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W. Linert:
"Iron acting as catalyst for oxidative stress in the pathogenesis of Parkinson's disease?";
Hauptvortrag: 5th International Scientific Conference on Applied Natural Sciences 2015, Jasna, Low Tatras Slovak Republik (eingeladen); 30.09.2015 - 02.10.2015; in: "Book ob Abstracts 5th International Scientific Conference on Applied Natural Sciences 2015", D. Chmelova, M. Ondrejovic (Hrg.); (2015), S. 17 - 18.

The mechanisms leading to degeneration of melanized dopaminergic neurons in the brain stem, and particularly in the substantia nigra (SN) in patients with Parkinson´s disease (PD) are still unknown. Demonstration of increased iron Fe(III) in SN of PD brain has suggested that Fe-melanin interaction may contribute to oxidative neuronal damage. Energy dispersive X-ray electron microscopic analysis of the cellular distribution of trace elements revealed significant Fe-peaks, similar to those of a synthetic melanin-Fe(III) complex in intrancytoplasmic electron- dense neuromelanin granules of SN neurons, with highest levels in a case of PD.


The relevance of chemical reactions of dopamine (DA), 5-hydroxydopamine (5-OHDA), and 6-hydroxydopamine (6-OHDA) with Fe(III) and with dioxygen for the pathogenesis of PD was investigated. An initiating mechanism related to interaction between Ferritin, free Fe(II) and hydrogenperoxid is suggested. A cycle of continuous production of cytotoxic species inducing a cascade of pathogenic reactions ultimately leading to neuronal death which becomes visible in accumulation of Fe(III) the (SN). The release of Fe(II) from Ferritine can be related to the redox potential of dopamines which in turn is associated on inner-sphere - outersphere redox reactions of Fe(III) (stored in Ferritine) and the respective dopamines. The scheme below outlines the mentioned cycle.

neurodegenerative disease, redox kinetics