Chapter 31 Reactions of nitric oxide, superoxide and peroxynitrite with superoxide dismutase in neurodegeneration

Beckman, Joseph S.; Chen, Jun; Crow, John P.; Ye, Yao Zu

doi:10.1016/s0079-6123(08)61151-6

Cited by 194 publications

(102 citation statements)

References 60 publications

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“…In neurodegenerative disorders, this imbalance in metal ion homeostasis can induce OS. If the levels of superoxide radicals are high and if there is an increased availability of nitric oxide, radical-radical recombination results in the formation of peroxynitrite, a highly reactive product with a half life of < 1 s that can lead to nitration of biomolecules, proteins, and lipids (38). Hence, markers of OS, levels of antioxidant enzymes, and elevation of cellular stress response proteins reflect the level of oxidative damage in, and fate of, the cell.…”

Section: Protein (/Lipid) Oxidation and Protein Dysfunctionmentioning

confidence: 99%

“…The first hypothesis states that mSOD1 proteins are or become misfolded and consequently oligomerize to form intracellular aggregates (106,387), which also include other essential proteins that are, therefore, no longer available to perform their correct function. The second-the oxidative damage hypothesis-proposes that toxicity is caused by aberrant chemistry of the active Cu/Zn sites of the misfolded enzyme (38), which contributes to further exacerbate OS conditions by increasing the levels of ROS within the cell (38,251). This latter mechanism can lead to misfolding of Cu, Zn SOD (315).…”

Section: G93amentioning

confidence: 99%

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Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Butterfield

Perluigi

Reed

et al. 2012

Antioxidants & Redox Signaling

156

142

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Several studies demonstrated that oxidative damage is a characteristic feature of many neurodegenerative diseases. The accumulation of oxidatively modified proteins may disrupt cellular functions by affecting protein expression, protein turnover, cell signaling, and induction of apoptosis and necrosis, suggesting that protein oxidation could have both physiological and pathological significance. For nearly two decades, our laboratory focused particular attention on studying oxidative damage of proteins and how their chemical modifications induced by reactive oxygen species/reactive nitrogen species correlate with pathology, biochemical alterations, and clinical presentations of Alzheimer's disease. This comprehensive article outlines basic knowledge of oxidative modification of proteins and lipids, followed by the principles of redox proteomics analysis, which also involve recent advances of mass spectrometry technology, and its application to selected age-related neurodegenerative diseases. Redox proteomics results obtained in different diseases and animal models thereof may provide new insights into the main mechanisms involved in the pathogenesis and progression of oxidativestress-related neurodegenerative disorders. Redox proteomics can be considered a multifaceted approach that has the potential to provide insights into the molecular mechanisms of a disease, to find disease markers, as well as to identify potential targets for drug therapy. Considering the importance of a better understanding of the cause/effect of protein dysfunction in the pathogenesis and progression of neurodegenerative disorders, this article provides an overview of the intrinsic power of the redox proteomics approach together with the most significant results obtained by our laboratory and others during almost 10 years of research on neurodegenerative disorders since we initiated the field of redox proteomics. Antioxid. Redox Signal. 17, 1610-1655.

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Section: Protein (/Lipid) Oxidation and Protein Dysfunctionmentioning

confidence: 99%

Section: G93amentioning

confidence: 99%

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Butterfield

Perluigi

Reed

et al. 2012

Antioxidants & Redox Signaling

156

142

View full text Add to dashboard Cite

show abstract

“…At high levels, however, its cytotoxicity is much increased by its reaction with superoxide anion to form peroxynitrite. 26,27 This causes oxidation of cell membrane lipids and DNA bases, thereby contributing to cell damage and injury, 26 and it has been implicated in a variety of clinical conditions, including rheumatoid arthritis, 21 atherosclerosis, 28 and adult respiratory distress syndrome. 29 NO can inactivate superoxide dismutase leading to an increased accumulation of superoxide anion, which itself can stimulate bone resorption, and also interfere with the glutathione-glutathione peroxidase system resulting in an increased production of hydrogen peroxide, a reactive oxygen species able to activate bone resorption.…”

