Restoration of enzymatic activity of energy related proteins in traumatically brain injured rats following the administration of gamma-glutamylcysteine ethyl ester

Presenter Hometown

Charlotte, NC

Major

Biology

Department

Biological Sciences

Degree

Graduate

Mentor

Tanea T. Reed

Mentor Department

Chemistry

Abstract

Biochemical processes such as the glycolytic pathway and Kreb’s cycle are important in producing ATP for the brain. Without a sufficient supply of glucose for energy metabolism, the brain cannot efficiently regulate or coordinate the actions and reactions of the body. The disruption of brain function resulting from an external force, such as a bump, is known as traumatic brain injury (TBI). Symptoms of TBI range from physical to psychological while effects are indicative of the severity of injury experienced. TBI is associated with reduced energy metabolism, as studies have demonstrated that protein nitration is consequential of TBI through the production of reactive oxygen/nitrogen species (ROS/RNS). Antioxidants, such as glutathione (GSH), combat the deleterious effects of oxidation by scavenging ROS/RNS, inhibiting propagation, and removing neurotoxic byproducts. Gamma-glutamylcysteine ethyl ester (GCEE) is an ethyl ester moiety of gamma-glutamylcysteine that exhibits antioxidant activity by increasing GSH production. Previous studies have demonstrated that the administration of GCEE following TBI has protective effects against protein nitration through the elevation of glutathione. This study investigates the enzymatic activity of energy related proteins that have been identified as nitrated in moderate TBI treated Wistar rats. To test the hypothesis that the elevation of GSH production upon administration of GCEE will normalize enzymatic activity post-TBI, adult male Wistar rats were equally divided 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 treated with saline or GCEE groups received 150 mg/kg of saline and GCEE, respectively. Upon sacrifice, brains were harvested and enzymatic activity was measured spectrophotometrically. Results demonstrate an increase in enzymatic activity upon GSH elevation via GCEE administration in several key enzymes, thereby indicating GCEE is a potential therapeutic strategy to restore energy related proteins in the brain post-TBI via GSH elevation.

Presentation format

Poster

Poster Number

001

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Restoration of enzymatic activity of energy related proteins in traumatically brain injured rats following the administration of gamma-glutamylcysteine ethyl ester

Biochemical processes such as the glycolytic pathway and Kreb’s cycle are important in producing ATP for the brain. Without a sufficient supply of glucose for energy metabolism, the brain cannot efficiently regulate or coordinate the actions and reactions of the body. The disruption of brain function resulting from an external force, such as a bump, is known as traumatic brain injury (TBI). Symptoms of TBI range from physical to psychological while effects are indicative of the severity of injury experienced. TBI is associated with reduced energy metabolism, as studies have demonstrated that protein nitration is consequential of TBI through the production of reactive oxygen/nitrogen species (ROS/RNS). Antioxidants, such as glutathione (GSH), combat the deleterious effects of oxidation by scavenging ROS/RNS, inhibiting propagation, and removing neurotoxic byproducts. Gamma-glutamylcysteine ethyl ester (GCEE) is an ethyl ester moiety of gamma-glutamylcysteine that exhibits antioxidant activity by increasing GSH production. Previous studies have demonstrated that the administration of GCEE following TBI has protective effects against protein nitration through the elevation of glutathione. This study investigates the enzymatic activity of energy related proteins that have been identified as nitrated in moderate TBI treated Wistar rats. To test the hypothesis that the elevation of GSH production upon administration of GCEE will normalize enzymatic activity post-TBI, adult male Wistar rats were equally divided 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 treated with saline or GCEE groups received 150 mg/kg of saline and GCEE, respectively. Upon sacrifice, brains were harvested and enzymatic activity was measured spectrophotometrically. Results demonstrate an increase in enzymatic activity upon GSH elevation via GCEE administration in several key enzymes, thereby indicating GCEE is a potential therapeutic strategy to restore energy related proteins in the brain post-TBI via GSH elevation.