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Cellular biomacromolecules, primarily DNA, proteins, and lipids, are the fundamental biological structures affected by ionizing radiation during cancer radiotherapy (Desouky et al., 2015, Journal of Radiation Research and Applied Sciences). The therapeutic efficacy of radiotherapy relies on the induction of complex damage to these molecules, most critically the generation of DNA double-strand breaks (DSBs) which lead to cell cycle arrest or apoptosis (Kuo and Yang, 2008, In Vivo). Radiation interacts with these macromolecules either directly through ionization or indirectly via the radiolysis of water, which produces reactive oxygen species (ROS) like hydroxyl radicals that oxidize lipids and proteins (Riley, 1994, International Journal of Radiation Biology). In clinical practice, drugs such as radiosensitizers are used to increase the susceptibility of DNA to radiation damage, while radioprotectors are employed to scavenge ROS and protect biomacromolecules in healthy tissues (PubChem CID 2124). Monitoring the integrity of these macromolecules, such as through gamma-H2AX assays for DNA damage, is vital for assessing treatment response and potential toxicity.
Radiosensitization (enhancing DNA damage or inhibiting repair) and Radioprotection (scavenging free radicals to prevent macromolecular oxidation).
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