Abstract
Protein oxidation and nitration have been described during spinal cord injury (SCI) in animal models. Herein, mass spectrometry unambiguously identified GDP-dissociation inhibitor-2 (GDI-2) in SCI with post-translational modifications of 3-aminotyrosine (8 h post-injury) and an acrolein adduct of GDI-2 (72 h post-injury). On the basis of mass spectrometry evidence, we conclude that lipid-peroxidation and protein nitration do take place on an important signalling protein that may be prevented by specific experimental therapeutic interventions.
MeSH terms
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Acrolein / analysis
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Amino Acid Sequence
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Animals
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Guanine Nucleotide Dissociation Inhibitors / chemistry
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Guanine Nucleotide Dissociation Inhibitors / metabolism*
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Lipid Peroxidation
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Male
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Molecular Sequence Data
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Nitric Oxide / metabolism*
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Oxidation-Reduction
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Oxidative Stress*
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Protein Processing, Post-Translational*
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Rats
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Rats, Sprague-Dawley
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Reactive Oxygen Species / metabolism*
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Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
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Spinal Cord Injuries / metabolism*
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Tyrosine / analogs & derivatives
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Tyrosine / analysis
Substances
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Gdi2 protein, rat
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Guanine Nucleotide Dissociation Inhibitors
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Reactive Oxygen Species
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3-aminotyrosine
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Nitric Oxide
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Tyrosine
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Acrolein