A review on regulation of autophagy by ROS (Reactive Oxygen Species)

ROS (Reactive Oxygen Species) are small, short-lived and highly reactive molecules that can oxidize proteins, lipids and DNA. ROS are formed by incomplete one-electron reduction of oxygen. ROS include oxygen anions, free radicals, including superoxide and hydroxyl radicals, and peroxides such as hydrogen peroxide (H2O2). Autophagy is a catabolic pathway for degradation of intracellular proteins and organelles via the lysosome. Autophagy is activated under stress conditions such as starvation, ischemia/reperfusion and pathogen infection, and is deregulated in various pathological conditions, including cancer and neurodegenerative diseases. It is generally accepted that ROS induce autophagy, and that autophagy, in turn, serves to reduce oxidative damage. Cells have developed various non-enzymatic and enzymatic antioxidizing agents to detoxify ROS and prevent oxidative stress. These include glutathione, thioredoxin, superopxide dismutase (SOD), catalase and peroxidases. ROS produced by damaged mitochondria might induce mitophagy, which in turn eliminates the damaged organelles. Two pathologies highly associated with the accumulation of ROS are cancer and ischemia/reperfusion. The role of mitochondria as ROS generators, essential for the activation of autophagy. Autophagy is a survival mechanism in response to ROS. Removal of damaged mitochondria and oxidized proteins, in most cases, supports survival.