Intracellular reactive oxygen species homeostasis (ROS homeostasis) (ROS homeostasis)

Intracellular reactive oxygen species (ROS) homeostasis is the physiological process of maintaining a dynamic equilibrium between the generation of reactive oxygen species and their elimination by endogenous antioxidant systems [5, 9]. ROS, such as superoxide and hydrogen peroxide, are primarily produced as byproducts of mitochondrial respiration and by specialized enzymes like NADPH oxidases [2, 7]. At physiological levels, these molecules act as essential secondary messengers in signal transduction pathways that regulate cell growth, differentiation, and immune responses [1, 8]. However, a disruption in this balance leads to oxidative stress, causing cumulative damage to cellular macromolecules and contributing to the pathogenesis of cancer, neurodegeneration, and cardiovascular disease [12, 13]. Pharmacological intervention typically involves either the use of antioxidants and Nrf2 activators to restore balance in chronic inflammatory conditions or the administration of pro-oxidants to selectively kill cancer cells by exceeding their ROS threshold [3, 10]. Achieving therapeutic efficacy remains challenging due to the dual nature of ROS and the difficulty of targeting specific redox environments without disrupting normal cellular signaling [6, 11].

Other names

Redox homeostasisCellular redox balanceROS regulationOxidative stress managementIntracellular redox state

The modulation of intracellular ROS homeostasis involves several mechanisms: direct scavenging of free radicals by antioxidants, activation of the Nrf2-Keap1 pathway to upregulate endogenous antioxidant enzymes, inhibition of ROS-generating enzymes such as NADPH oxidases (NOX), and the induction of ROS to toxic levels (pro-oxidant therapy) to trigger apoptosis in cancer cells [3, 7, 10].