研究人員早已注意到,，人體中缺乏一種多數(shù)動物甚至植物帶有的能夠修復嚴重太陽灼傷的酶,。美國俄亥俄州立大學的科學家在《自然》（Nature）雜志網(wǎng)站上撰文表示,，他們首次觀察到了這種酶是如何修復受損DNA的。該發(fā)現(xiàn)有望幫助人們開發(fā)新的曬傷療法和皮膚癌預防方法,。
俄亥俄州立大學物理學家和化學家仲東平與同事介紹說,，他們觀察到光解酶（photolyase）向受損的DNA鏈注射一個電子和一個質(zhì)子、在10億分之數(shù)秒內(nèi)修復損傷的情況,。仲東平表示,，這聽起來簡單，但實際上電子和質(zhì)子注入后產(chǎn)生了一系列非常復雜的化學反應,。這一切雖然發(fā)生在瞬間,，時機卻十分恰當。
在實驗中,，仲東平他們將自己合成的DNA放在紫外線下照射,，讓DNA出現(xiàn)類似于曬傷的損傷，然后加入光解酶,，并用超快光脈沖成像技術(shù)獲得了揭示光解酶修復受損DNA過程的系列圖片,。
紫外線導致人類患上皮膚癌的原因是它使得細胞中沿著DNA分子不正確的地方出現(xiàn)了化學鍵。仲東平的研究顯示,，光解酶能夠解散這些錯誤的化學鍵,，讓DNA的原子重新回到原來的位置,。同時，他們還發(fā)現(xiàn),，修復完成后,，DNA螺旋鏈會自動向光解酶發(fā)射出電子和質(zhì)子，這讓光解酶能繼續(xù)修復其他受損的DNA,。
人類被陽光曬傷后,，其體內(nèi)的酶沒有能力修復DNA損傷，皮膚細胞出現(xiàn)死亡,?？茖W家將慢性皮膚曬傷同DNA變異聯(lián)系起來，認為DNA變異導致了諸如皮膚癌等疾病,。仲東平表示,，現(xiàn)在人們認識了光解酶的作用機理，有望利用該信息設計出治療陽光曬傷的藥物或皮膚霜,。
科學家表示,，常見的防曬霜的作用是將紫外線轉(zhuǎn)變成熱能或反射紫外光。含有光解酶的防曬霜則有可能治療穿透進皮膚的紫外線所引起的損害,。(生物谷Bioon.com)
生物谷推薦原文出處：
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.
