Intracellular Trafficking Pathway and ROS Scavenging Activity of Glycol Chitosan‐Coated Cerium Oxide Nanoparticles in a Pathological AMD‐Like Model

Abstract

AbstractAge‐related macular degeneration (AMD) is a degenerative eye disease that primarily affects the macula. AMD is a leading cause of vision loss in individuals over the age of 65, particularly more common in Caucasians than in other racial groups. Cerium oxide nanoparticles (CNPs) have emerged as highly promising nanomaterials in the treatment of AMD due to their potent antioxidant properties. In pathological damages of AMD conditions, characterized by oxidative stress resulting from an overproduction of reactive oxygen species (ROS), CNPs possess significant promise for attenuating the pathogenic processes and advancing therapeutic interventions. Despite their potential clinical applications, the widespread use of CNPs is greatly hampered by limited water solubility, and concerns have arisen about their potential impact on normal ROS production in mitochondria. Here, the antioxidative activity of glycol chitosan‐coated CNPs (namely, GCCNPs) and their behavior in mouse primary RPE (mRPE) cells are reported through an in vitro trafficking study. This findings demonstrate that GCCNPs effectively neutralize excessive ROS and prefer to exclusively accumulate in cytosol without any uptake in the nucleus and mitochondria of the mRPE cells. Moreover, GCCNPs demonstrated therapeutic effects by reducing the ROS level in a laser‐induced choroidal neovascularization (CNV) AMD‐like murine model.