Absorption of UV-radiation in nucleotides initiates a number of photophysical and photochemical processes, which may finally cause DNA damage. One major decay channel of photoexcited DNA leads to reactive charge transfer states. This study shows that these states trigger self-repair of DNA photolesions. The experiments were performed by UV spectroscopy and HPLC on different single and double stranded oligonucleotides containing a cyclobutane pyrimidine dimer (CPD) lesion. In a first experiment we show that photoexcitation of adenine adjacent to a CPD has no influence on this lesion. However, excitation of a guanine (G) adenine (A) sequence leads to reformation of the intact thymine (T) bases. The involvement of two bases for the repair points to a long-living charge transfer state between G and A to be responsible for the repair. The negatively charged A radical anion donates an electron to the CPD, inducing ring splitting and repair. In contrast, a TA sequence, having an inverted charge distribution (T radical anion, A radical cation), is not able to repair the CPD lesion. The investigations show that the presence of an adjacent radical ion is not sufficient for repair. More likely it is the driving power represented by the oxidation potential of the radical ion, which controls the repair. Thus, repair capacities are strongly sequence-dependent, creating DNA regions with different tendencies of self-repair. This self-healing activity represents the simplest sequence-dependent DNA repair system.

Excited-state dynamics are essential to understanding the formation of DNA lesions induced by UV light. By using femtosecond IR spectroscopy, it was possible to determine the lifetimes of the excited states of all four bases in the double-stranded environment of natural DNA. After UV excitation of the DNA duplex, we detected a concerted decay of base pairs connected by Watson-Crick hydrogen bonds. A comparison of single- and double-stranded DNA showed that the reactive charge-transfer states formed in the single strands are suppressed by base pairing in the duplex. The strong influence of the Watson-Crick hydrogen bonds indicates that proton transfer opens an efficient decay path in the duplex that prohibits the formation or reduces the lifetime of reactive charge-transfer states.

Die Dynamik des angeregten Zustands ist wesentlich für ein Verständnis der UV‐Licht‐induzierten Schadensbildung der DNA. Mithilfe von Femtosekunden‐IR‐Spektroskopie konnten wir die Lebenszeit des angeregten Zustands aller vier Nukleobasen in der doppelsträngigen natürlichen DNA bestimmen. Wir stellten einen konzertierten Zerfall des angeregten Zustands von Watson‐Crick‐Basenpaaren nach UV‐Anregung fest. Durch einen Vergleich von einzelsträngiger und doppelsträngiger DNA konnten wir zeigen, dass die in Einzelsträngen auftretenden reaktiven, ladungsgetrennten Zustände durch Basenpaarung im Duplex unterdrückt werden. Der starke Einfluss der Watson‐Crick‐Wasserstoffbrücken deutet auf einen Protonentransfer hin, der einen neuen Zerfallskanal eröffnet und damit die Bildung von reaktiven ladungsgetrennten Zuständen vermeidet oder deren Lebenszeit verkürzt.