Eastern Kentucky University

Poster Title

The Effects of Gamma-glutatmylcystein Ethyl Ester on Glutathione Elevation as a Post Treatment to Moderate Traumatic Brain Injury

Institution

Eastern Kentucky University

Abstract

A moderate traumatic brain injury causes irreversible protein damage due to oxidative stress. Oxidative stress is caused by an imbalance between harmful free radical species and protective antioxidants, the most prominent being glutathione (GSH). The GSH protects proteins from irreversible damage through a reversible protein modification. This covalent modification is reversed once the concentration of free radical species is below the toxic threshold. The GSH is produced through a recycling assay that is halted by feedback inhibition. In the event of an injury, gamma-glutamylcysteine ethyl ester (GCEE) is being studied as a possible post-treatment to prevent inhibition and increase the production of GSH. This study focuses on enzymatic recycling assays and Western Blotting as a means to quantify the amount of GSH present in brain tissue samples that have a moderate traumatic brain injury. These methods have determined the concentration and protein protection of GSH in samples treated with GCEE were greater than that of a non-injured or non-treated sample. The information from this study can be used as a means to assess the viability of GCEE as a post-injury treatment for moderate traumatic brain injury.

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The Effects of Gamma-glutatmylcystein Ethyl Ester on Glutathione Elevation as a Post Treatment to Moderate Traumatic Brain Injury

A moderate traumatic brain injury causes irreversible protein damage due to oxidative stress. Oxidative stress is caused by an imbalance between harmful free radical species and protective antioxidants, the most prominent being glutathione (GSH). The GSH protects proteins from irreversible damage through a reversible protein modification. This covalent modification is reversed once the concentration of free radical species is below the toxic threshold. The GSH is produced through a recycling assay that is halted by feedback inhibition. In the event of an injury, gamma-glutamylcysteine ethyl ester (GCEE) is being studied as a possible post-treatment to prevent inhibition and increase the production of GSH. This study focuses on enzymatic recycling assays and Western Blotting as a means to quantify the amount of GSH present in brain tissue samples that have a moderate traumatic brain injury. These methods have determined the concentration and protein protection of GSH in samples treated with GCEE were greater than that of a non-injured or non-treated sample. The information from this study can be used as a means to assess the viability of GCEE as a post-injury treatment for moderate traumatic brain injury.