Date of Award

January 2016

Degree Type

Open Access Thesis

Document Type

Master Thesis

Degree Name

Master of Science (MS)

Department

Biological Sciences

First Advisor

Tanea T. Reed

Department Affiliation

Biological Sciences

Second Advisor

Lindsay E. Calderon

Department Affiliation

Biological Sciences

Third Advisor

Marcia M. Pierce

Department Affiliation

Biological Sciences

Abstract

The brain is one of the most important organs in the body. It functions as a control center by regulating and coordinating actions and reactions, which is facilitated via signal transduction pathways. Its function is primarily dependent upon sufficient supply of glucose for energy metabolism. The dysfunction of the brain resulting from an external force is known as traumatic brain injury (TBI). Symptoms range from physical to psychological and effects can be mild, moderate, or severe depending on the extent of injury. TBI is associated with oxidative damage, the overproduction of reactive oxygen/nitrogen species. Reduced energy metabolism is a consequence of traumatic brain injury, while reduced purine salvage is associated with deficient cell signaling. Previous studies have demonstrated that the administration of gamma-glutamylcysteine ethyl ester (GCEE) following TBI has protective effects against protein nitration. This study investigates the enzymatic activity of energy related and salvage related enzymes, glyceraldehyde-3-phosphate dehydrogenase, pyruvate kinase, lactate dehydrogenase, aspartate aminotransferase, malate dehydrogenase, cytochrome C oxidase, ATP synthase, and hypoxanthine-guanine phosphoribosyltransferase, that have been identified as excessively nitrated following the administration of GCEE post-TBI. Adult male Wistar rats were divided equally into three groups: sham, saline, and GCEE. Rats in all groups (except sham) were subjected to a craniotomy and a moderate TBI via cortical contusion. Post-TBI rats in the saline group received an administration of saline (150mg/kg), and rats in the GCEE treatment group received an administration of GCEE (same dosage). Upon sacrifice, brains were harvested and enzymatic activity was indirectly measured spectrophotometrically. Data demonstrates that the administration of GCEE following brain trauma increases enzymatic activity. Our results are promising and indicate potential therapeutic strategies to restore energy and salvage related enzymatic activity in the brain post-TBI.

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