Potassium bromate-induced cell model of age-related macular degeneration in vitro

Age‑related macular degeneration (AMD) progression occurs due to oxidative stress in retinal pigment epithelium (RPE) cells. To develop a new model of AMD, the present study investigated the effects of potassium bromate (KBrO 3 ) on ARPE‑19 cells. Incubation with KBrO 3 for 24 h significantly decreased ARPE‑19 cell viability in a concentration‑dependent manner compared with the control group. The MTT and lactate dehydrogenase assay results indicated that KBrO 3 induced cell apoptosis. Compared with the control group, KBrO 3 reatment significantly decreased the Bcl2/Bax ratio, as determined via western blotting, and caspase‑3 mRNA expression levels. Fluorescence microscopy indicated the increased ROS levels in cells treated with KBrO 3 . Endogenous antioxidant enzyme activities, including superoxide dismutase and glutathione peroxidase, were significantly inhibited by KBrO 3 compared with the control group. Moreover, the antioxidants tiron and phloroglucinol inhibited KBrO 3 ‑mediated effects on ARPE‑19 cells in a dose‑dependent manner. Additionally, GPR109A is the binding site of 4‑hydroxynonenal (4‑HNE). KBrO 3 displayed cytotoxic effects in 293 cells, which naturally lack the GPR109A gene, but these effects were not observed in 4‑HNE‑treated 293 cells, suggesting that KBrO 3 induced apoptosis without increasing endogenous 4‑HNE levels in cells. Moreover, the results suggested that KBrO 3 ‑induced oxidative stress may activate STAT3 to increase VEGF expression in ARPE‑19 cells. Collectively, the results of the present study supported the potential use of KBrO 3 o induce an in vitro model of AMD in ARPE‑19 cells.