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Cellular biomolecules in irradiated cells refers to the collective set of intracellular components, including genomic DNA, structural and functional proteins, and membrane lipids, that are altered by exposure to ionizing radiation. Radiation induces damage through direct ionization of these molecules or indirectly via the radiolysis of water, which produces reactive oxygen species (ROS) that cause oxidative modifications (Desouky et al., 2015, Journal of Radiation Research and Applied Sciences). DNA is considered the primary biological target; radiation-induced double-strand breaks can lead to cell death, senescence, or oncogenic mutations if not accurately repaired by cellular pathways (Jackson & Bartek, 2009, Nature). Proteins and lipids are also susceptible to carbonylation and peroxidation, respectively, which can disrupt cellular signaling and membrane integrity. Pharmacological intervention typically involves radioprotectors, such as Amifostine, which scavenge free radicals to prevent biomolecular damage in healthy tissues. Conversely, radiosensitizers like PARP inhibitors or cisplatin are used to block repair mechanisms and enhance the lethality of radiation in tumor cells (Hall & Giaccia, 2018, Radiobiology for the Radiologist). Because this term describes a broad state of multiple molecular classes rather than a single protein, enzyme, or receptor, it is classified as a descriptive category rather than a specific therapeutic target.
Radioprotectors act as free radical scavengers to prevent oxidative damage to biomolecules, while radiosensitizers and DNA repair inhibitors prevent the restoration of damaged biomolecules to promote cell death in target tissues.
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