A detailed knowledge of DNA damage induced by lowenergy
electrons (LEE) are of crucial importance both for the
advancement of theoretical models of cellular radiolysis and
for the development of new methods of radiotherapy.[1]
Studies on various DNA fragments have demonstrated that
near 0 eV energy, electron attachment may induce strand
breaks in DNA.[2–15] Strand-breaking mechanisms have been
proposed to elucidate the nature of DNA damage by
LEE.[7, 9–15] Both experimental and theoretical studies suggest
that the base-hosted radical anions might be responsible for
the LEE-induced DNA single-strand breaks.[3, 9, 11,13–15] These
electronically stable radical anions (covalent-bonded
anions)[13–15] are capable of undergoing either CO rupture
or glycosidic bond breaking (forming an abasic site). However,
as far as cytosine is concerned, this pathway might be
retarded in double-stranded DNA. Although the pairing
between cytosine (C) and guanine (G) dramatically increases
the electron affinity of C (from 0.1 eV for C to 0.4 eV for a
GC pair),[16, 17] a minor activation barrier (4 kcalmol1,
which is lower than the activation energy (6 kcalmol1) for
the LEE-induced C3’-O3’ bond breaking in DNA single
strands[15]) for proton transfer (PT) from the N1 of G to the
N3 of C in the GC pair might neutralize the negative charge of
the cytosine (forming a C(N3H)C neural radical) before
possible cleavage reactions.[17, 18]