Traumatic brain injury (TBI) is damage that occurs suddenly to the brain that can become permanent. During the primary injury, the initial external force encountering the brain and secondary injury, the biochemical cascade that can occur up to months after the primary injury. Oxidative damage is a result of TBI that is referred to as an imbalance of reactive oxygen species (ROS) and antioxidants. Protein carbonyls can be used as a biological marker for oxidative damage to the brain. As the levels of ROS increase during oxidative stress, apoptosis occurs in excess, cell communication is inhibited, and proteins and lipids are altered from their native conformations. Gamma-glutamylcysteine ethyl ester (GCEE), a glutathione (GSH) mimetic, is an antioxidant that occurs naturally in the brain. Glutathione can counteract the increased levels of ROS in brain. GCEE may be used as a potential therapy for TBI due to its ability to upregulate GSH in brain. This work investigates protein carbonylation levels after administration of GCEE 30 minutes post injury in moderate TBI rats. Slot blot and 2D gel electrophoresis were used to obtain results. Slot blot analysis, an immunochemical tool, yielded overall protein carbonylation while 2D gel electrophoresis identified specific protein spots. Our findings showed a significant difference in the number of proteins expressed between all three groups (sham, saline, and GCEE treatment). These results provide evidence that GCEE treatment reduces protein carbonylation to create a more homeostatic state in the brain and prevent further oxidative damage.

Semester/Year of Award

Fall 12-11-2017


Tanea T. Reed

Department/Professional Affiliation


Access Options

Restricted Access Dissertation

Degree Name

Honors Scholars