Cellular DNA (radiotherapy-induced species) (DNA)

Cellular DNA is the primary biological target of ionizing radiation used in cancer radiotherapy. Radiation induces a variety of lesions, including single-strand breaks (SSBs), double-strand breaks (DSBs), base damage (e.g., 8-oxoguanine), and DNA-protein crosslinks (Desouky et al., 2015, Journal of Radiation Research and Applied Sciences). These radiotherapy-induced species are formed either through direct ionization of the DNA atoms or indirectly via the radiolysis of water, which generates reactive oxygen species (ROS) like hydroxyl radicals (Hall & Giaccia, 2018, Radiobiology for the Radiologist). The accumulation of complex DNA damage, particularly unrepaired or misrepaired DSBs, leads to cell cycle arrest, senescence, or cell death via apoptosis or mitotic catastrophe, which is the fundamental goal of oncological radiation treatment (NIH/NCI, 2023). Pharmacological intervention often involves radiosensitizers like Nimorazole that enhance the fixation of these species in tumor cells, or radioprotectors like Amifostine that scavenge radicals to shield healthy tissues (PubChem, CID 2124). Monitoring the induction and repair of these species is typically achieved through biomarkers such as gamma-H2AX foci, which serve as a surrogate for double-strand breaks (Kuo & Yang, 2008, In Vivo).

Other names

Ionizing radiation-induced DNA damageRadiogenic DNA lesionsDNA double-strand breaksDNA single-strand breaksOxidized DNA basesRadiation-induced DNA damage (RIDD)

Ionizing radiation induces DNA damage through direct ionization of the phosphodiester backbone or indirect action via the radiolysis of water, which generates reactive oxygen species (ROS) like hydroxyl radicals that cause strand breaks and base oxidation (Hall & Giaccia, 2018).