DNA oxidative damage (null)

DNA oxidative damage refers to a spectrum of chemical modifications to DNA bases and the sugar-phosphate backbone, primarily induced by reactive oxygen species such as hydroxyl radicals, superoxide, and hydrogen peroxide[2][7]. The most common lesions include 8-oxoguanine, base modifications, single- and double-strand breaks, and DNA-protein crosslinks[1][7]. These lesions threaten genome stability and, when not properly repaired (chiefly by base excision repair mechanisms), can lead to mutagenesis, genomic instability, cell death, or disease states including cancer, neurodegenerative disorders, and aging[1][2][3][4][7]. DNA oxidative damage is a hallmark of both endogenous metabolic stress and exogenous insults (e.g., ionizing radiation, toxins), and is often studied as a biomarker of cellular stress or pathogenesis, not as a direct therapeutic target[1][2]. Summary: "DNA oxidative damage" should not be catalogued as a canonical drug target; it is a lesion/process with many upstream effectors (ROS) and downstream consequences but is not itself a receptor, protein, or enzyme. If pursuing drug discovery or pathway analysis, the appropriate targets are DNA repair enzymes such as 8-oxoguanine DNA glycosylase (OGG1), MUTYH, or signaling proteins like ATM, all of which directly interact with or repair oxidative DNA lesions[4].

Other names

Oxidative DNA damageOxidatively induced DNA lesionsROS-induced DNA damageDNA oxidation8-oxoguanine lesions

Drugs can reduce oxidative DNA damage by scavenging ROS (antioxidants); Some treatments increase DNA oxidative damage to trigger cancer cell death (radiation/chemotherapy); PARP inhibitors modulate DNA repair after oxidative lesions; OGG1 modulators alter repair of oxidized bases such as 8-oxoguanine