Section: From the Royal Postgraduate Medical School London Englandmentioning

confidence: 99%

Aseptic Loosening Of Total Hip Replacement: Macrophage Expression Of Inducible Nitric Oxide Synthase And Cyclo-oxygenase-2, Together With Peroxynitrite Formation, As A Possible Mechanism For Early Prosthesis Failure

Hukkanen¹,

Corbett²,

Batten³

et al. 1997

The Journal of Bone and Joint Surgery

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Aseptic loosening is a major cause of failure of total hip arthroplasty. The adverse tissue response to prosthetic wear particles, with activation of cytokine and prostanoid production, contributes to bone loss around the implants. We have investigated the possibility that inducible nitric oxide synthase (iNOS) and cyclo-oxygenase-2 (COX-2) are expressed in macrophages in the pseudomembrane at the bone-implant interface, thereby contributing to the periprosthetic bone resorption.We also assessed whether peroxynitrite, a nitric oxide (NO)-derived oxidant associated with cellular injury, is generated in the membrane. Enzymatic activity of iNOS was measured using the arginine-citrulline assay technique and prostaglandin E 2 (PGE 2 ), as an indicator of COX-2 activity, was measured using an enzyme immunoassay.Cellular immunoreactivity for iNOS, nitrotyrosine (a marker of peroxynitrite-induced cellular injury) and COX-2 was assessed by quantitative peroxidase immunocytochemistry while immunofluorescence methods were used for subsequent co-localisation studies with CD68 + macrophages.

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“…6 One such ROS, namely NO, has major cytotoxic effects within the secondary lesion. 7 For example, peroxynitrite is a superoxide derivative of NO that has been shown to destroy proteins, lipids, and DNA. 8,9 The neurotoxic effects of NO vary according to the concentration of NO, redox conditions, cell type, and the tissue milieu.…”

Section: Introductionmentioning

confidence: 99%

Changes in nitric oxide synthase expression in young and adult rats after spinal cord injury

2007

Spinal Cord

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Objective: To examine the clinical meaning of the changes in nitric oxide synthase (NOS) expression and activity after spinal cord injury (SCI) according to the age of the experiment animal. Material and method: Ten 5-and 16-week-old Sprague-Dawley rats were laminectomized at T10 and SCI induced at this level using a New York impactor. Outcome measures to assess SCI utilized the Basso-Beatti-Bresnahan scale to quantitate hind limb motor dysfunction as a functional outcome measure. NOS isoforms (nNOS, neuronal NOS; iNOS, inducible NOS; and eNOS, endothelial NOS) were also immunolocalized in sections of control and spinal cord injury in the two sample groups using specific monoclonal antibodies. Student's t-test evaluated the difference between the young and adult rats, and Po0.05 was considered as significant value. Result: As the expression of nNOS on the spinal gray matter of the adult rat decreased, eNOS activity increased. Different from the adult rat, expression of the nNOS in the young rat was maintained until 1 day after SCI, and compared with the adult rat; eNOS activity was increased in the vessels from the damaged gray matter area after 7 days of SCI. iNOS expression was maintained until the 7th day of SCI on the adult rat, but iNOS expression after 7 days of SCI on young rat decreased. The young rat showed relatively less motor disability on the hind limb when compared with the adult rat, and had a rapid recovery. Conclusion: Neural protective eNOS activity increased after SCI in the young rat, and neural destructive iNOS expression was more remarkable in the adult rat.

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Chapter 31 Reactions of nitric oxide, superoxide and peroxynitrite with superoxide dismutase in neurodegeneration

Cited by 194 publications

References 60 publications

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Aseptic Loosening Of Total Hip Replacement: Macrophage Expression Of Inducible Nitric Oxide Synthase And Cyclo-oxygenase-2, Together With Peroxynitrite Formation, As A Possible Mechanism For Early Prosthesis Failure

Changes in nitric oxide synthase expression in young and adult rats after spinal cord injury

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