The reactions of
dopamine (1-amino-2-(3,4-dihydroxyphenyl)-ethane, DA),
5-hydroxydopamine (5-OHDA), and
6-hydroxydopamine (6-OHDA), with molecular
oxygen-with and without the addition of catalytic amounts of
iron(III) and other
metal ions-have been studied and the implication of these results with respect to the chemistry involved in the progress of
Parkinson's disease is discussed. In the presence of O2 DA reacts spontaneously without the necessity of
metal-ion catalysis under the production of stoichiometric amounts of H2O2, to form initially pink
dopaminochrome, which is not stable and reacts further (without the consumption of
dioxygen) to form the insoluble polymeric material known as 'melanine'. DA reacts with
iron(III) yielding an intermediate 1:1 complex, which decomposes releasing Fe(II) and the semiquinone, which reacts further under involvement of both Fe(III) and
dioxygen.
6-OHDA reacts without showing the necessity of such an intermediate, and it is shown to be able to release
iron as Fe(II) from ferritine. On the other hand, it is shown (in vitro) that Fe(II) reacts in a Fenton type reaction with DA and the present H2O2 producing 5-OHDA and especially
6-OHDA. Based on these mutual interacting reactions a mechanism for the initiation and progress of
Parkinson's disease is suggested. The catalytic effects of some other transition-
metal ions are presented and an explanation for the peculiarly toxic effects of
manganese(II) is put forward. Finally, a possible reason for the effect that
nicotine has in the mitigation of
Parkinson's disease is discussed.