Multiple disorders are linked to overproduction of reactive oxygen species (ROS) that form as side-products of normal cell respiration in mitochondria. The relationship between ROS and mitochondria suggests association between pathology causing mechanisms. Defects in oxidative phosphorylation have been shown to elevate ROS levels, whereas ROS-induced deleterious effects on organic matter can directly compromise the function of the electron transport components. This paper will present the molecular mechanisms of ROS production, as well as the existing evidence of mitochondrial ROS involvement in Alzheimer's disease (AD).
Oxygen is damaging to aerobic organisms at levels higher than are found in the atmosphere. Frank (1985) found that the deleterious effects are caused by reactive oxygen species (ROS) free radical formation after intracellular oxygen reduction (as cited in Lagouge & Larrson, 2013). Free radicals are inorganic molecules that have unpaired or odd number of electrons (Brand et al. 2004; Turrens, 2003). The most common ROS found in biological systems are hydrogen peroxide (H2O2), superoxide anion (O2 -), and hydroxyl radical ( ·OH). .
According to Forman and Torres (2002), free radicals can protect from disease causing agents (pathogens), however they also assist in monitoring of glucose metabolism, cell growth and division, as proposed by Rhee (1999) (found in Kumar et al. 2012). The control of ROS levels is of high importance for normal functioning of organisms, as impairment of free radical signalling might lead to the activation of dangerous enzymatic cascades and stimulation of different pathologies, for example, cardiovascular diseases, inflammation, cancer, and ageing (Afanas'ev, 2010).The main place of radical synthesis is mitochondria (Mt) the eukaryotic ˜power house' that produces adenosine triphosphate (ATP) and allows the cells to carry out all of their functions (Figge et al.