NUR KALUÇ, PINAR BUKET THOMAS
Journal of Clinical Practice and Research - 2025;47(4):407-414
Objective: Astaxanthin (ATX) is a well-known antioxidant and cytoprotective natural xanthophyll carotenoid that exhibits protective effects against a wide range of pathological conditions. However, its underlying mechanisms and the contribution of autophagy remain unclear. This study aimed to investigate the potential role of autophagy in ATX-mediated cytoprotection under oxidative stress conditions through a genetic approach. Materials and Methods: Wild-type and autophagy-deficient (atg8Δ) Saccharomyces cerevisiae strains were exposed to 1, 3, or 8 mM H2O2 for up to three hours. Cell viability and intracellular reactive oxygen species (ROS) levels were measured using the colony-forming unit assay and H2DCFDA staining, respectively. To evaluate the contribution of autophagy to ATX-mediated cytoprotection, wild-type and atg8Δ cells were pretreated with or without 30 µM ATX for three hours, followed by exposure to 3 mM H2O2 for one hour. Viability and ROS levels were compared between wild-type and atg8Δ strains. Results: H2O2 reduced cell viability in both strains in a dose- and time-dependent manner, with atg8Δ cells showing increased sensitivity. ROS levels also showed a dose-dependent increase in both strains and were higher in atg8Δ cells after prolonged H2O2 exposure. ATX pretreatment effectively reduced intracellular ROS levels in both strains. While ATX improved viability in wild-type cells, it failed to enhance viability in autophagy-deficient cells. Conclusion: Autophagy may not be required for the ROS-reducing effects of ATX but may be essential for protection against oxidative stress-induced cell death, highlighting the importance of autophagy in ATX-mediated cytoprotection.
