1. Oxidative stress and mitochondrial dysfunction in sepsis
H.F. Galley 
British Journal of Anaesthesia 
Volume 107, Issue 1, Pages (July 2011)
DOI: /bja/aer093
Copyright © 2011 The Author(s) Terms and Conditions

2. Fig 1
Schematic diagram showing the sources of electrons in the electron transport chain of mitochondria (indicated by a red star). The proton flux is denoted by H+. CoQ, coenzyme Q10 (ubiquinone); Cyt c, cytochrome c. See the text for other abbreviations.
British Journal of Anaesthesia  , 57-64DOI: ( /bja/aer093)
Copyright © 2011 The Author(s) Terms and Conditions

3. Fig 2
Overview of mitochondrial ROS production. ROS production within mitochondria can lead to oxidative damage to mitochondrial proteins, membranes, and mtDNA. Mitochondrial oxidative damage leads to the release of cytochrome c (cyt c) into the cytosol resulting in apoptosis. Increased permeability makes the inner membrane permeable to small molecules. Mitochondrial ROS are also important in cell signalling pathways which modulate several cellular functions. Figure reproduced with permission, from Murphy MP (2009).2 © The Biochemical Society.
British Journal of Anaesthesia  , 57-64DOI: ( /bja/aer093)
Copyright © 2011 The Author(s) Terms and Conditions

4. Fig 3
Antioxidants conjugated to the lipophilic cation TPP, accumulate specifically within mitochondria, and block mitochondrial oxidative damage and redox cell signalling. Antioxidants which have been attached to TPP include co-enzyme Q10 (ubiquinone) to form MitoQ and α-tocopherol to form MitoVitE.
British Journal of Anaesthesia  , 57-64DOI: ( /bja/aer093)
Copyright © 2011 The Author(s) Terms and Conditions