Oxidative stress and antioxidant defense systems

Oxidative stress and antioxidant defense systems represent the complex biochemical network responsible for maintaining cellular redox homeostasis. Oxidative stress arises from an imbalance where the production of reactive oxygen species (ROS) overwhelms the cellular antioxidant capacity, leading to oxidative damage of proteins, lipids, and nucleic acids (Sies et al., 2017, Nature Reviews Molecular Cell Biology). The defense system includes enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), alongside non-enzymatic molecules like glutathione and vitamins C and E (Halliwell & Gutteridge, 2015, Free Radicals in Biology and Medicine). This system plays a dual role: while excessive ROS drive the progression of diseases like Alzheimer's, atherosclerosis, and cancer, basal ROS levels are essential for intracellular signaling and immune function (Finkel, 2011, Nature). Pharmacological intervention often targets the Nrf2 (Nuclear factor erythroid 2-related factor 2) pathway to upregulate endogenous defenses or utilizes direct-acting scavengers to mitigate tissue damage (He et al., 2020, Signal Transduction and Targeted Therapy). Understanding the balance within this system is crucial for developing therapies that mitigate damage without disrupting vital physiological signaling.

Other names

Redox homeostasisAntioxidant defense systemOxidative stress responseCellular redox system

Mechanisms include the direct scavenging of reactive oxygen species (ROS), activation of the Nrf2-KEAP1 signaling pathway to induce phase II antioxidant enzymes, replenishment of endogenous thiol pools such as glutathione, and inhibition of ROS-generating enzymes like NADPH oxidase or xanthine oxidase.