当你走到太阳下,感受阳光的不只是你的双眼。你的皮肤也与视网膜一样含有光感受器,从而能够迅速对有害的紫外线辐射采取防御。
皮肤通过产生黑色素而变黑,黑色素可以保护DNA不受紫外线的损伤。我们已经知道,在被太阳暴晒几天后,阳光中的UVB紫外线才会使皮肤增加黑色素的产生,以应对皮肤中的DNA损伤。但是,阳光中的UVA紫外线却可以在几分钟内就促进黑色素的产生。
布朗大学的埃琳娜·万恰和同事认为他们知道其中的原因。他们分析了负责生产黑色素的黑素细胞的基因表达,发现这些细胞也能产生视紫红质,即存在于视网膜中的光敏物质。
当研究小组用UVA紫外线照射黑素细胞时,他们发现黑色素分泌量有所上升。在24小时内,黑色素的分泌增加了4倍。而去掉黑素细胞中负责分泌视紫红质的基因,也就阻断了其对
UVA紫外线的这种即刻反应能力。万恰认为,这种即刻“变黑”的过程尽管不那么明显,却可以帮助保护皮肤抵御早期的DNA受损。
不过,澳大利亚昆士兰大学的里克·斯特姆并不相信皮肤“看到”阳光的功能可以使之获得很大程度的保护。他说:“即刻变黑并不能抵御紫外线引起的晒伤或DNA损伤。” (生物谷 Bioon.com)
doi:10.1016/j.cub.2011.09.047
PMC:
PMID:
UVA Phototransduction Drives Early Melanin Synthesis in Human Melanocytes
Nadine L. Wicks, Jason W. Chan, Julia A. Najera, Jonathan M. Ciriello, Elena Oancea
Exposure of human skin to solar ultraviolet radiation (UVR), a powerful carcinogencomprising 95% ultraviolet A (UVA) and 5% ultraviolet B (UVB) at the Earth's surface, promotes melanin synthesis in epidermal melanocytes , which protects skin from DNA damage . UVB causes DNA lesions that lead to transcriptional activation of melanin-producing enzymes, resulting in delayed skin pigmentation within days . In contrast, UVA causes primarily oxidative damage and leads to immediate pigment darkening (IPD) within minutes, via an unknown mechanism . No receptor protein directly mediating phototransduction in skin has been identified. Here we demonstrate that exposure of primary human epidermal melanocytes (HEMs) to UVA causes calcium mobilization and early melanin synthesis. Calcium responses were abolished by treatment with G protein or phospholipase C (PLC) inhibitors or by depletion of intracellular calcium stores. We show that the visual photopigment rhodopsin is expressed in HEMs and contributes to UVR phototransduction. Upon UVR exposure, significant melanin production was measured within one hour; cellular melanin continued to increase in a retinal- and calcium-dependent manner up to 5-fold after 24 hr. Our findings identify a novel UVA-sensitive signaling pathway in melanocytes that leads to calcium mobilization and melanin synthesis and may underlie the mechanism of IPD in human skin. P>