European Neurology
Does Oxidative Stress Participate in Nerve Cell Death in Parkinson’s Disease?Hirsch E.C. · Hirsch E.C.INSERM U-289, Hôpital de la Salpêtrière, Paris, France
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Article / Publication Details
Published online: February 20, 2008
Issue release date: 1993
Number of Print Pages: 8
Number of Figures: 0
Number of Tables: 0
ISSN: 0014-3022 (Print)
eISSN: 1421-9913 (Online)
For additional information: https://www.karger.com/ENE
Abstract
Parkinson’s disease is characterized by a massive neuronal loss in several cell groups of the midbrain. However, the most consistent lesions are observed in dopaminergic systems including nigral neurons. Although the cause of this neuronal loss remains unknown, oxidative stress has been suspected to participate in the mechanism of nerve cell death for several reasons. (1) Lipid peroxidation, a consequence of oxygen free radical production, has been found to be elevated in the substantia nigra in Parkinson’s disease. (2) Catecholaminergic neurons containing neuromelanin, an autooxidation by-product of catecholamines, are more vulnerable in Parkinson’s disease than non-melanized catecholaminergic neurons. (3) Catecholaminergic neurons surrounded by a low density of cells containing glutathione peroxidase, a free radical scavenging enzyme, are more susceptible to degeneration in Parkinson’s disease than those well protected against oxidative stress. (4) The content of iron, a compound which exacerbates the production of free radicals in catecholaminergic neurons, is increased in the substantia nigra in Parkinson’s disease. It remains, however, to be determined whether oxidative stress participates to the cause of the disease or only represents a consequence of nerve cell death.
© 1993 S. Karger AG, Basel
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Article / Publication Details
Published online: February 20, 2008
Issue release date: 1993
Number of Print Pages: 8
Number of Figures: 0
Number of Tables: 0
ISSN: 0014-3022 (Print)
eISSN: 1421-9913 (Online)
For additional information: https://www.karger.com/ENE
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