Regulation of Oxidative Imbalances in Mitochondria and Endoplasmic Reticulum | Biomedgrid

Intracellular oxidative stress has been described as a double-edged sword, at the physiological level these molecules complements cellular functioning, but excessive burden may cause damaged to cellular macromolecules and organelles [1, 2]. Notably, cells dissipate the reactive oxygen species (ROS) induced oxidative stress through arsenal of antioxidant enzymes (such as glutathione peroxidase, catalase, thioredoxin reductase and superoxide dismutase) and by redox systems (such as oxidized glutathione/ reduced glutathione (GSSG/GSH), NAD+/NADH, NADP+/NADPH) to maintain cellular homeostasis [3]. Interestingly, the oxidative imbalance in the cells are mostly generated through organelles in the process of building cellular architecture [4, 5]. For instance, the mitochondrial respiratory chain or electron transport chain (ETC) comprises of complex I to IV are the prime site for production of reactive oxygen species (ROS). The mitochondrial ETC generates superoxide anion that converts to hydrogen peroxide (H2O2) through mitochondrial dismutase and may generates highly reactive hydroxyl radical such as super oxide (O2•−) and hydroxyl radical (OH•) [5, 6]. Similarly, reactive nitrogen species (RNS) is derived from nitrogen species also known as call peroxynitrite (ONOO−) in the term of ions.