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.
Keywords: 3-Nitrotyrosine (3-NT); Nitrosative stress; Protein nitration; Reactive nitrogen species (RNS); Traumatic brain injury (TBI).
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