Amino-functionalized carbon dots disrupt lipid metabolism to impair zebrafish embryogenesis

Carbon dots (CDs) are versatile nanomaterials with broad biomedical applications; yet their in vivo toxicity mechanisms remain poorly understood. Here, we report a one-step hydrothermal synthesis of amino-functionalized CDs from p-phenylenediamine (PCDs). Exposure of zebrafish embryos to PCDs induced dose-dependent developmental defects-including pericardial edema, spinal curvature, and impaired hatching-with malformation rates reaching 94 % at 200 μg mL^-1. Oxidative stress assays revealed significant elevations in malondialdehyde alongside altered superoxide dismutase, glutathione S-transferase, and catalase activities, implicating reactive oxygen species as primary mediators of toxicity. Integrated metabolomic and lipidomic profiling further uncovered pronounced disruptions in glycerophospholipid and arachidonic acid metabolic pathways, linking surface amino groups to lipid peroxidation-driven membrane damage. We propose a unified mechanistic model in which PCD surface chemistry initiates oxidative lipid perturbations, culminating in embryotoxicity. These insights establish a molecular framework for assessing and mitigating the biosafety risks of surface-functionalized CDs in biomedical and environmental applications.