Base stacking in DNA is related to long-living excited states whose molecular nature is still under debate. To elucidate the molecular background we study well-defined oligonucleotides with natural bases, which allow selective UV excitation of one single base in the strand. IR probing in the picosecond regime enables us to dissect the contribution of different single bases to the excited state. All investigated oligonucleotides show long-living states on the 100-ps time scale, which are not observable in a mixture of single bases. The fraction of these states is well correlated with the stacking probabilities and reaches values up to 0.4. The longliving states show characteristic absorbance bands that can be assigned to charge-transfer states by comparing them to marker bands of radical cation and anion spectra. The charge separation is directed by the redox potential of the involved bases and thus controlled by the sequence. The spatial dimension of this charge separation was investigated in longer oligonucleotides, where bridging sequences separate the excited base from a sensor base with a characteristic marker band. After excitation we observe a bleach of all involved bases. The contribution of the sensor base is observable even if the bridge is composed of several bases. This result can be explained by a charge delocalization along a well-stacked domain in the strand. The presence of charged radicals in DNA strands after light absorption may cause reactions-oxidative or reductive damagecurrently not considered in DNA photochemistry.DNA photophysics | DNA damage | DNA electron transfer | ultrafast vibrational spectroscopy D NA photophysics is crucial for the understanding of lightinduced damage of the genetic code (1). The excited state of single DNA bases is known to decay extremely fast on the subpicosecond time scale, predominantly via internal conversion (2, 3). This ultrafast decay is assumed to suppress destructive decay channels, thereby protecting the DNA from photodamage and avoiding disintegration of the genetic information. In contrast to this ultrafast deactivation of single nucleobases, the biological relevant DNA strands show further long-living states (4, 5). Several explanations for these long-living states and the size of their spatial extent have been discussed in the literature (5-9). Delocalized excitons (9); excitons that decay to charge-separated states or neutral excimer states (10, 11); exciplexes located on two neighboring bases (5, 8, 12, 13); or even excited single bases, where steric interactions in the DNA strand impedes the ultrafast decay (14), have been proposed. Further computations suggest a decay of an initially populated delocalized exciton to localized neutral or charged excimer states (15-17). However, to our knowledge, a final understanding of the nature of these longliving states has not been reached. Related experiments were performed in the last decade to investigate charge transport processes in DNA, motivated by DNA electronics and oxidative damage (18,19). Charge ...

The importance of a backbone: The mechanism of formation of Dewar lesions has been investigated by using femtosecond IR spectroscopy and ab initio calculations of the exited state. The 4π electrocyclization is rather slow, occurs with an unusual high quantum yield, and--surprisingly--is controlled by the phosphate backbone.

UV-induced formation of the cyclobutane pyrimidine dimer (CPD) lesion is investigated by stationary and time-resolved photosensitization experiments. The photosensitizer 2'-methoxyacetophenone with high intersystem crossing efficiency and large absorption cross-section in the UV-A range was used. A diffusion controlled reaction model is presented. Time-resolved experiments confirmed the validity of the reaction model and provided information on the dynamics of the triplet sensitization process. With a series of concentration dependent stationary illumination experiments, we determined the quantum efficiency for CPD formation from the triplet state of the thymine dinucleotide TpT to be 4 ± 0.2%.