Reactive oxygen species and cellular redox system (ROS/Redox system)

Reactive oxygen species (ROS) and the cellular redox system encompass a complex network of oxygen-derived molecules and the enzymatic and non-enzymatic mechanisms that regulate their levels. ROS, including superoxide and hydrogen peroxide, are generated primarily as byproducts of mitochondrial respiration and by specialized enzymes like NADPH oxidases [1]. At physiological levels, ROS function as essential signaling molecules that regulate cell growth, differentiation, and immune responses [2]. However, an imbalance between ROS production and antioxidant defense leads to oxidative stress, causing oxidative damage to DNA, lipids, and proteins [3]. This dysregulation is a hallmark of numerous pathologies, including cancer, neurodegenerative disorders like Alzheimer's, and cardiovascular diseases [4]. Pharmacological intervention typically targets specific components of this system, such as activating the Nrf2-Keap1 pathway to boost antioxidant gene expression or using small-molecule scavengers to neutralize excess radicals [3][5]. Sources: [1] Sies, H., & Jones, D. P. (2020). Nature Reviews Molecular Cell Biology; [2] Pizzino, G., et al. (2017). Oxidative Medicine and Cellular Longevity; [3] Forman, H. J., & Zhang, H. (2021). Nature Reviews Drug Discovery; [4] Di Meo, S., et al. (2016). Journal of Physiology and Biochemistry; [5] Hayes, J. D., & Dinkova-Kostova, A. T. (2014). Trends in Biochemical Sciences.

Other names

Reactive oxygen speciesRedox homeostasisOxidative stress systemAntioxidant defense systemCellular redox state

Modulation of the redox balance occurs through direct scavenging of reactive species, induction of endogenous antioxidant enzymes via the Nrf2-Keap1 signaling pathway, or the inhibition of ROS-generating enzymes such as NADPH oxidase and xanthine oxidase [3][5].