一项研究发现，紫外线暴露的时间可能影响小鼠皮肤癌的出现。
暴露在紫外线辐射中能引发可能导致皮肤癌的DNA损伤。此前对小鼠的研究已经显示了一种称为XPA的蛋白质—它参与了紫外线引发的DNA损伤的修复—的水平在一天中涨落，在下午4—6点达到峰值，在上午4—6点达到低谷，这与生物钟的节律一致。
Aziz Sancar及其同事发现，在小鼠的皮肤细胞中，这种蛋白质的水平和活性在上午4点最低，在下午4点最高。这组作者让两组小鼠暴露在紫外线辐射下——一组在上午4点，另一组在下午4点——并且监测皮肤癌的出现。
在修复活动处于最低点的时候接受辐射的小鼠比在这种蛋白质的修复功能最强的时候接受辐射的小鼠出现肿瘤的速度远远更快，而且出现的频率是后者的5倍。当这组作者在一种缺乏生物钟的两个关键成分的小鼠身上重复这一实验的时候，紫外线暴露的时间没有遵循这种蛋白质的修复活动或者皮肤癌的出现，这提示XPA蛋白质的生物钟控制可能影响皮肤癌的发病率。这组作者说，由于小鼠和人类的生物钟类似，紫外线暴露的时间可能同样地决定了它在人类身上的致癌潜力。(生物谷 Bioon.com)
doi:10.1073/pnas.1115249108
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Control of skin cancer by the circadian rhythm
Shobhan Gaddameedhi, Christopher P. Selby, William K. Kaufmann, Robert C. Smart, and Aziz Sancar
Skin cancer is the most common form of cancer in the United States. The main cause of this cancer is DNA damage induced by the UV component of sunlight. In humans and mice, UV damage is removed by the nucleotide excision repair system. Here, we report that a rate-limiting subunit of excision repair, the xeroderma pigmentosum group A (XPA) protein, and the excision repair rate exhibit daily rhythmicity in mouse skin, with a minimum in the morning and a maximum in the afternoon/evening. In parallel with the rhythmicity of repair rate, we find that mice exposed to UV radiation (UVR) at 4:00 AM display a decreased latency and about a fivefold increased multiplicity of skin cancer (invasive squamous cell carcinoma) than mice exposed to UVR at 4:00 PM. We conclude that time of day of exposure to UVR is a contributing factor to its carcinogenicity in mice, and possibly in humans.
