Effect of Buffer Capacity and Ascorbic Acid on the Cyclization Reaction of Electrochemically Oxidized Dopamine, Levodopa, and Adrenaline on the Glassy Carbon Electrode

The intramolecular cyclization step of oxidized catecholamines is crucial for neuromelanin (NM) and polydopamine (PDA). The product of the cyclization reaction of catecholamines has electrochemical activity, and its anodic and cathodic peaks occur at a more negative position than that of catecholamines. Moreover, in low pH, the amine group is protonated to a considerable extent; thus, the cyclization reaction is precluded. Our cyclic voltammetric results show that, in dilute buffer solution, the buffer concentration promotes the extent of the cyclization reaction of dopamine (DA), levodopa (L-D), and adrenaline (AD). A buffer component accepts the protons released by oxidized catecholamines, which suppresses the pH decrease near the electrode surface and protonation of amine group. Ascorbic acid (AA) more significantly inhibits the cyclization reaction of oxidized DA than those of L-D and AD. AA reduces catecholamine–quinone, and the cyclization rate constant of oxidized DA is smaller than those of L-D and AD. Consequently, buffer capacity and AA can be used to regulate the synthesis of NM and PDA.