研究人员早已注意到，人体中缺乏一种多数动物甚至植物带有的能够修复严重太阳灼伤的酶。美国俄亥俄州立大学的科学家在《自然》（Nature）杂志网站上撰文表示，他们首次观察到了这种酶是如何修复受损DNA的。该发现有望帮助人们开发新的晒伤疗法和皮肤癌预防方法。
俄亥俄州立大学物理学家和化学家仲东平与同事介绍说，他们观察到光解酶（photolyase）向受损的DNA链注射一个电子和一个质子、在10亿分之数秒内修复损伤的情况。仲东平表示，这听起来简单，但实际上电子和质子注入后产生了一系列非常复杂的化学反应。这一切虽然发生在瞬间，时机却十分恰当。
在实验中，仲东平他们将自己合成的DNA放在紫外线下照射，让DNA出现类似于晒伤的损伤，然后加入光解酶，并用超快光脉冲成像技术获得了揭示光解酶修复受损DNA过程的系列图片。
紫外线导致人类患上皮肤癌的原因是它使得细胞中沿着DNA分子不正确的地方出现了化学键。仲东平的研究显示，光解酶能够解散这些错误的化学键，让DNA的原子重新回到原来的位置。同时，他们还发现，修复完成后，DNA螺旋链会自动向光解酶发射出电子和质子，这让光解酶能继续修复其他受损的DNA。
人类被阳光晒伤后，其体内的酶没有能力修复DNA损伤，皮肤细胞出现死亡。科学家将慢性皮肤晒伤同DNA变异联系起来，认为DNA变异导致了诸如皮肤癌等疾病。仲东平表示，现在人们认识了光解酶的作用机理，有望利用该信息设计出治疗阳光晒伤的药物或皮肤霜。
科学家表示，常见的防晒霜的作用是将紫外线转变成热能或反射紫外光。含有光解酶的防晒霜则有可能治疗穿透进皮肤的紫外线所引起的损害。(生物谷Bioon.com)
生物谷推荐原文出处：
Nature doi:10.1038/nature09192
Dynamics and mechanism of repair of ultraviolet-induced (6–4) photoproduct by photolyase
Jiang Li1, Zheyun Liu1, Chuang Tan1, Xunmin Guo1, Lijuan Wang1, Aziz Sancar2 & Dongping Zhong1
1 Departments of Physics, Chemistry and Biochemistry, Programs of Biophysics, Chemical Physics and Biochemistry, 191 West Woodruff Avenue, The Ohio State University, Columbus, Ohio 43210, USA
2 Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599, USA
One of the detrimental effects of ultraviolet radiation on DNA is the formation of the (6–4) photoproduct, 6–4PP, between two adjacent pyrimidine rings1. This lesion interferes with replication and transcription, and may result in mutation and cell death2. In many organisms, a flavoenzyme called photolyase uses blue light energy to repair the 6–4PP (ref. 3). The molecular mechanism of the repair reaction is poorly understood. Here, we use ultrafast spectroscopy to show that the key step in the repair photocycle is a cyclic proton transfer between the enzyme and the substrate. By femtosecond synchronization of the enzymatic dynamics with the repair function, we followed the function evolution and observed direct electron transfer from the excited flavin cofactor to the 6–4PP in 225?picoseconds, but surprisingly fast back electron transfer in 50?picoseconds without repair. We found that the catalytic proton transfer between a histidine residue in the active site and the 6–4PP, induced by the initial photoinduced electron transfer from the excited flavin cofactor to 6–4PP, occurs in 425?picoseconds and leads to 6–4PP repair in tens of nanoseconds. These key dynamics define the repair photocycle and explain the underlying molecular mechanism of the enzyme’s modest efficiency.
