Radiation-induced DNA damage and cellular apoptosis

Radiation-induced DNA damage and cellular apoptosis refers to the process by which exposure to ionizing radiation leads to various forms of DNA damage—primarily double-strand and single-strand breaks—within the genome. This damage is sensed by cellular kinases such as ATM and ATR, triggering a cascade of events involving cell cycle arrest, DNA repair, and, if damage is irreparable, activation of apoptotic cell death pathways. Radiation also generates reactive oxygen species (ROS), amplifying DNA damage and contributing to cytotoxicity. The apoptosis that follows can proceed via intrinsic (mitochondrial), extrinsic (death receptor), or ceramide-mediated pathways, all converging on executioner caspases. These responses are critical for the therapeutic effects of radiotherapy in cancer but can also impact normal tissues, leading to side effects.

Other names

Radiation-induced apoptosisDNA damage response to radiationRadiation-induced cell death

Induction of DNA breaks (single- and double-strand) Generation of reactive oxygen species (ROS) Activation of DNA damage response (ATM/ATR/Chk1/Chk2/p53) Arrest of cell cycle and activation of apoptosis (caspase-3, PARP cleavage, mitochondrial and death receptor pathways)