Kwok Wai-Ming, Ma Chensheng, Phillips David Lee
Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong, China.
J Am Chem Soc. 2008 Apr 16;130(15):5131-9. doi: 10.1021/ja077831q. Epub 2008 Mar 13.
Ultraviolet irradiation of DNA produces electronic excited states that predominantly eliminate the excitation energy by returning to the ground state (photostability) or following minor pathways into mutagenic photoproducts (photodamage). The cyclobutane pyrimidine dimer (CPD) formed from photodimerization of thymines in DNA is the most common form of photodamage. The underlying molecular processes governing photostability and photodamage of thymine-constituted DNA remain unclear. Here, a combined femtosecond broadband time-resolved fluorescence and transient absorption spectroscopies were employed to study a monomer thymidine and a single-stranded thymine oligonucleotide. We show that the protecting deactivation of a thymine multimer is due to an ultrafast single-base localized stepwise mechanism where the initial excited state decays via a doorway state to the ground state or proceeds via the doorway state to a triplet state identified as a major precursor for CPD photodamage. These results provide new mechanistic characterization of and a dynamic link between the photoexcitation of DNA and DNA photostability and photodamage.
DNA的紫外线照射会产生电子激发态，这些激发态主要通过回到基态（光稳定性）或通过次要途径形成诱变光产物（光损伤）来消除激发能。由DNA中胸腺嘧啶的光二聚化形成的环丁烷嘧啶二聚体（CPD）是最常见的光损伤形式。控制胸腺嘧啶构成的DNA的光稳定性和光损伤的潜在分子过程仍不清楚。在这里，我们采用飞秒宽带时间分辨荧光和瞬态吸收光谱相结合的方法来研究单体胸苷和单链胸腺嘧啶寡核苷酸。我们表明，胸腺嘧啶多聚体的保护性失活是由于一种超快的单碱基局域逐步机制，其中初始激发态通过一个门道态衰减到基态，或通过门道态进入一个三重态，该三重态被确定为CPD光损伤的主要前体。这些结果为DNA的光激发与DNA光稳定性和光损伤之间提供了新的机制表征和动态联系。
