Interruption of the MnO2 oxidative process on dopamine and L-dopa by the action of S2O3(2-)

The oxidation effects of Mn2+, Mn3+ or MnO2 on dopamine can be studied in vitro and, therefore, this offers a model of the auto-oxidation process that appears naturally in neurons causing Parkinson's disease. The use of MnO, as an oxidizer in aqueous solution at pH 7 causes the oxidation of catecholamines (L-dopa, dopamine, noradrenaline and adrenaline) to melanin. However, this work shows that, in water at pH 6-7, the oxidation of catecholamines by MnO2 in the presence of sodium thiosulphate (Na2S2O3) occurs by other mechanisms. For dopamine and L-dopa, MLCT complexes were formed with bands at 312, 350 (sh), 554 (sh) nm, and an intense band at 597 nm (epsilon approximately/= 4 x 10(3) M(-1) cm(-1)) and at ca. 336, 557 (sh) nm, and an intense band at 597 nm (epsilon approximately 6 x 10(3) M(-1) cm(-1)), respectively. The latter transitions were assigned to d(pi)-->pi*-SQ. Noradrenaline and adrenaline do not form this blue complex in solution, but generate soluble oxidized compounds. The resonance Raman spectra of these complexes in solution showed bands at 950, 1006, 1258, 1378, 1508 and 1603 cm(-1) for the complex derivation of L-dopa and at 948, 1010, 1255, 1373, 1510 and 1603 cm(-1) for the dopamine-derived compound. The most intense Raman band at ca. 1378 cm(-1) was assigned to C-O stretching with major C1-C2 characteristics and indicated that dopamine and L-dopa do not occur complexed with manganese in the catecholate or quinone form, but suggests an intermediate compound such as an anionic o-semiquinone (SQ-), forming a complex such as Mn(II)(SQ-)3]-. All enhanced Raman frequencies are characteristic of the benzenic ring without the participation of the aminic nitrogen. A mechanism is proposed for the formation of the dopamine and L-dopa complexes and a computational simulation was performed to support it.