内吞作用
细胞内
网格蛋白
碱性磷酸酶
细胞生物学
细胞凋亡
活力测定
平衡
化学
受体介导的内吞作用
细胞
生物
生物化学
酶
作者
Lie-Jun Huang,Guifan Sun,Xu Wang,Shufang Li,Xiujun Qin,Quan An,Zhongwen Wang,Jianguo Li
标识
DOI:10.1016/j.etap.2023.104171
摘要
The objective of this study was to explore the endocytosis mechanisms of uranium uptake in HK-2 cells and its toxic effects. Our results demonstrated that uranium exposure impairs redox homeostasis and increases the permeability of the cell membrane and mitochondrial membrane, which may induce cell apoptosis by cytochrome-c leakage. Alkaline phosphatase activity increased after uranium exposure, which may be involved in the process of intracellular mineralisation of uranium, leading to severe cell necrosis. Furthermore, our findings demonstrated that the clathrin-mediated endocytosis process contributed substantially to uranium uptake in HK-2 cells and the total uranium uptake was highly correlated with cell viability, reaching a high correlation coefficient (r = −0.853) according to Pearson correlation analysis. In conclusion, the uptake of uranium into mammalian cells was mainly facilitated by the clathrin-mediated endocytosis pathway and induced dose-dependent cellular toxicity, including redox homeostasis imbalance, membrane injury, cell apoptosis and necrosis.
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