Ionizing radiation is extensively employed in medical procedures, particularly for cancer therapy and diagnostic imaging. Although the biological effects of medium- and high-dose radiation on human health have been established over the past century, the consequences of exposures below 0.5 Gy remain ambiguous. Damage to DNA arises through both direct and indirect mechanisms, resulting in single- and double-strand breaks. Clustered double-strand breaks are especially deleterious due to their complexity and the considerable difficulty involved in repair. The DNA damage response is predominantly mediated via non-homologous end-joining, an error-prone repair pathway that can engender chromosome aberrations and genomic instability, thereby contributing to carcinogenesis. Dose rate critically influences the extent of cellular damage: high dose rates provoke rapid energy deposition, overwhelming repair processes, whereas low dose rates afford temporal windows for repair, mitigating adverse effects. A sophisticated understanding of these underlying biological consequences is imperative for optimizing clinical application of ionizing radiation.
| Mualliflar | Hussein, Mohammed Qasim Mansour, Hassan , Rawaq Taleb, Aate , Khetam Haithem |
|---|---|
| Jurnal | Innovative Multidisciplinary Journal of Applied Technology |
| Nashr sanasi | 2025-10-09 |
| Jild | 3 |
| Son | 10 |
| Betlar | 13-27 |
| Til | Ingliz |
| DOI | 10.51699/9da4rz32 |
DOI: 10.51699/9da4rz32 · Maqolaning asl sahifasi
Radiation, DNA, Carcinogenesis
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