Theoretical insights on the excited-state-deactivation mechanisms of protonated thymine and cytosine†

Ab initio and surface-hopping nonadiabatic dynamics simulation methods were employed to investigate relaxation mechanisms in protonated thymine (TH+) and cytosine (CH+). A few conical intersections were located between (1)pi pi* and S-0 states for each system with the CASSCF (8,8) theoretical model and relevant contributions to the deactivation mechanism of titled systems were addressed by the determination of potential energy profiles at the CASPT2 (12,10) theoretical level. It was revealed that the relaxation of the (1)pi pi* state of the most stable conformer of both systems to the ground state is mostly governed by the accessible S-1/S-0 conical intersection resulting from the barrier-free out-of-plane deformation. Interestingly, it was exhibited that the ring puckering coordinate driven from the C-6 position of the heterocycle ring in TH+ and CH+ plays the most prominent role in the deactivation mechanism of considered systems. Our ab initio results are also supported by excited-state nonadiabatic dynamics simulations based on ADC(2), describing the ultrashort S-1 lifetime of TH+/CH+ by analyzing trajectories leading excited systems to the ground. It was confirmed that the excited-state population mostly relaxes to the ground via the ring puckering coordinate from the C-6 moiety. Overall, the theoretical results of this study shed light on the deactivation mechanism of protonated DNA bases.

Automated summary

The study utilizes ab initio and surface-hopping nonadiabatic dynamics simulation methods to investigate relaxation mechanisms in protonated thymine (TH+) and cytosine (CH+). Multiple conical intersections were located between (1)pi pi* and S-0 states for each system, with particular focus on the barrier-free out-of-plane deformation governing relaxation from the (1)pi pi* state to the ground state. The ring puckering coordinate from the C-6 position of the heterocycle ring was found to play a prominent role in the deactivation mechanism of the considered systems, supported by excited-state nonadiabatic dynamics simulations.