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Retinal pigment epithelial (RPE) cells occupy the outer layer of the retina and perform various biological functions. Oxidative damage to RPE cells is a major risk factor for retinal degeneration that ultimately leads to vision loss. In this study, we investigated the role of spermidine in a hydrogen peroxide (H 2 O 2 )-induced oxidative stress model using human RPE cells. Our findings showed that 300 μM H 2 O 2 increased cytotoxicity, apoptosis, and cell cycle arrest in the G2/M phase, whereas these effects were markedly suppressed by 10 μM spermidine. Furthermore, spermidine significantly reduced H 2 O 2 -induced mitochondrial dysfunction including mitochondrial membrane potential and mitochondrial activity. Although spermidine displays antioxidant properties, the generation of intracellular reactive oxygen species (ROS) upon H 2 O 2 insult was not regulated by spermidine. Spermidine did suppress the increase in cytosolic Ca 2+ levels resulting from endoplasmic reticulum stress in H 2 O 2 -stimulated human RPE cells. Treatment with a cytosolic Ca 2+ chelator markedly reversed H 2 O 2 -induced cellular dysfunction. Overall, spermidine protected against H 2 O 2 -induced cellular damage by blocking the increase of intracellular Ca 2+ independently of ROS. These results suggest that spermidine protects RPE cells from oxidative stress, which could be a useful treatment for retinal diseases.

Spermidine Attenuates Oxidative Stress-Induced Apoptosis via Blocking Ca2+ Overload in Retinal Pigment Epithelial Cells Independently of ROS