Ab initio study of a biradical radiationless decay channel of the lowest excited electronic state of cytosine and its derivatives.

A theoretical model for the ultrafast S1-->S0 internal conversion of cytosine is presented, in which a state switch from the initially prepared 1pipi* state to the out-of-plane deformed excited state of biradical character controls the rate of the S1(1pipi*) decay. This mechanism successfully accounts for the dramatically longer S1 lifetimes of 5-fluorocytosine and N-acetylcytosine relative to cytosine. The replacement of the C5 hydrogen atom by a methyl group is predicted to lead to a substantial, but not dramatic, increase in the S1 lifetime, also consistent with experiment. It is this ability to correctly predict the substituent effects that distinguishes the present model from the previously proposed mechanisms.