Cellular reactive oxygen species homeostasis (ROS homeostasis)

Cellular reactive oxygen species (ROS) homeostasis is the physiological process of maintaining a dynamic balance between the generation of ROS and their neutralization by antioxidant defense systems (Chen et al., 2025). ROS, including superoxide anions and hydrogen peroxide, are primarily produced as byproducts of mitochondrial oxidative phosphorylation and serve as vital secondary messengers in signaling pathways that regulate cell growth, differentiation, and immune responses (Steven et al., 2022). When this balance is disrupted, the resulting oxidative stress leads to cumulative damage to DNA, proteins, and lipids, which is a hallmark of aging and various chronic diseases such as cancer and neurodegeneration (Marrocco et al., 2017). Therapeutic strategies targeting ROS homeostasis aim to either bolster antioxidant defenses using Nrf2 activators or direct scavengers, or conversely, to induce lethal ROS levels in cancer cells to trigger selective apoptosis (Chen et al., 2025). However, because ROS are essential for normal physiological signaling, non-specific modulation can lead to significant toxicity or the "antioxidant paradox," where supplementation fails to provide therapeutic benefit or potentially increases mortality (Steven et al., 2022).

Other names

Redox homeostasisOxidative stress regulationROS balanceCellular redox stateOxidative equilibrium

Modulation of ROS levels through direct scavenging of free radicals, activation of the Nrf2-mediated antioxidant response element (ARE) pathway to induce endogenous enzymes, or inhibition of ROS-generating enzymes such as NADPH oxidases (NOX) and xanthine oxidase.