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

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

Methods: 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 Ca release experiments, mitochondrial membrane depolarization, glutathione (GSH), glutathione peroxidase (GSH-Px) and ROS experiments, and apoptosis assay.

Results: 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 Ca 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.

Conclusion: 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, Ca release and excess production of ROS with antiapoptotic effect. This study proposes a new therapeutic approach for the treatment of age-related macular degeneration.