Exposure of polystyrene nanoplastics led to ferroptosis on cardiomyocytes.

Recent studies have revealed that nanoplastics (nm-sized nanoplastics may induce oxidative stress) can translocate into human cardiovascular tissues and potentially contribute to pathophysiological processes through mechanisms involving reactive oxygen species (ROS) generation. However, the exact role of these materials in inducing iron-related diseases such as ferroptosis remains unclear. In this investigation, we demonstrated that 100 nm polystyrene nanoparticles (PS-NPs) can be taken up by primary rat cardiomyocytes and induce mitochondrial reactive oxygen species (ROS) elevation, mitochondrial membrane potential decrease, ferrrous iron accumulation, and lipid peroxidation. These changes ultimately result in significant reduction of cell viability alongside upregulation of pro-ferroptotic proteins such as COX2, ACSL4, and downregulation of antioxidant proteins like GPX4. Furthermore, ferrous deferoxamine (DFO) effectively restored cellular viability by inhibiting the increase in ferrrous iron and lipid peroxidation. Additionally, autophagy and NF-κB-IL6 signaling pathways were activated in response to PS-NPs exposure. These findings suggest that PS-NPs may serve as a novel agent inducing ferroptosis in cardiomyocytes.