Effects of astaxanthin on antioxidant parameters in ARPE-19 cells on oxidative stress model

To observe the protective effect of astaxanthin (AST) against hydroquinone (HQ) mediated cell death in the apoptotic cascade and evaluate intracellular Ca²⁺ release, caspase-3, and -9 activation, reactive oxygen species (ROS) production in ARPE-19 cells.

We cultured ARPE-19 cells in special mediums and performed MTT tests to determine protective effect of AST, before exposing the cells to HQ in an incubator. We analyzed intracellular Ca²⁺ release experiments, mitochondrial membrane depolarization, glutathione (GSH), glutathione peroxidase (GSH-Px) and ROS experiments, and apoptosis assay.

ROS production ranges depend on the amount of cell death. We computed the correlation between ROS ranges and cell death by 20,70-dichlorofluorescein fluorescence, and Ca²⁺ levels by Fura-2-AM. HQ-induced cell death found out to rise ranges of caspase-3 and -9, and mitochondrial depolarization. These three steps were delayed by AST management.

ARPE-19 cells are avoided from HQ-induced ROS production and caspase-3 and -9 activation by AST. AST may limit the range of caspase synthesis, Ca²⁺ release and excess production of ROS with antiapoptotic effect. This study proposes a new therapeutic approach for the treatment of age-related macular degeneration.