Cellular reactive oxygen species and antioxidant systems (ROS/Antioxidant System)

Cellular reactive oxygen species (ROS) and antioxidant systems constitute a fundamental biological framework responsible for maintaining redox homeostasis (Sies et al., 2017, Nature Reviews Molecular Cell Biology). ROS, such as superoxide and hydrogen peroxide, are generated primarily as byproducts of mitochondrial respiration and by specialized enzymes like NADPH oxidases (Lambeth, 2004, Nature Reviews Immunology). While they function as essential secondary messengers in signal transduction and immune defense, their overproduction leads to oxidative stress, causing damage to DNA, proteins, and lipids (Ray et al., 2012, Cell Signaling). The antioxidant system, which includes enzymes like superoxide dismutase (SOD), catalase, and the glutathione system, works to neutralize these reactive species (Halliwell & Gutteridge, 2015, Oxford University Press). Dysregulation of this balance is a hallmark of various pathologies, including cancer, neurodegenerative disorders, and cardiovascular disease (Forman & Zhang, 2021, Nature Reviews Drug Discovery). Therapeutic strategies often focus on enhancing antioxidant capacity or inhibiting specific ROS sources, though clinical success has been limited by the complexity of redox signaling and the potential for unintended interference with normal cellular functions (Gutteridge & Halliwell, 2018, Free Radical Biology and Medicine). Consequently, this system is viewed more as a complex pathway of multiple targets rather than a single therapeutic entity.

Other names

Oxidative stress pathwayRedox signaling networkROS scavenging systemCellular redox homeostasis

Pharmacological modulation involves direct scavenging of free radicals, inhibition of ROS-producing enzymes (e.g., NOX inhibitors), or induction of endogenous antioxidant gene expression via the Nrf2-Keap1 pathway.