This article is part of a series on Translational Research, edited by Dr John Kellum.

Review

Bench-to-bedside review: Mitochondrial injury, oxidative stress and apoptosis – there is nothing more practical than a good theory

Hülya Bayir^1,2 and Valerian E Kagan²

¹Safar Center for Resuscitation Research, Department of Critical Care Medicine, School of Medicine, University of Pittsburgh, PA, USA

²Center for Free Radical and Antioxidant Health, Department of Environmental and Occupational Health, School of Public Health, University of Pittsburgh, PA, USA

author email corresponding author email

Critical Care 2008, 12:206doi:10.1186/cc6779

Published:	18 February 2008

Abstract

Apoptosis contributes to cell death in common intensive care unit disorders such as traumatic brain injury and sepsis. Recent evidence suggests that this form of cell death is both clinically relevant and a potential therapeutic target in critical illness. Mitochondrial reactive oxygen species (ROS) have become a target for drug discovery in recent years since their production is characteristic of early stages of apoptosis. Among many antioxidant agents, stable nitroxide radicals targeted to mitochondria have attracted attention due to their ability to combine electron and free radical scavenging action with recycling capacities. Specific mechanisms of enhanced ROS generation in mitochondria and their translation into apoptotic signals are not well understood. This review focuses on several contemporary aspects of oxidative stress-mediated mitochondrial injury, particularly as they relate to oxidation of lipids and their specific signaling roles in apoptosis and phagocytosis of apoptotic cells.