Radioisotope-mediated cytotoxicity

Radioisotope-mediated cytotoxicity refers to a therapeutic mechanism in which radioactive isotopes are delivered to diseased cells, usually cancer, by targeting specific molecular markers. The radioactive decay of these isotopes produces ionizing radiation (most commonly alpha or beta particles) that causes DNA double-strand breaks and generates reactive oxygen species, leading to apoptosis or necrosis of the target cell. The selectivity of damage is determined not by the radioisotope itself, but by the delivery vector (e.g., antibody, peptide, small molecule) that localizes the isotope to the tumor[4][2]. This entry is not a molecular entity (such as a receptor, enzyme, or channel) but rather a therapeutic concept or mechanism. Structured pharmacological databases would not treat this as an individual target, but would instead reference the actual molecular target to which the radioisotope-conjugated drug binds (for instance, "Somatostatin receptor 2" or "Prostate-specific membrane antigen") rather than the downstream cytotoxic effect of the radioisotope itself[4]. If "radioisotope-mediated cytotoxicity" appears as a target entry, it is considered incorrect and should be replaced with the specific molecular target being exploited by the radiopharmaceutical agent.

Induction of DNA double-strand breaks through emission of ionizing radiation (α, β, or γ particles), generating free radicals and direct DNA damage[4][2]. Apoptosis or necrosis secondary to DNA damage or oxidative stress[4][2].