This study aims to investigate the role of ferroptosis in human bronchial epithelial cells injury following exposure to seawater.

bronchial epithelial cells were cultured to the logarithmic growth phase and divided into four groups: Control (Con), Seawater treated (SW), Fer-1 treated control (Con+ F), and Fer-1 treated seawater (SW+ F) groups. The Con group was cultured with DMEM complete medium, the Con+ F group was cultured with DMEM complete medium containing 10 μM Fer-1 for 6 hours, the SW group was cultured with DMEM complete medium containing 25% Chinese primary standard seawater for 6 hours, and the SW+ F group was cultured with DMEM complete medium containing 25% primary standard seawater and 10 μM Fer-1 for 6 hrs. Subsequently, the cell viability, GSH and MDA levels, SOD vigor, and protein expression levels of GPX4, FTH1, COX2, and ACSL4 were measured.

The viability of cells in the seawater group significantly decreased (P<0.0001), following a time-dependent pattern, with an average decrease of 13% every two hours. However, treatment with Fer-1 was able to significantly ameliorate this decline in cell viability (P<0.0001), resulting in a relative increase of 8.897%. Moreover, Fer-1 was capable of significantly mitigating the reduction in cellular GSH, MDA accumulation, and SOD activity induced by seawater (P<0.001). Compared to the seawater group, treatment with Fer-1 led to an increase of 3.985 μmol/gprot, a decrease of 1.414 nM/mgprot, and an increase of 1.288 U/mgprot. Furthermore, Fer-1 was able to mitigate the reduction in cellular FTH1 and GPX4 expression levels and the increase in COX2 and ACSL4 expression levels induced by seawater (P<0.05), resulting in relative increases of 25.02% and 29.84% and reductions of 68.98% and 39.17%, respectively.

Seawater exposure induces ferroptosis in bronchial epithelial cells, while Fer-1 attenuates the seawater-induced cell injury.