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Developmental cardiovascular disruption triggered by polystyrene nanoplastics in zebrafish mediated through oxidative stress
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Researchers exposed zebrafish embryos to polystyrene nanoplastics and observed disrupted heart development, including abnormal heart rate, swelling around the heart, and impaired blood vessel formation. The damage was linked to oxidative stress, and treatment with the antioxidant glutathione significantly reduced the harmful effects. The findings suggest that nanoplastic pollution in waterways may pose risks to cardiovascular development and that antioxidant-based strategies could help counteract the damage.
The rising prevalence of polystyrene nanoplastics (PSNPs) in aquatic ecosystems poses not only ecological threats but also growing concerns for human health, particularly through their potential to interfere with cardiovascular development and function. This study investigated the cardiotoxic effects of PSNPs (25 nm) exposure on zebrafish embryos, a well-established vertebrate model in toxicology. PSNPs were exposed on Tg(fli1: EGFP) zebrafish embryos at concentrations of 0.01, 0.1, 1, and 10 μg/mL for 96 h post-fertilization (hpf). Cardiovascular function and morphology were evaluated during early development. The exposure disrupted cardiovascular development, leading to abnormalities such as altered heart rate, pericardial edema, impaired blood vessel formation, reduced red blood cell velocity, and decreased aortic diameter and ventricular volume between 48 and 96 hpf. Increased reactive oxygen species and apoptosis suggest oxidative stress is a key mechanism of toxicity. Gene expression analysis showed that PSNP exposure disrupted genes related to cardiovascular development, apoptotic signaling, as well as antioxidant defense mechanisms. Co-exposure of glutathione (GSH) at 50 μM, a powerful antioxidant, significantly mitigated the harmful effects of PSNPs, suggesting that oxidative stress is crucial to PSNP-induced cardiovascular toxicity. The results demonstrate the urgency of addressing nanoplastic pollution and highlight potential antioxidant-based strategies for mitigating its health impacts.
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Polystyrene nanoplastics cause developmental abnormalities, oxidative damage and immune toxicity in early zebrafish development
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Zebrafish embryos exposed to polystyrene nanoplastics showed dose-dependent developmental problems including delayed hatching, reduced survival, smaller body size, and the nanoplastics accumulated in critical organs like the eyes, heart, liver, and brain. The particles triggered oxidative stress that damaged cells and activated inflammatory immune responses, demonstrating how nanoplastic contamination in water can cause widespread harm to developing organisms.
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.
Polystyrene Nanoplastic Exposure Induces Developmental Toxicity by Activating the Oxidative Stress Response and Base Excision Repair Pathway in Zebrafish (Danio rerio)
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Researchers exposed zebrafish embryos to polystyrene nanoplastics at various concentrations and found significant developmental abnormalities including reduced hatching rates and increased malformations. The nanoplastics activated oxidative stress responses and DNA repair pathways, indicating cellular damage during critical early development stages. The study provides mechanistic evidence for how nanoplastic exposure can disrupt normal embryonic development in aquatic organisms.
Embryonic exposure of polystyrene nanoplastics affects cardiac development
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Researchers found that polystyrene nanoplastics disrupted the development of heart cells grown from human embryonic stem cells, producing smaller and weaker heart tissue in the lab. The nanoplastics caused oxidative stress in mitochondria and blocked important cellular cleanup processes, reducing the stem cells' ability to properly form heart cells. In zebrafish embryos, nanoplastic exposure also reduced heart contractions and blood flow, suggesting that nanoplastic exposure during pregnancy could pose risks to fetal heart development.
Cardiovascular toxicity assessment of polyethylene nanoplastics on developing zebrafish embryos
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Researchers assessed the cardiovascular effects of polyethylene nanoplastics on developing zebrafish embryos and found that exposure above 50 micrograms per milliliter caused pericardial edema, reduced cardiac output, and impaired blood vessel formation. The nanoplastics also triggered oxidative stress and inflammation, which contributed to blood clot formation in the embryos. The study suggests that nanoplastic exposure could pose risks to cardiovascular development in living organisms.
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