Microsolvation Controls Ultrafast Relaxation Pathways in Hydrated Pyridine

Abstract Hydration critically reshapes ultrafast electronic relaxation in biorelevant molecules, yet its mechanistic role remains poorly understood. Here, we investigate intermolecular Coulombic decay (ICD) following medium-energy (E0 = 103 eV) electron impact ionization of hydrated pyridine, a prototypical nucleobase analogue. Combining multiparticle momentum coincidence spectroscopy with high-level electronic structure calculations, we identify water-initiated ICD and find evidence consistent with an additional pyridine-initiated ICD pathway, in which inner-valence ionization leads to ionization of the neighboring molecule. Water vacancies decay exclusively via the ICD, establishing a highly efficient direct channel. In contrast, pyridine vacancies compete with Auger decay, reducing the efficiency of the pyridine-to-water ICD pathway. As in pyridine dimers, heterocycle-initiated ICD is dominated by N 2s vacancy states. Our results reveal a dual role of water: it opens a highly efficient direct ICD pathway via O 2s vacancy states and acts as an energy-accepting partner following biomolecular inner-valence ionization. These results reveal how microsolvation governs ultrafast relaxation and shapes radiation-induced damage pathways in DNA-related systems.