Radiation chemical methods were used to investigate the reactions of glycine anions, H2NCH2CO2 - (Gly-), with •OH, (CH3)2C•OH, and •CH3 radicals. A major and most significant product from all of these processes is CO2. Pulse-radiolysis revealed that the initial step in the •OH-induced mechanism is oxidation of the amino group, producing +H2N•-CH2-CO2 - and HN•-CH2-CO2 - with yields of 63% and 37%, respectively. The amino radical cation, +H2N•-CH2-CO2 -, suffers fast (≤100 ns) fragmentation into CO2 + •CH2NH2. The other primary radical, HN•-CH2-CO2 -, can also be converted into the decarboxylating +H2N•-CH2-CO2 - by reaction with proton donors such as phosphate (H2PO4 -/k = 7.4 × 107 M-1 s-1, and HPO4 2-/k = 2.5 × 105 M-1 s-1) or the glycine zwitterion, Gly± (k = 3.9 × 105 M-1 s-1), but only on a much longer (typically μs to ms) time scale (k ≈ 4 × 105 M-1 s-1). Competitively, the HN•-CH2-CO2 - transforms into a carbon-centered radical H2N-C•H-CO2 - either by an intramolecular 1,2-H-atom shift (k = (1.2 ± 1.0) × 103 s-1) or by bimolecular reaction with Gly- (k = (3.0 ± 0.2) × 104 M-1 s-1). Both C-centered radicals, H2N-C•H-CO2 - and •CH2NH2, are reductants as verified through their reactions with Fe(CN)6 3- and methyl viologen (MV2+) in pulse-radiolysis experiments (k ≈ 4 × 109 M-1 s-1). The eventual complete transformation of all primary radicals into H2N-C•H-CO2 - and •CH2NH2 was further substantiated by γ-radiolytic reduction of Fe(CN)6 3-. In the presence of suitable electron donors, the HN•-CH2-CO2 - radical acts as an oxidant. This was demonstrated through its reaction with hydroquinone (k = (7.4 ± 0.5) × 107 M-1 s-1). Although the C-centered H2N-C•H-CO2 - radical is not generated in a direct H-atom abstraction by •OH, this radical appears to be the exclusive product in the reaction of Gly- with (CH3)2C•OH, •CH2NH2, and •CH3 (k ≈ 102 M-1 s-1). A most significant finding is that H2N-C•H-CO2 - can be converted into the decarboxylating N-centered radical cation +H2N•-CH2-CO2 - by reaction with proton donors such as Gly± (k ≈ 3 × 103 M-1 s-1) or phosphate and thus also becomes a source of CO2. The •CH2NH2-induced route establishes, in fact, a chain mechanism which could be proven through dose rate effect experiments and suppression of the chain upon addition of Fe(CN)6 3- or MV2+ as a scavenger for the reducing precursor radicals. The possible initiation of amino acid decarboxylation by C-centered radicals and the assistance of proton donors at various stages within the overall mechanism are considered to be of general significance and interest in chemical and biological systems.

The oxidation of simple aliphatic sulphides [MeSMe, EtSEt, (CH,),S] by hydroxyl radicals occurs via a complex reaction mechanism. The first step is addition of the OH* to sulphur to form R2SOH radicals. At low sulphide concentrations ( < ~O -* M ) R,SOH rapidly eliminates H 2 0 to form a RSR(-H)* radical which may be described by the mesomeric forms -CH-S-and -CH=S-.This radical is ultimately also formed at higher sulphide concentrations but via a different pathway. R2SOH increasingly reacts with another R2S molecule to form a short lived (R,S),OH* radical complex which dissociates to (R,S),+ and OH-. The (R,S),+ complex ion seems to be relatively stable and decays essentially via equilibration to the molecular cation R2S+. This ion in its reaction with the solvent, OHions, and through a bimolecular process with another R2S+ cation is effectively deprotonated to form the RSR( -H). radical. The reaction route a t high concentration includes the formation of transient species with oxidizing properties; Fe(CN)64is rapidly oxidized by (R,S),+ [and possibly (R,S),OH*].The RSR(-H).radical partially disproportionates to negative and long lived (>I ms) positive ions. The stable oxidation product, sulphoxide, has been identified.

Aminyl radicals, HN•−CR2−CO2 - (R = H, CH3) have been identified as significant transients in the hydroxyl radical-induced oxidation of the anions of glycine (Gly-), alanine (Ala-), and α-methylalanine (MeAla-) at relative yields of 37%, 43%, and 56%, respectively. Quantification has been achieved by two independent pulse radiolysis methods. Direct titration of the aminyl radicals made use of their capability to oxidize hydroquinone to the easily detectable semiquinone radical. The rate constant for this reaction involving the aminyl radical from alanine is 1.1 × 108 M-1 s-1 (at pH 11.0). An alternative method relied on the titration with methyl viologen and 4-carboxybenzophenone of the reducing radicals, which are formed as the result of secondary reactions of the aminyl radicals. In fact, several processes may occur and compete with each other in this case:  (i) In the presence of proton donors the aminyl radicals can effectively be converted into H2N•+−CR2−CO2 - radical zwitterions (even in basic solution), which immediately decarboxylate and leave strongly reducing α-aminoalkyl radicals, •CR2NH2. The rate-determining step in this reaction sequence has been shown to be the protonation of the aminyl function by, e.g., the respective zwitterions of the amino acids, or hydrogen phosphate. Absolute rate constants for these proton-transfer processes cover a 105−108 M-1 s-1 range (including previously published values for the glycine-derived aminyl radical). (ii) The aminyl radicals are further capable of abstracting a Cα-bound H atom (applicable for glycine and alanine), thereby generating C-centered α-amino-α-carboxyl radicals. A rate constant of 1.7 × 105 M-1 s-1 has been obtained for this process in the alanine system. (ii) A third competing process of significance has been identified to be β-fragmentation of the aminyl radicals into the respective imines and CO2 •-. The latter radical anion was identified through its electron transfer to 4-carboxybenzophenone (k = 3.3 × 107 M-1 s-1). Rate constants for the β-fragmentation itself have been determined to be 2.3 × 104 s-1 for HN•−CH(CH3)−CO2 -, and 7.4 × 104 s-1 for HN•−C(CH3)2−CO2 -. They follow the trend predicted by density functional theory (DFT) calculations on the free energies of reaction and activation.