Beta particle emission (Beta emission)

Beta particle emission is a physical process of radioactive decay where an unstable atomic nucleus releases a high-speed electron or positron to reach a more stable state [7, 12]. In clinical oncology, beta-minus emission is primarily used as the effector mechanism for targeted radionuclide therapies (TRT), where radionuclides like Lutetium-177 or Yttrium-90 are delivered to specific cancer sites [1, 9]. These emitted electrons travel a moderate distance in biological tissue (typically 1 to 12 mm), enabling a 'cross-fire' effect that destroys nearby tumor cells, including those not directly bound by the drug [8, 13]. The therapeutic effect is achieved through the induction of lethal DNA damage and the generation of destructive free radicals within the tumor environment [3, 10]. While critical for the function of many radiopharmaceuticals, beta emission is a physical modality of action rather than a biological target such as a receptor, enzyme, or signaling protein [1, 8]. Safety considerations involve managing the risk of collateral damage to healthy organs, particularly the bone marrow and kidneys, which can be affected during the systemic circulation and excretion of these isotopes [1, 5].

Other names

Beta decayBeta-minus decayBeta-plus decayElectron emissionPositron emissionBeta radiationBeta ray

The process involves the radioactive decay of an atomic nucleus resulting in the emission of a high-energy electron (beta-minus) or positron (beta-plus). In therapeutic applications, these particles travel short distances (millimeters) through tissue, causing localized ionization of atoms and molecules. This ionization leads to the formation of reactive oxygen species (ROS) and direct damage to cellular DNA, including single and double-strand breaks, which eventually trigger apoptosis or necrosis in the targeted cells [1, 3, 10].