Airborne PM₁₀ Decreases Ku80 Expression and Ku70-Ku80 Heterodimer Levels of the Non-Homologous End Joining Repair Pathway in Lung Epithelial Cells.

ABSTRACT: The global population constantly breathes particulate matter with an aerodynamic diameter of ≤10 µm (PM₁₀)-a human carcinogen linked to lung cancer. Previous studies have indicated that PM₁₀ causes DNA damage, including double-strand breaks (DSBs). In particular, DSBs are primarily repaired by the non-homologous end joining (NHEJ) pathway, which is essential for maintaining genomic stability; however, the effects of PM₁₀ exposure on this pathway are unknown. To address this, A549 lung epithelial cells were exposed to 10 µg/cm² of PM₁₀ for 6, 12, and 24 h. We determined that DSBs increased with prolonged exposure, and an increase in the frequency of micronuclei was found. Despite the accumulated DNA damage, no changes in the cell cycle

SUBMITTER: Quezada-Maldonado EM 

PROVIDER: S-EPMC12469928 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature