Cellular oxidative balance

Cellular oxidative balance, or redox homeostasis, is the physiological state of equilibrium between the generation of reactive oxygen species (ROS) and the capacity of the cell's antioxidant defense systems to neutralize them [3, 5]. This balance is fundamental for various cellular functions, as low levels of ROS act as essential signaling molecules in processes such as cell proliferation, differentiation, and the innate immune response [10, 12]. When ROS production exceeds the antioxidant capacity, a state of oxidative stress occurs, leading to the damaging of proteins, lipids, and nucleic acids [3, 9]. Chronic disruption of this balance is a central hallmark in the pathogenesis of many diseases, including cancer, neurodegenerative disorders, and cardiovascular diseases [2, 11]. Pharmacological intervention typically focuses on restoring this balance by either enhancing endogenous antioxidant defenses—often through the Nrf2-KEAP1 pathway—or by directly scavenging radicals and inhibiting pro-oxidant enzymes [4, 7]. However, achieving therapeutic efficacy is challenging because excessive suppression of ROS can lead to 'reductive stress,' which may impair essential physiological signaling and immune defenses [11, 12].

Other names

Redox homeostasisRedox balanceCellular redox stateOxidative stress regulation

Drugs influencing cellular oxidative balance act by activating the Nrf2/KEAP1 signaling pathway to induce antioxidant enzymes, directly scavenging reactive oxygen and nitrogen species, or inhibiting enzymatic sources of ROS such as NADPH oxidase and xanthine oxidase [3, 4, 11].