Reactive oxygen species-mediated oxidative stress and DNA integrity (ROS/DNA Integrity)

Reactive oxygen species (ROS)-mediated oxidative stress and DNA integrity refers to a pathological state where an imbalance between the production of reactive oxygen species and cellular antioxidant defenses leads to oxidative damage of the genome. ROS, including superoxide and hydroxyl radicals, induce a variety of DNA lesions such as base modifications (e.g., 8-OHdG), single-strand breaks, and double-strand breaks (Sies et al., 2017; Nature Reviews Molecular Cell Biology). This process is a fundamental driver of mutagenesis and genomic instability in cancer, and it plays a central role in the loss of post-mitotic cells in neurodegenerative diseases like Alzheimer's (PubMed, 2022). While not a single molecular target, this pathway is modulated by therapeutic agents that either scavenge ROS, such as N-acetylcysteine, or target the cellular response to DNA damage, such as PARP inhibitors (Olaparib) (PubChem; NIH). Monitoring DNA integrity often relies on biomarkers like 8-hydroxy-2'-deoxyguanosine (8-OHdG) and gamma-H2AX to quantify the extent of oxidative damage and the efficacy of protective interventions (Valavanidis et al., 2009).

Other names

Oxidative DNA damageROS-induced genomic instabilityOxidative stress-mediated DNA damageRedox-induced DNA lesions

The mechanism involves the neutralization of reactive oxygen species through scavenging, the induction of endogenous antioxidant enzymes via the NRF2 pathway, or the inhibition of DNA repair proteins like PARP to prevent the resolution of oxidative DNA lesions.