Electronic and Inertial Effects of Methylation on Excited-State Hydrogen Transfer

甲基化对激发态氢转移的电子效应和惯性效应

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Abstract

Excited-state intramolecular hydrogen transfer (ESIHT) is among the fastest chemical reactions and is a key design element in photoprotective molecules and functional chromophores. Despite the apparent simplicity of the symmetric HO-C═C-C═O ESIHT prototype, its multifunctional nature enables competing nonradiative decay channels, including C═C torsional motion. Here, we compare malonaldehyde (MA), the minimal motif, with its methylated derivative acetylacetone (AcAc) to investigate how electronic and inertial effects of methylation shape the ultrafast dynamics initiated on S(2)(ππ*). XMS-CASPT2 nonadiabatic dynamics on the singlet manifold reveal bond-length alternation that drives the wavepacket toward the H-transfer intersection seam rather than undergoing torsional motion directly out of the Franck-Condon region. Methylation destabilizes the S(1)(nπ*) state, reducing the S(2)/S(1)-energy gap and enhancing the asymmetry of the H-transfer intersection seam. As a result, S(2)/S(1)-decay precedes H-transfer, which mostly takes place only after the population arrives on S(1). Moreover, the methyl groups in AcAc introduce an inertial mismatch between the central methine hydrogen and the terminal methyl groups, which gives rise to two distinct behaviors on S(1): (i) an early ballistic rise in ground-state population within ∼75 fs via twist-pyramidalized geometries akin to the behavior of α,β-enones and (ii) a slower repopulation through torsional motion, with the majority of the population remaining near the planar S(1)-minimum. In contrast, MA displays no ballistic channel. Our results for AcAc are consistent with recent time-resolved photoelectron spectroscopy, confirming the ultrafast S(2)-lifetime. We propose extending such experiments into the X-ray regime, where the evolution of the oxygen 1s binding energies offers direct, site-specific sensitivity to the H-transfer-mediated motion governing the early decay.

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