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Updated: May 27, 2026

Revealing the Ferroptotic Phenotype of Medulloblastoma
Published on: March 15, 2024
PFOA/PFOS induce ferroptosis in bladder epithelial cells through inhibition of ACSL4 ubiquitination
Hao Xu1,2, Zhihua Ye1,2, Juan Liu2,3
1Department of Urology, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Huangshi, Hubei, China.
Introduction:
Perfluoroalkyl and polyfluoroalkyl substances (PFAS) are persistent environmental pollutants, but their role in bladder epithelial injury remains unclear.
Methods:
SV-HUC-1 cells were exposed to PFOA and PFOS. Cell viability, lipid peroxidation, and ROS levels were assessed using CCK-8 assay, flow cytometry, and transmission electron microscopy. Protein expression and ubiquitination were analyzed by Western blotting and molecular docking.
Results:
PFOA and PFOS induced ferroptosis in bladder epithelial cells, characterized by increased lipid peroxidation and ROS levels. Mechanistically, PFOA/PFOS inhibited ACSL4 ubiquitination at K593 and K690, leading to its stabilization and promoting ferroptosis. Knockdown of ACSL4 significantly reversed these effects.
Discussion:
These findings reveal a novel mechanism by which PFAS induce ferroptosis via regulation of ACSL4 ubiquitination, providing new insights into PFAS-induced bladder toxicity.
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