Vitamin E inhibits the UVAI induction of "light" and "dark" cyclobutane pyrimidine dimers, and oxidatively generated DNA damage, in keratinocytes
Vitamin E inhibits the UVAI induction of "light" and "dark" cyclobutane pyrimidine dimers, and oxidatively generated DNA damage, in keratinocytes
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DOI：
10.1038/s41598-017-18924-4
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发表时间：
2018-01-11
影响因子：
4.6
通讯作者：
Young, Antony R.
中科院分区：
文献类型：
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作者：
Delinasios, George J.;Karbaschi, Mahsa;Young, Antony R.
太阳紫外线辐射（UVR）引起的DNA损伤对皮肤有急性和长期的不良影响。这种损伤直接由紫外线的吸收引起，间接通过光敏反应引起。本研究的目的是评估维生素E对体外uvai诱导的角化细胞DNA损伤的影响。暴露于UVAI之前用维生素E孵育可减少氧化嘌呤（细胞内氧化物质减少）和环丁烷嘧啶二聚体（CPD）的形成。当紫外线辐射暴露后补充维生素E获得类似结果时，排除了可能的防晒作用。我们的数据表明，uva诱导的光敏反应对DNA的损伤可以通过在照射前或照射后引入维生素E来抑制，无论是氧化嘌呤还是CPD（包括所谓的“暗”CPD）。这些数据验证了UVAI最初通过光敏诱导CPD，一些通过化学激发诱导CPD的证据，并支持维生素E可以干预这一途径以防止角化细胞形成CPD的证据。我们建议在局部防晒霜和晒后制剂中加入类似的制剂，特别是后者，即使在阳光照射结束后，也能减轻正在进行的DNA损伤形成。
Solar ultraviolet radiation (UVR)-induced DNA damage has acute, and long-term adverse effects in the skin. This damage arises directly by absorption of UVR, and indirectly via photosensitization reactions. The aim of the present study was to assess the effects of vitamin E on UVAI-induced DNA damage in keratinocytes in vitro. Incubation with vitamin E before UVAI exposure decreased the formation of oxidized purines (with a decrease in intracellular oxidizing species), and cyclobutane pyrimidine dimers (CPD). A possible sunscreening effect was excluded when similar results were obtained following vitamin E addition after UVAI exposure. Our data showed that DNA damage by UVA-induced photosensitization reactions can be inhibited by the introduction of vitamin E either pre- or post-irradiation, for both oxidized purines and CPD (including so-called "dark" CPDs). These data validate the evidence that some CPD are induced by UVAI initially via photosensitization, and some via chemoexcitation, and support the evidence that vitamin E can intervene in this pathway to prevent CPD formation in keratinocytes. We propose the inclusion of similar agents into topical sunscreens and aftersun preparations which, for the latter in particular, represents a means to mitigate on-going DNA damage formation, even after sun exposure has ended.