  Joint femtosecond fluorescence upconversion experiments and theoretical
calculations provide a hitherto unattained degree of characterization and
understanding of the mutagenic etheno adduct 3,N4-etheno-2'-deoxycytidine
($\epsilon$dC) excited state relaxation. This endogenously formed lesion is
attracting great interest because of its ubiquity in human tissues and its
highly mutagenic properties. The $\epsilon$dC fluorescence is modified with
respect to that of the canonical base dC, with a 3-fold increased lifetime and
quantum yield at neutral pH. This behavior is amplified upon protonation of the
etheno ring ($\epsilon$dCH+). Quantum mechanical calculations show that the
lowest energy state $\pi$$\pi$*1 is responsible for the fluorescence and that
the main nonradiative decay pathway to the ground state goes through an
ethene-like conical intersection, involving the out-of-plane motion of the C5
and C6 substituents. This conical intersection is lower in energy than the
$\pi$$\pi$* state ($\pi$$\pi$*1) minimum, but a sizable energy barrier explains
the increase of $\epsilon$dC and $\epsilon$dCH+ fluorescence lifetimes with
respect to that of dC.
