Traumatic Brain Injury and Mitochondrial Dysfunction

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Presentation transcript:

Traumatic Brain Injury and Mitochondrial Dysfunction John B. Hiebert, MD, Qiuhua Shen, PhD, APRN, Amanda R. Thimmesch, BA, Janet D. Pierce, PhD The American Journal of the Medical Sciences Volume 350, Issue 2, Pages 132-138 (August 2015) DOI: 10.1097/MAJ.0000000000000506 Copyright © 2015 Southern Society for Clinical Investigation Terms and Conditions

Figure 1 An illustration superoxide to the hydroxyl radical leading to cellular damage. Included are the 2 antioxidants, glutathione and catalase. The American Journal of the Medical Sciences 2015 350, 132-138DOI: (10.1097/MAJ.0000000000000506) Copyright © 2015 Southern Society for Clinical Investigation Terms and Conditions

Figure 2 An imbalance between reactive oxygen species (ROS) and antioxidants when traumatic brain injury (TBI) occurs. This is called oxidative stress. The American Journal of the Medical Sciences 2015 350, 132-138DOI: (10.1097/MAJ.0000000000000506) Copyright © 2015 Southern Society for Clinical Investigation Terms and Conditions

Figure 3 Traumatic brain injury (TBI) affects the mitochondrial neuron and damages the supercomplexes within the electron transport chain. The American Journal of the Medical Sciences 2015 350, 132-138DOI: (10.1097/MAJ.0000000000000506) Copyright © 2015 Southern Society for Clinical Investigation Terms and Conditions

Figure 4 The pathophysiologic sequence of traumatic brain injury (TBI) damaging the electron transport chain resulting in reactive oxygen species and subsequent apoptosis and necrosis. The American Journal of the Medical Sciences 2015 350, 132-138DOI: (10.1097/MAJ.0000000000000506) Copyright © 2015 Southern Society for Clinical Investigation Terms and Conditions