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.
","abstract_html":"<p>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. </p>","abstract_has_math":false,"creators":["Rice, Brittany"],"institution":"Eastern Kentucky University","degree_name":"Master of Science (MS)","degree_level":"Master's","degree_discipline":"Biological Sciences","degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2016,"date_issued":"2016-01-01T08:00:00Z","date_published":"2016-01-01T08:00:00Z","updated_at":"2026-07-24T02:15:39Z","subjects":["GCEE","TBI","Biochemistry","Neuroscience and Neurobiology"],"languages":[],"rights":["Copyright 2016 Brittany Rice"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://encompass.eku.edu/etd/417","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Rice, Brittany"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:publisher","label":"Institution","values":["Encompass Digital Archive, Eastern Kentucky University"]},{"key":"dc:type","label":"Dc Type","values":["Master Thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biological Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Master's"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science (MS)"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["Eastern Kentucky University"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["GCEE","TBI","Biochemistry","Neuroscience and Neurobiology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["Copyright 2016 Brittany Rice"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://encompass.eku.edu/etd/417"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["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.
"]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:source","label":"Dc Source","values":["Encompass Digital Archive: Online Theses and Dissertations"]},{"key":"dc:title","label":"Title","values":["Enzyme Analysis of Oxidatively Modified Proteins Post-TBI"]}]}],"canonical_facts":{"dc:creator":["Rice, Brittany"],"dc:description.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.
"],"dc:format":["application/pdf"],"dc:identifier":["https://encompass.eku.edu/etd/417"],"dc:publisher":["Encompass Digital Archive, Eastern Kentucky University"],"dc:rights":["Copyright 2016 Brittany Rice"],"dc:source":["Encompass Digital Archive: Online Theses and Dissertations"],"dc:subject":["GCEE","TBI","Biochemistry","Neuroscience and Neurobiology"],"dc:title":["Enzyme Analysis of Oxidatively Modified Proteins Post-TBI"],"dc:type":["Master Thesis"],"thesis:degree_discipline":["Biological Sciences"],"thesis:degree_level":["Master's"],"thesis:degree_name":["Master of Science (MS)"],"thesis:institution_name":["Eastern Kentucky University"]},"updated_at":"2026-07-24T02:15:39Z"}