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Additionally, GPR109A is the binding site of 4‑hydroxynonenal (4‑HNE). KBrO3 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 KBrO3 induced apoptosis without increasing endogenous 4‑HNE levels in cells. Moreover, the results suggested that KBrO3‑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 KBrO3 to induce
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