Radiation-induced DNA damage via beta emission

Radiation-induced DNA damage via beta emission" refers not to a discrete molecular target but rather to the **process** by which ionizing radiation—specifically in the form of energetic electrons known as **beta particles**—causes chemical alterations in cellular DNA. When tissues are exposed to radionuclides that emit beta particles or external sources of electron irradiation, these high-energy electrons interact with biological molecules primarily through ionization and excitation events. This leads directly or indirectly (via reactive oxygen species) to various forms of **DNA lesions**, including single-strand breaks, base modifications, and most critically for cell fate decisions, **double-strand breaks** (DSBs)[1][3][4]. DSBs are particularly lethal if unrepaired or misrepaired. The complexity and clustering of these lesions depend on the energy deposition pattern; clustered/complex DSBs are more difficult for cells to repair accurately than isolated ones. The biological consequences include cell death (apoptosis), mutations leading potentially to cancer development if cells survive with misrepaired genomes, and genomic instability. In cancer therapy contexts such as targeted radionuclide therapy using agents like ^177Lu-DOTATATE—which emits therapeutic-range beta particles—the intent is selective induction of irreparable DSBs in tumor cells while sparing normal tissue as much as possible[5]. Because this entry describes a physical/chemical process rather than a specific gene product or protein target typically modulated by drugs, it is not considered a canonical "therapeutic target" in the conventional sense used for receptors or enzymes. Instead, it represents an endpoint/process exploited therapeutically. Notable biomarkers used experimentally and clinically for monitoring this type of damage include γ-H2AX foci formation—a marker for DSB presence—and 53BP1 accumulation at sites of complex chromatin-associated damage[1][3]. Safety concerns center on off-target effects leading to healthy tissue injury and increased risk for secondary cancers due to induced mutations. In summary: "Radiation-induced DNA damage via beta emission" is best classified as a damaging process/mechanism rather than an actionable molecular target; thus its use as a "target name" is incorrect per standard pharmacological nomenclature conventions.[1][3][4]

Other names

Radiation-induced DNA double-strand breaks via beta emissionBeta particle-induced DNA damageIonizing radiation-induced DNA lesions (via beta particles)

Induction of direct and indirect DNA strand breaks by ionizing radiation from beta emissions[4][5]