Radiation-induced cytotoxicity

Radiation-induced cytotoxicity refers to the various forms of cell death and cellular damage caused by exposure to ionizing radiation. When cells are irradiated, direct damage to DNA—particularly double strand breaks—triggers multiple forms of cell death such as apoptosis, necrosis, autophagy-dependent cell death, pyroptosis, ferroptosis, and immunogenic cell death[2][5]. In addition to DNA damage, radiation generates reactive oxygen species (ROS), induces endoplasmic reticulum stress, and activates damage-associated molecular patterns (DAMPs) like calreticulin, HMGB1, and ATP, which promote immune responses and inflammation[1][2][3]. Radiation cytotoxicity also involves the release of cytokines such as IL-1, IL-6, TNF-α, and TGF-β, leading to chronic inflammation and tissue fibrosis in normal tissues[3]. This process is clinically relevant in both radiation therapy for cancer—where it is exploited to kill tumor cells—and in the context of normal tissue toxicity and side effects of radiotherapy[3][5].\n \n**Note:** "Radiation-induced cytotoxicity" is a process, not a single druggable target. If you are seeking specific molecular targets involved in mediating or sensing radiation cytotoxicity (such as DNA damage response proteins, purinergic receptors, or cytokine receptors), these should be named specifically (e.g., "DNA-dependent protein kinase," "P2X7 purinergic receptor") for structured data extraction[1][2][3].

Other names

Radiation-induced cell deathRadiation cytotoxicityRadiation-induced cellular cytotoxicity