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Review
. 2003 Jan;111(2):163-9.
doi: 10.1172/JCI17638.

Oxidative stress and nitration in neurodegeneration: cause, effect, or association?

Harry Ischiropoulos  1 , Joseph S Beckman
Affiliations
Review

Oxidative stress and nitration in neurodegeneration: cause, effect, or association?

Harry Ischiropoulos et al. J Clin Invest. 2003 Jan.
No abstract available

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Figures

Figure 1
Figure 1
Specific antibodies against nitrated α-synuclein recognize synuclein inclusions. Immunostaining with the mAb nSyn24, a nitrated α-synuclein–specific antibody, reveals staining in nigral Lewy bodies of Parkinson disease and dementia with Lewy bodies (a), glial cytoplasmic inclusions of multiple system atrophy (b), and the Lewy body–like inclusions, neuroaxonal spheroids, and dystrophic neurites of neurodegeneration with brain iron accumulation type 1 (c). The image was provided by John Duda and Benoit Giasson (Center for Neurodegenerative Disease Research, University of Pennsylvania, Philadelphia, USA).
Figure 2
Figure 2
Common reactions of oxygen radicals and nitric oxide in a biological setting. NADPH oxidase and xanthine oxidase transfer a single electron to oxygen to form superoxide anion, while other flavoproteins can transfer two electrons to form hydrogen peroxide directly. SODs scavenge superoxide, which forms additional hydrogen peroxide. Peroxidases use hydrogen peroxide to oxidize a wide range of substrates to produce many different reactive species. Nitric oxide reacts with superoxide to form peroxynitrite. Carbon dioxide reacts catalytically with peroxynitrite to form nitrogen dioxide and carbonate radical. These two radicals nitrate tyrosine, which is blocked by the competitive inhibitor urate. Nitric oxide can also react with these radicals to form nitrosating intermediates that can produce, among other things, S-nitrosothiols. MPO, myeloperoxidase; RS-NO, S-nitrosothiols.
Figure 3
Figure 3
Proposed model for a central but not initiating role of oxidative processes in the pathogenesis of Parkinson disease. The model is based on published data and incorporates elements of the existing working hypothesis that places oxidative processes at the narrowest point of a funnel through which environmental, genetic, and endogenous risk factors flow to adversely impact cellular function and viability.
See this image and copyright information in PMC

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