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

被引：0
作者：
Zhang, Mingxia [1 ,2 ]
Zhou, Han [2 ]
Liu, Lei [2 ,3 ]
Song, Wencheng [1 ,2 ,3 ,4 ]
机构：
[1] College of Life Sciences, Anhui Normal University, Wuhu
[2] Anhui Province Key Laboratory of Medical Physics and Technology, Institute of Health & Medical Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei
[3] Hefei Cancer Hospital, Chinese Academy of Sciences, Hefei
[4] Collaborative Innovation Center of Radiation Medicine, Jiangsu Higher Education Institutions and School for Radiological and Interdisciplinary Sciences, Soochow University, Suzhou
来源：
Chemosphere | 2024年 / 366卷
基金：
中国国家自然科学基金;
关键词：
BEAS-2B cells; Cell cycle; Cytotoxicity; U(VI);
D O I：
10.1016/j.chemosphere.2024.143451
中图分类号：
学科分类号：
摘要：
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. © 2024 Elsevier Ltd
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