Sepsis related organ dysfunction remains the most common cause of death on the intensive care unit despite advances in healthcare and science. Oxidative stress has been consistently reported in patients with sepsis and is thought to result in mitochondrial dysfunction which may contribute to organ failure. Normally a complex system of interacting antioxidant defences are able to combat oxidative stress and prevent damage to mitochondria. Protection of mitochondrial function with antioxidants can reduce organ damage, inflammation and mitochondrial damage in models of sepsis. We are investigating the ways in which novel compounds can regulate inflammation and mitochondrial function using cellular models mimicking conditions seen during sepsis.