Is Oxidative Damage by β-Amyloid and Prion Peptides Mediated by Hydrogen Atom Transfer from Glycine α-Carbon to Methionine Sulfur within β-Sheets?

摘要: Methionine in glycine-rich regions of both β-amyloid peptide and prion is thought to be crucial their neurotoxic properties. We postulate here a role for methionine the propagation oxidative damage. The S−H bond dissociation enthalpies, BDE(S−H)s, dimethylsulfonium ion (CH3)2SH+ S-protonated residue polypeptide strand are estimated 351 326−331 kJ mol-1, respectively, by application calculations at B3LYP level with large basis sets. These species direct products H atom abstraction radical cations sulfides. reactions between glycine (CH3)2S Met were investigated transition structures transfer located. results suggest that it thermodynamically feasible S-ionized form cause damage αC−H site almost any amino acid nearby (BDE(αC−H) = 330−360 mol-1) or lipids bis(allylic) methyle...