Differential Expression of Oxidized Proteins in Moderate TBI
Grade Level at Time of Presentation
Junior
Major
Chemistry
Minor
N/A
Institution
Eastern Kentucky University
KY House District #
74
KY Senate District #
28
Faculty Advisor/ Mentor
Dr. Tanea T. Reed
Department
Chemistry Dept.
Abstract
Traumatic brain injuries (TBI) are the result of injuries to the brain that lead to primary and secondary injuries. Primary injuries include the initial force causing damage to the brain and secondary injuries consist of chemical cascades as a result of primary injury. Secondary injuries produce reactive oxygen species ultimately causing oxidative damage in the brain. Protein carbonyls are an indicator of oxidative damage and are used to measure the level of oxidative damage and efficacy of treatment. Gamma-glutamylcysteine ethyl ester (GCEE), a moiety of gamma-glutamylcysteine, can upregulate glutathione in the brain and reduce protein carbonyl levels. Glutathione has shown to be a strong antioxidant that can reduce oxidative stress in the brain. Oxidative stress is created through the imbalance of reactive oxygen species and antioxidants resulting in damaged brain tissue. The purpose of this study was to determine if GCEE is a suitable treatment in reducing oxidative damage caused by TBI. GCEE was administered sixty minutes post-injury to determine if brain damage was reduced at this time point. A proteomic approach was used to investigate specific proteins that underwent differential expression in tissue samples, while slot blot analyzed the levels of protein carbonyls. Results using these techniques demonstrated significant differences between control and saline treatments with promising results from GCEE treatment. Annually, there are 10 million cases of TBI in the world with no cure or successful treatment to prevent or reverse subsequent secondary damage. Results from this project could lead to more effective treatments for traumatic brain injury.
Differential Expression of Oxidized Proteins in Moderate TBI
Traumatic brain injuries (TBI) are the result of injuries to the brain that lead to primary and secondary injuries. Primary injuries include the initial force causing damage to the brain and secondary injuries consist of chemical cascades as a result of primary injury. Secondary injuries produce reactive oxygen species ultimately causing oxidative damage in the brain. Protein carbonyls are an indicator of oxidative damage and are used to measure the level of oxidative damage and efficacy of treatment. Gamma-glutamylcysteine ethyl ester (GCEE), a moiety of gamma-glutamylcysteine, can upregulate glutathione in the brain and reduce protein carbonyl levels. Glutathione has shown to be a strong antioxidant that can reduce oxidative stress in the brain. Oxidative stress is created through the imbalance of reactive oxygen species and antioxidants resulting in damaged brain tissue. The purpose of this study was to determine if GCEE is a suitable treatment in reducing oxidative damage caused by TBI. GCEE was administered sixty minutes post-injury to determine if brain damage was reduced at this time point. A proteomic approach was used to investigate specific proteins that underwent differential expression in tissue samples, while slot blot analyzed the levels of protein carbonyls. Results using these techniques demonstrated significant differences between control and saline treatments with promising results from GCEE treatment. Annually, there are 10 million cases of TBI in the world with no cure or successful treatment to prevent or reverse subsequent secondary damage. Results from this project could lead to more effective treatments for traumatic brain injury.