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补骨脂素诱导的黑色素生成对小鼠表皮DNA光损伤的体内光保护作用。

Photoprotection by furocoumarin-induced melanogenesis against DNA photodamage in mouse epidermis in vivo.

作者信息

Kinley J S, Brunborg G, Moan J, Young A R

机构信息

Department of Photobiology, St. John's Institute of Dermatology, St. Thomas' Hospital, London, UK.

出版信息

Photochem Photobiol. 1997 Mar;65(3):486-91. doi: 10.1111/j.1751-1097.1997.tb08595.x.

DOI:10.1111/j.1751-1097.1997.tb08595.x
PMID:9077137
Abstract

The photoprotective properties of furocoumarin plus UVA-induced epidermal melanogenesis were assessed in hairless mice. The ear and dorsal surfaces were topically treated with 6,4,4'-trimethylangelicin (TMA), 5-methoxypsoralen (5-MOP), 8-methoxypsoralen (8-MOP) or psoralen and exposed to UVA for 12 consecutive week-days. The TMA treatment induced intense tanning whereas modest tanning was seen with the other compounds. Seven days after the last treatment, the mice were challenged with a DNA damaging dose of UV radiation. Single strand breaks (SSB) in epidermal DNA were assessed by alkaline elution. Photoprotection was assessed by comparing SSB in furocoumarin-treated mice with control mice (vehicle plus UVA and also no treatment). No photoprotection was seen, with any compound, in dorsal epidermis despite intense pigmentation induced by TMA. Modest photoprotection with all compounds was seen in ear epidermis that was independent of the level of pigmentation. These data show that induced melanogenesis is not always associated, with photoprotection.

摘要

在无毛小鼠中评估了呋喃香豆素加紫外线A诱导的表皮黑色素生成的光保护特性。对耳朵和背部表面进行局部处理,分别涂抹6,4,4'-三甲基当归素(TMA)、5-甲氧基补骨脂素(5-MOP)、8-甲氧基补骨脂素(8-MOP)或补骨脂素,并连续12个工作日暴露于紫外线A下。TMA处理导致强烈晒黑,而其他化合物则导致适度晒黑。在最后一次处理7天后,用具有DNA损伤剂量的紫外线辐射对小鼠进行攻击。通过碱性洗脱评估表皮DNA中的单链断裂(SSB)。通过比较呋喃香豆素处理小鼠与对照小鼠(赋形剂加紫外线A以及未处理)中的SSB来评估光保护作用。尽管TMA诱导了强烈色素沉着,但在背部表皮中未观察到任何化合物具有光保护作用。在耳朵表皮中,所有化合物均表现出适度的光保护作用,且与色素沉着水平无关。这些数据表明,诱导的黑色素生成并不总是与光保护作用相关。

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Photoprotection by furocoumarin-induced melanogenesis against DNA photodamage in mouse epidermis in vivo.补骨脂素诱导的黑色素生成对小鼠表皮DNA光损伤的体内光保护作用。
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