Aged polystyrene nanoplastics induce cardiac developmental toxicity associated with mitochondrial dysfunction in zebrafish larvae.

Environmental aging alters the physicochemical properties of micro/nanoplastics (MNPs) and may modify their biological effects; however, the cardiac developmental toxicity of aged MNPs remains poorly understood. In this study, ultraviolet-aged polystyrene nanoplastics (aged PSNPs) were prepared as a laboratory model of photoaged nanoplastics, and zebrafish embryos were exposed to pristine or aged PSNPs for 7 days to evaluate developmental cardiotoxicity and mitochondrial mechanisms. UV aging increased surface roughness and cracks, reduced particle diameter from 93.43 nm to 87.5 nm, shifted zeta potential from -33.3 mV to -21.8 mV, and increased oxygen-containing functional groups. Both pristine and aged PSNPs disrupted early development, including accelerated hatching at 3 dpf, reduced final hatching rate, increased mortality, and elevated cardiac malformation. Cardiac defects were mainly characterized by pericardial edema and cardiac enlargement. PSNP exposure increased heart rate and blood flow velocity while reducing BA-SV distance, with aged PSNPs inducing stronger effects. Mechanistically, both pristine and aged PSNPs decreased ATP levels, whereas aged PSNPs caused greater ROS accumulation and calcium overload. Aged PSNPs also broadly suppressed mitochondrial function related genes and disrupted cardiac developmental signaling, as indicated by altered Notch/Wnt-related and myocardial maturation gene expression. These findings demonstrate that aged PSNPs exert stronger developmental cardiotoxicity than pristine PSNPs and suggest that mitochondrial dysfunction may represent a potential mechanistic contributor associated with impaired early cardiac development.