Purpose: The aims of this study are to establish a time point to determine the most beneficial time to administer GCEE post incident to reduce oxidative damage and second, by using redox proteomics, to determine if GCEE can readily suppress 3-NT modification in TBI animals. Experimental design: By using a moderate traumatic brain injury model with Wistar rats, it is hypothesized that the role of 3-nitrotyrosine (3-NT) formation as an intermediate will predict the involvement of protein nitration/nitrosation and oxidative damage in the brain. Results: In this experiment, the levels of protein carbonyls, 4-hydroxynonenal, and 3-nitrotyrosine were significantly elevated in TBI injured, saline treated rats compared with those who sustained an injury and were treated with 150 mg/kg of the glutathione mimetic, GCEE. Conclusion and clinical relevance: Determining the existence of elevated 3-NT levels provides insight into the relationship between the protein nitration/nitrosation and the oxidative damage, which can determine the pathogenesis and progression of specific neurological diseases.
|Number of pages||7|
|Journal||Proteomics - Clinical Applications|
|State||Published - Dec 1 2016|
Bibliographical noteFunding Information:
This work was funded by the National Institute for Neurological Disorders and Stroke grant (1R15NS072870-01A1).
© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
- 3-Nitrotyrosine (3–NT)
- Nitrosative stress
- Protein nitration
- Reactive nitrogen species (RNS)
- Traumatic brain injury (TBI)
ASJC Scopus subject areas
- Clinical Biochemistry