A multicoincidence study of fragmentation dynamics in collision of γ-aminobutyric acid with low-energy ions.

Fragmentation of the γ-aminobutyric acid molecule (GABA, NH(2)(CH(2))(3)COOH) following collisions with slow O(6+) ions (v≈0.3 a.u.) was studied in the gas phase by a combined experimental and theoretical approach. In the experiments, a multicoincidence detection method was used to deduce the charge state of the GABA molecule before fragmentation. This is essential to unambiguously unravel the different fragmentation pathways. It was found that the molecular cations resulting from the collisions hardly survive the interaction and that the main dissociation channels correspond to formation of NH(2)CH(2)(+), HCNH(+), CH(2)CH(2)(+), and COOH(+) fragments. State-of-the-art quantum chemistry calculations allow different fragmentation mechanisms to be proposed from analysis of the relevant minima and transition states on the computed potential-energy surface. For example, the weak contribution at [M-18](+), where M is the mass of the parent ion, can be interpreted as resulting from H(2)O loss that follows molecular folding of the long carbon chain of the amino acid.

Ion-induced fragmentation of amino acids: effect of the environment.

In general, radiation-induced fragmentation of small amino acids is governed by the cleavage of the C-C(α) bond. We present results obtained with 300 keV Xe(20+) ions that allow molecules (glycine and valine) to be ionised at large distances without appreciable energy transfer. Also in the present case, the C-C(α) bond turns out to be the weakest link and hence its scission is the dominant fragmentation channel. Intact ionised molecules are observed with very low intensities. When the molecules are embedded in a cluster of amino acids, a protective effect of the environment is observed. The fragmentation pattern changes: the C-C(α) bond becomes more protected and stable amino acid cations are observed as fragments of the molecular clusters. Evidently, the molecular cluster acts as a "buffer" for the excess energy, capable of rapidly redistributing excess energy and charge.

On the hydrogen loss from protonated nucleobases after electronic excitation or collisional electron capture.

In this work, we have subjected protonated nucleobases MH(+) (M = guanine, adenine, thymine, uracil and cytosine) to a range of experiments that involve high-energy (50 keV) collision induced dissociation and electron capture induced dissociation. In the latter case, both neutralisation reionisation and charge reversal were done. For the collision induced dissociation experiments, the ions interacted with O(2). In neutral reionisation, caesium atoms were used as the target gas and the protonated nucleobases captured electrons to give neutrals. These were reionised to cations a microsecond later in collisions with O(2). In choosing Cs as the target gas, we have assured that the first electron transfer process is favourable (by about 0.1-0.8 eV depending on the base). In the case of protonated adenine, charge reversal experiments (two Cs collisions) were also carried out, with the results corroborating those from the neutralisation reionisation experiments. We find that while collisional excitation of protonated nucleobases in O(2) may lead to hydrogen loss with limited probabilities, this channel becomes dominant for electron capture events. Indeed, when sampling reionised neutrals on a microsecond timescale, we see that the ratio between MH(+) and M(+) is 0.2-0.4 when one electron is captured from Cs. There are differences in these ratios between the bases but no obvious correlation with recombination energies was found.