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5-甲氧基补骨脂素晒黑对紫外线辐射诱导的人体皮肤DNA损伤的抑制作用。

Inhibition of UV radiation-induced DNA damage by a 5-methoxypsoralen tan in human skin.

作者信息

Young A R, Potten C S, Chadwick C A, Murphy G M, Cohen A J

机构信息

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

出版信息

Pigment Cell Res. 1988;1(5):350-4. doi: 10.1111/j.1600-0749.1988.tb00131.x.

Abstract

Previously untanned buttock skin of 4 volunteers (skin type II; tan with difficulty as they sunburn easily) was treated with various sunscreen preparations and solar--simulated radiation (SSR) or SSR alone for 2 weeks. One week later, the treatment sites were challenged with a DNA-damaging dose of SSR--twice the minimal erythema dose (2 MED). Skin biopsy samples were assayed for the levels of unscheduled DNA synthesis (a measure of DNA damage), melanin distribution, and skin thickening. 5-Methoxypsoralen-containing sunscreen preparations plus SSR or SSR alone induced melanogenesis and increased the stratum corneum thickness, but only the former regimen afforded a high degree of protection against subsequent SSR-induced DNA damage. 5-Methoxypsoralen-free sunscreen preparations plus SSR induced negligible tanning, skin thickening, and photoprotection. These findings are relevant to the risk-benefit analysis of sunscreen preparations, especially in skin type II, as they provide evidence that a 5-methoxypsoralen-induced tan is protective against the DNA-damaging effects of solar UV radiation, and thus has the potential to reduce the carcinogenic risk of exposure to such radiation.

摘要

4名志愿者(皮肤类型为II型,容易晒伤,难以晒黑)先前未晒黑的臀部皮肤分别用各种防晒制剂处理,并接受太阳模拟辐射(SSR)或仅接受SSR照射,为期2周。一周后,对处理部位给予双倍最小红斑量(2MED)的DNA损伤剂量的SSR照射。对皮肤活检样本进行非定时DNA合成水平(一种DNA损伤的测量指标)、黑色素分布和皮肤增厚情况的检测。含5-甲氧基补骨脂素的防晒制剂加SSR或仅加SSR均可诱导黑色素生成并增加角质层厚度,但只有前一种方案能高度保护皮肤免受随后SSR诱导的DNA损伤。不含5-甲氧基补骨脂素的防晒制剂加SSR诱导的晒黑、皮肤增厚和光保护作用可忽略不计。这些发现与防晒制剂的风险效益分析相关,特别是对于II型皮肤,因为它们提供了证据表明5-甲氧基补骨脂素诱导的晒黑可保护皮肤免受太阳紫外线辐射的DNA损伤作用,因此有可能降低暴露于此类辐射的致癌风险。

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