Radiation damage

Radiation damage encompasses the direct deposition of energy into biomolecules (e.g., DNA/RNA/proteins) and the indirect generation of reactive species via radiolysis of water and enzymatic sources, leading to base damage, single-strand breaks, double-strand breaks (including complex/clustered lesions), protein and lipid modifications, and membrane reorganization. Key cellular responses engage the DNA damage response kinases ATM, ATR, and DNA-PK through MRN-mediated sensing, orchestrating repair pathways such as homologous recombination and nonhomologous end joining; failure or overload of these systems results in cell death or mutagenesis. Indirect effects predominate in aqueous tissues, with hydroxyl radicals and related ROS/RNS mediating much of the injury, while high-LET radiation produces more complex, locally clustered damage with increased lethality and repair resistance. Sphingolipid and lipid-raft signaling, notably ceramide generation via acid sphingomyelinase, modulate membrane platforms and stress responses after irradiation, influencing bystander effects and therapy responses.

Other names

radiation-induced damageradiation-induced DNA damageionizing-radiation damagebiomolecular radiation damage

Radiosensitizers: inhibit DNA repair (e.g., PARP inhibition) to convert radiation-induced SSBs into lethal DSBs or exacerbate DSB repair defects; increase oxygen effect to stabilize DNA radicals. Radioprotectors: scavenge free radicals from water radiolysis or modulate signaling to reduce ROS-mediated damage to DNA and membranes.