spectrum than their antioxidant functions per se and extend their role on more subtle regulatory mechanisms of the gene expression.
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