Eastern Kentucky University

Study 1 (Johnson, Henderson, Sellers, & Williams): Analysis of Antioxidant Enzymes in Wistar Rats with a Moderate Traumatic Brain Injury: A Dosage Dependent Approach

Institution

Eastern Kentucky University

Abstract

Imbalances in the production of ROS and native antioxidant mechanisms have been shown to increase oxidative stress. Glutathione peroxidase (GPx) is the central enzyme used for reduction of peroxides in the brain through the catalyzed reaction with reduced glutathione. Oxidized glutathione is then reduced to allow further protection against oxidative stress via the oxidation of β-nicotinamide adenine dinucleotide phosphate (β-NADPH) by glutathione reductase (GR). GCEE was administered using a dosage dependent approach, and the significance of each dose was determined by examining the activity of GPx and GR in the brain samples. Each sample was treated with 150 mg/kg of body weight of GCEE or saline at a time interval of 30 or 60 minutes post injury. Using spectrometric analysis, brain samples treated with GCEE had an increase in the activity GPx and GR compared to those treated with saline. The increased activity of these enzymes correlates with elevated antioxidant capacity and lowers overall oxidative stress making this a potential post therapeutic strategy for moderate TBI.

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Study 1 (Johnson, Henderson, Sellers, & Williams): Analysis of Antioxidant Enzymes in Wistar Rats with a Moderate Traumatic Brain Injury: A Dosage Dependent Approach

Imbalances in the production of ROS and native antioxidant mechanisms have been shown to increase oxidative stress. Glutathione peroxidase (GPx) is the central enzyme used for reduction of peroxides in the brain through the catalyzed reaction with reduced glutathione. Oxidized glutathione is then reduced to allow further protection against oxidative stress via the oxidation of β-nicotinamide adenine dinucleotide phosphate (β-NADPH) by glutathione reductase (GR). GCEE was administered using a dosage dependent approach, and the significance of each dose was determined by examining the activity of GPx and GR in the brain samples. Each sample was treated with 150 mg/kg of body weight of GCEE or saline at a time interval of 30 or 60 minutes post injury. Using spectrometric analysis, brain samples treated with GCEE had an increase in the activity GPx and GR compared to those treated with saline. The increased activity of these enzymes correlates with elevated antioxidant capacity and lowers overall oxidative stress making this a potential post therapeutic strategy for moderate TBI.