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DNA damage via beta radiation from iodine-131 decay is a biological outcome occurring when cells are exposed to beta particles released during the radioactive decay of I-131. Beta particles penetrate tissues and cause DNA damage primarily by generating reactive oxygen species (ROS), leading to single- and double-strand breaks, base modifications, and lesions within DNA. These DNA lesions trigger cellular repair pathways, cell cycle arrest, and often apoptosis. This mechanism is exploited in cancer therapy (notably for thyroid cancers) but carries risks of genotoxicity, secondary cancer, and normal-tissue toxicity. Biomarkers like γ-H2AX and micronuclei frequency are used to assess this damage. Importantly, this term describes a physical process and its biological effects, not a discrete molecular target[2][1][3][4][5][6][8].
Indirectly: Generation of reactive oxygen species (ROS) leading to DNA single-strand breaks (SSBs), double-strand breaks (DSBs), base and sugar modifications; Directly: Beta particles can physically ionize DNA bonds, causing SSBs and DSBs.
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