DNA damage via localized beta radiation from iodine-131

Iodine-131 emits beta particles that deposit energy over millimeter-scale paths; when localized near or within cells (e.g., thyroid tissue taking up radioiodide), these beta emissions produce predominantly indirect DNA damage through ROS, along with some direct ionization, resulting in SSBs, DSBs, and base damage. Cells mount a DNA damage response involving ATM/ATR signaling, γ-H2AX and 53BP1 foci formation, and engage BER and NHEJ (and HR in S/G2); outcomes include cell-cycle arrest, apoptosis, or mutagenesis. Experimental studies show I-131 beta particles induce measurable strand breaks in cultured cells, and can trigger apoptosis and G2/M arrest; in patients and lymphocyte models, genotoxicity can be monitored by micronuclei. While therapeutically exploited in thyroid disease, off-target genomic damage underlies radiation toxicity and secondary cancer risks.

Other names

Beta-radiation–induced DNA damageDNA lesions from beta particlesGenomic damage by beta radiationIodine-131–induced DNA damage

Indirect DNA damage via reactive oxygen species from water radiolysis leading to single-strand breaks, double-strand breaks, and base/sugar modifications Direct ionization of DNA by beta particles causing SSBs and reversible DSBs Downstream activation of DNA damage response pathways (BER for SSB/base damage; NHEJ for DSBs; HR in S/G2)