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Ionizing radiation-induced DNA damage encompasses a spectrum from simple base changes up through complex clustered breaks that challenge cellular repair systems. The outcome depends on dose/type/LET characteristics as well as intrinsic cellular capacity for detection and accurate repair. It includes direct effects like DNA strand breaks and base modifications, as well as indirect effects mediated by reactive oxygen species (ROS). The cellular response involves the DNA Damage Response (DDR), activating repair pathways such as homologous recombination (HR) and non-homologous end joining (NHEJ). If unrepaired, this damage can lead to cell death, mutations, and cancer. Detection methods focus on identifying markers like γ-H2AX foci formation at DSB sites. Understanding individual susceptibility based on genetic background helps predict radiosensitivity—a key consideration in personalized medicine approaches for cancer therapy.
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