Cellular redox systems and reactive oxygen species (ROS) generation (ROS/Redox systems)

Cellular redox systems and reactive oxygen species (ROS) generation refer to the integrated network of enzymes and molecules that regulate the production and neutralization of oxygen-derived free radicals. ROS, such as superoxide and hydrogen peroxide, are generated primarily through mitochondrial oxidative phosphorylation and the activity of NADPH oxidases (NOX) (Sies & Jones, 2020, Nature Reviews Molecular Cell Biology). While physiological levels of ROS are critical for cell signaling and immune defense, an imbalance—termed oxidative stress—leads to the degradation of cellular components and is implicated in the pathogenesis of cancer, cardiovascular diseases, and neurodegeneration (NIH, National Cancer Institute). Pharmacological intervention in these systems typically involves either the use of antioxidants to prevent tissue damage or pro-oxidant agents, such as arsenic trioxide, to induce apoptosis in malignant cells (PubChem). However, targeting these systems is challenging due to the "antioxidant paradox," where reducing ROS may inadvertently promote the survival of certain cancer cells or disrupt essential redox-sensitive signaling pathways (Hallmark et al., 2015, Antioxidants & Redox Signaling). Key components of these systems include enzymes like superoxide dismutase, catalase, and the glutathione system, as well as the Nrf2 transcription factor which coordinates the antioxidant response. Therapeutic development often focuses on specific nodes within this network to achieve selectivity and minimize off-target effects. Monitoring efficacy often involves measuring secondary products of oxidative damage, such as malondialdehyde or 8-hydroxy-2'-deoxyguanosine.

Other names

Redox homeostasisOxidative stress pathwayROS signalingAntioxidant defense system

Modulation of cellular oxidative state through the inhibition or activation of ROS-producing enzymes, scavenging of reactive species, or induction of endogenous antioxidant defense pathways.