Oxidative stress is a state of redox imbalance in various diseases caused by increased reactive oxygen species (ROS)(Bansal et al. 2014). ROS are metabolic products which originate from different cells but are best associated with mitochondrial metabolism (Alfadda and Sallam 2012). In normal conditions, the final oxygen electron receptor reduces down to water in the mitochondria, however, under pathological conditions, the electrons leak out of the electron transport chain system and generates ROS (Turrens 2003). During times of environmental stress, these ROS levels can increase dramatically. While it is known that lower concentrations of ROS have effects through regulation of cell signaling cascades like redox signaling from the organelle to the rest of the cell, prolonged exposure of increased ROS concentrations may lead to injury to proteins, lipids, and nucleic acids (Brieger et al. 2012; Chung et al. 2006). This augmented ROS production then contributes to mitochondrial damage in a range of pathologies (Chung et al. 2006). Mitochondrial dysfunction results in oxidative stress and inflammatory response, underlying factors in a variety of diseases including acute lung injury, pulmonary fibrosis, neurodegenerative diseases, diabetes, cardiovascular diseases, and cancer (Bandyopadhyay et al. 2013; Bansal et al. 2014; Namsolleck and Unger 2014).

In addition to the well-established role of the mitochondria in energy metabolism, regulation of cell death has recently emerged as a second major function of these organelles. This seems to be intimately linked to the role of mitochondria as the major intracellular source of ROS, which are mainly generated at complex I and III of the respiratory chain (Cogliati et al. 2013). Excessive ROS production can lead to oxidation of macromolecules and has been implicated in mtDNA mutations, ageing, and cell death (Semenzato and Scorrano 2014). Although mitochondrial dysfunction can cause ATP depletion and necrosis, these organelles are also involved in the regulation of apoptotic cell death by mechanisms which have been conserved through evolution. Thus, many lethal agents target the mitochondria and cause release of cytochrome c and other pro-apoptotic proteins, which can trigger caspase activation and apoptosis (Semenzato and Scorrano 2014).