[How can an electron induce oxidative damage in DNA in solution].

DNA damage caused by the dissociative electron attachment (DEA) has been well-studied in the gas and solid phases. However, understanding of this process at the fundamental level in solution is still a challenge. The electrons, after losing their kinetic energy via ionization and excitation events, are thermalized and undergo a multistep hydration process with a time constant of ca. ≤1 ps, to becoming fully trapped as a hydrated or solvated electron (e_sol ^- or e_aq ^-). Prior to the formation of e_sol ^-, the electron exists in its presolvated (or prehydrated) state (e_pre ^-) with no kinetic energy. We used picosecond pulse radiolysis to generate electrons in water or in liquid diethylene glycol (DEG) to observe the dynamics of capture of these electrons by DNA/RNA bases, nucleosides, and nucleotides. Contrary to the hypotheses in the literature that the presolvated electrons (e_pre ^-) are captured well by the DNA-nucleosides/tides and the transient negative ions (TNIs) cause strand breaks, we first show that the quasi-free electrons with kinetic energy (e_qf ^-) or e_pre ^-cannot be captured by guanine and adenine at very long distances in aqueous solutions with concentrations lower than 50 mM. However, the observation of a substantial decrease in the initial yield of e_sol ^- as a function of nucleoside/nucleotide concentrations accompanied by the formation of the nucleotide anion radicals provides direct evidence of an ultrafast step involving radiation-produced electron-mediated DNA damage via DEA. Transient signal analysis suggests that the dissociation channel of TNIs in nucleotide solutions is not even probable up to 0.25 M. On the other hand, in diethylene glycol, we demonstrate that unlike e_sol ^- and e_pre ^-, e_qf ^- effectively attaches itself to the RNA-nucleoside, ribothymidine, forming the TNI in the excited state (TNI*) that undergoes the N1-C1' glycosidic bond dissociation. Thanks to DEA, this process induced by e_qf ^-, in fact, leads to an oxidation of the parent molecule similar to the hydroxyl radical (^•OH) leading to the same glycosidic bond (N1-C1') cleavage.