Biological effect of U(VI) exposure on lung epithelial BEAS-2B cells.

In this study, the biological effects of U(VI) exposure on lung epithelial cells were investigated by MTT assay, immunofluorescence, flow cytometry, and Western blotting. U(VI)-induced stress triggers oxidative stress in cells, activates MAPK signaling pathways, and promotes inflammation. Additionally, U(VI) causes damage to the cell membrane structure and severe DNA injury, impacting the accuracy of transcription and translation. The results demonstrate that U(VI) exposure significantly inhibits cell proliferation and migration. This is attributed to the disruption of the PI3K/AKT/GSK-3β/β-catenin signaling pathway and the reduction in CyclinD1 expression, leading to a delayed cell cycle, decreased growth rate, mitochondrial damage, and reduced energy metabolism. This study provides a comprehensive understanding of the molecular mechanisms underlying uranium-induced cellular toxicity in lung epithelial cells.