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Nanoplastics Mitigate 6PPD-Induced Zebrafish Cardiac Ferroptosis Mediated by the GRK5/p53/SLC7A11 Pathway
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A study in zebrafish and rat heart cells found that 6PPD, a tire rubber chemical, damages heart cells through a specific chain of molecular changes. When nanoplastics were also present, less 6PPD reached the heart, and this heart cell damage was reduced.
Abstract 6PPD, as an antioxidant in tire rubber, constitutes an emerging pollutant together with nanoplastics (NPs) widely present in the environment. This study explored the potential combined toxicity risk of 6PPD and 50 nm polystyrene nanoplastics (PS-NPs) to aquatic ecosystems. The study found that the presence of PS-NPs altered the physicochemical behavior of 6PPD and was associated with reduced cardiac accumulation of 6PPD and its oxidation product 6PPD-Q. The experiment showed that 6PPD activated the p53 signaling pathway by upregulating the expression of GRK5, thereby inhibiting the expression of SLC7A11 and GPX4, leading to increased ROS, iron overload, lipid peroxidation, and mitochondrial damage in zebrafish heart and rat cardiomyocytes (H9C2), thereby triggering ferroptosis. After coexposure of PS-NPs and 6PPD, physicochemical interactions between PS-NPs and 6PPD altered the colloidal state and environmental behavior of the mixture, while the cardiac levels of both 6PPD and 6PPD-Q were reduced, accompanied by weakened ferroptosis-related responses. This study revealed the cardiotoxic mechanism of 6PPD and the mitigation effect of PS-NPs after coexposure, providing a basis for environmental pollution risk assessment.
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Effects of co-exposure of polyethylene nanoplastics and 6PPD on cardiac function in the early developmental stage of zebrafish
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Tire particles from car tires wash into waterways carrying both nanoplastics and a chemical called 6PPD, and this study found that when zebrafish embryos were exposed to both together, the combo caused worse heart damage than either one alone—weaker heartbeats, cell death, and oxidative stress in developing hearts. While this research was done in fish, it highlights a growing concern: everyday pollution from tires may combine with plastics in our water in ways that are more harmful than scientists previously realized, which matters since these same particles can end up in rivers, drinking water sources, and eventually the food chain.
Exposure to Polystyrene Nanoplastics Induces Ferroptosis-Associated Cardiac Injury: Cell-Based Evidence for Lysosome-Associated NLRX1 Loss and an NLRX1–STING–NCOA4 Response
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In mouse heart cells and in mice given polystyrene nanoplastics by mouth for eight weeks, the particles lowered the proteins NLRX1 and GPX4 and promoted iron buildup and lipid damage. The mice developed cardiac dysfunction and fibrosis.
Micro‐Nano Plastics and 6‐ PPD ‐Q in Cardio‐Pulmonary Health: Environmental Sources, Systemic Exposure, and Mechanistic Insights
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This review examines how micro- and nanoplastics along with 6-PPD-Quinone, a toxic chemical from tire wear, affect heart and lung health. These pollutants cause oxidative stress, inflammation, mitochondrial damage, and blood vessel injury in cardiovascular and respiratory tissues. The detection of these particles in human tissues underscores the urgency of understanding how everyday exposure to tire and plastic pollution may contribute to heart and lung disease.
Polystyrene nanoplastics exert cardiotoxicity through the Notch and Wnt pathways in zebrafish (Danio rerio)
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Researchers exposed zebrafish embryos to polystyrene nanoplastics and found dose-dependent cardiac developmental defects linked to disruption of the Notch and Wnt signaling pathways — key regulators of heart development — alongside oxidative stress, endoplasmic reticulum stress, and reduced mitochondrial activity.
Exposure of polystyrene nanoplastics led to ferroptosis on cardiomyocytes
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Researchers exposed rat heart cells to 100-nanometer polystyrene nanoparticles and found that the particles were taken up by the cells and triggered a form of iron-dependent cell death called ferroptosis. The nanoparticles caused a buildup of reactive oxygen species in mitochondria, iron accumulation, and damage to cell membranes. The study suggests that nanoplastic exposure may pose risks to heart health through this specific cell death pathway.
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