Sequence-Specific Damage Induced by the Impact of 3–30 eV Electrons on Oligonucleotides

Abdoul-Carime, H. and Sanche, L. Sequence-Specific Damage Induced by the Impact of 3–30 eV Electrons on Oligonucleotides. Radiat. Res. 156, 151–157 (2001). The ability of low-energy electrons to induce single- and double-strand breaks in DNA has recently been demonstrated. Here we show the propensity of 3–30 eV electrons to initiate base sequence-dependent damage to a short single DNA strand. Solid monolayer films of homogeneous thymidine (T9) and deoxycytidine (dCy9) and heterogeneous oligomers (T6dCy3) are bombarded with 1–30 eV electrons in an ultrahigh-vacuum system. CN, OCN and/or H2NCN are detected by a mass spectrometer as the most intense neutral fragments desorbing in vacuum. A weaker signal of CH3CCO is also detected, but only from oligonucleotides containing thymine. Below 17 eV, the energy dependence of the yields of CN, OCN and CH3CCO exhibits resonance-like structures, attributed to dissociative electron attachment (DEA). Above 17 eV, the monotonic increase in the fragment yields indicates that nonresonant processes (i.e. dipolar dissociation) control the fragmentation of these molecules. Within the energy range investigated, comparison of the magnitude of the total fragment yields produced by electron attack on dCy9, T6-dCy3 and T9 suggests the following order in the sensitivity of single-strand DNA: dCy9 > T6-dCy3 > T9. At 12 eV, the total fragment yields are found to be 5.8, 5.0 and 3.9 × 10–3 fragment/electron, respectively. From the yields obtained with the two homo-oligonucleotides, we differentiate between contributions arising from the chemical nature of the base and the effect of environment (i.e. the sequence) when a thymidine unit in T9 is replaced by dCy. The base sequence-dependent damage is found to vary with incident electron energy. These results reinforce the idea that genomic sensitivity to ionizing radiation depends on local genetic information. Furthermore, they underscore the possible role of low-energy electrons in the pathways responsible for the induction of specific genomic lesions.