Is Parkinson's disease a progressive siderosis of substantia nigra resulting in iron and melanin induced neurodegeneration?

Is Parkinson's disease a progressive siderosis of substantia nigra resulting in iron and melanin... Abstract– Razor sharp and high iron deposits are present in the substantia nigra (SN). Although the function of such high iron content is not known, the homeostatis of brain iron is important for normal brain function. The participation of free tissue iron in oxidative stress (OS), resulting in the formation of cytotoxic hydroxyl radical (·OH) from H2O2 (Fenton reaction) and promotion of membrane lipid peroxides by ·OH can no longer be questioned as a biological phenomenon. The highly selective increase of Fe2+ and Fe3+ and lipid peroxidation observed in parkinsonian SN points to OS in such brains. Lipid peroxidation proceeds with either Fe2+ or Fe3+ provided a mechanism exists to facilitate the interconversion of iron between its redox states. Indeed H2O2 derived from MAO B reaction and autooxidation of dopamine to melanin in the SN can drive the iron dependent Fenton reaction. Furthermore, interaction of iron with melanin may be even more important considering that melanin avidly binds Fe3+ and reduce it to Fe2+, resulting in ·OH generation. Thus, without evoking environmental neurotoxins, the excessive accumulation of free iron in the SN and “melanintrap'’could be the trigger for accelerated cell death and Parkinsonism. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Acta Neurologica Scandinavica Wiley

Is Parkinson's disease a progressive siderosis of substantia nigra resulting in iron and melanin induced neurodegeneration?

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Publisher
Wiley
Copyright
Copyright © 1989 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0001-6314
eISSN
1600-0404
D.O.I.
10.1111/j.1600-0404.1989.tb01782.x
Publisher site
See Article on Publisher Site

Abstract

Abstract– Razor sharp and high iron deposits are present in the substantia nigra (SN). Although the function of such high iron content is not known, the homeostatis of brain iron is important for normal brain function. The participation of free tissue iron in oxidative stress (OS), resulting in the formation of cytotoxic hydroxyl radical (·OH) from H2O2 (Fenton reaction) and promotion of membrane lipid peroxides by ·OH can no longer be questioned as a biological phenomenon. The highly selective increase of Fe2+ and Fe3+ and lipid peroxidation observed in parkinsonian SN points to OS in such brains. Lipid peroxidation proceeds with either Fe2+ or Fe3+ provided a mechanism exists to facilitate the interconversion of iron between its redox states. Indeed H2O2 derived from MAO B reaction and autooxidation of dopamine to melanin in the SN can drive the iron dependent Fenton reaction. Furthermore, interaction of iron with melanin may be even more important considering that melanin avidly binds Fe3+ and reduce it to Fe2+, resulting in ·OH generation. Thus, without evoking environmental neurotoxins, the excessive accumulation of free iron in the SN and “melanintrap'’could be the trigger for accelerated cell death and Parkinsonism.

Journal

Acta Neurologica ScandinavicaWiley

Published: Nov 1, 1989

References

  • Transition metals, ferritin, glutathione and ascorbic acid in Parkinsonian brain
    Riederer, Riederer; Sofic, Sofic; Rausch, Rausch; Schmidt, Schmidt; Reynolds, Reynolds; Kellinger, Kellinger; Youdim, Youdim
  • In vivo lipid peroxidation in rat brain following intracortical Fe ++ injection
    Triggs, Triggs; Willmore, Willmore
  • Parkinson Plus Syndrome: Diagnosis Using High Field MR Imaging of Brain Iron
    Drayer, Drayer; Olanow, Olanow; Burger, Burger; Johnson, Johnson; Herfkens, Herfkens; Riederer, Riederer

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