Hydroxydopamine and Ferritin

By making use of the intense color of the deprotonated quinone of 6-OHDA, Jameson et al. [49] were able to demonstrate that this catecholamine can enter the ferritin and reduce the iron present, reaching redox equilibrium. Importantly, they also demonstrated that this alone did not explain the liberation of iron from this storage protein - an external complexing agent is required to remove the iron(II) produced, disturb the equilibrium within the protein, and thus continuously remove iron (Figure 8).

It has been shown that dopamine itself is able to fulfil this role [50], but as has been pointed out above there are many other potential complexing agents present within the cell (e.g., citrate, amino acids, and nucleotides) that could also fulfil this role. These observations would further appear to add credence to the idea [35] that the neurotoxin 6-OHDA has an essential role to play in the progression of PD.

Figure 8. Schematic diagram illustrating the entrance of 6-OHDA into ferritin and reaching redox equilibrium with the iron core. This equilibrium is disturbed if a com-plexing agent is present.

Figure 8. Schematic diagram illustrating the entrance of 6-OHDA into ferritin and reaching redox equilibrium with the iron core. This equilibrium is disturbed if a com-plexing agent is present.

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