Each year 1.4 million cases of traumatic brain injury (TBI) occur in the United States. Traumatic brain injury can cause serious damage to the brain due to oxidative stress. Currently, there is no treatment available to reduce this damage. Oxidative stress is caused by an imbalance of protective antioxidants and free radical oxygen and nitrogen species, which bind to proteins causing irreversible function loss. Antioxidants prevent this damage from occurring through a reversible covalent bond with the protein. The most prominently produced antioxidant in the brain is glutathione (GSH). To maintain a balance of antioxidants to free radical species, the concentration of GSH is regulated through feedback inhibition of the first step of its synthesis. This study focuses on elevating glutathione levels beyond the inhibited concentration as a therapeutic strategy for moderate TBI. A possible post-treatment that can increase GSH levels is the natural mimetic gamma-glutamylcysteine ethyl ester (GCEE). GCEE increases GSH production by bypassing the inhibited step and restarting production. To determine if the concentration of GSH is increased due to GCEE, Western Blotting and enzymatic recycling assays are utilized to directly quantify the concentration of GSH present in brain tissue samples. These methods are used to determine if TBI samples that have been treated with GCEE post-injury have an increased concentration of glutathione compared to non-injured or non-treated samples. The data collected through this study can be used to determine if GCEE is a viable post-treatment for moderate TBI.

Semester/Year of Award

Spring 5-10-2014


Tanea T. Reed

Mentor Department Affiliation


Access Options

Restricted Access Thesis

Document Type

Bachelor Thesis

Degree Name

Honors Scholars

Degree Level