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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.
The ubiquity of micro(nano)plastics has raised significant concerns among people. Their accumulation in the cardiovascular system necessitates attention to their cardiotoxicity. However, research on the cardiotoxicity of micro(nano)plastics remains scarce. Our study exposed zebrafish embryos to four different concentrations (0, 1, 10, 100 μg/mL) of polystyrene nanoplastics (PSNPs) for a period of 7 days. The results indicated that PSNPs noticeably decreased the hatching and survival rates of zebrafish and also induced cardiac developmental abnormalities. The mRNA level analysis revealed significant upregulations of heart development-related genes nkx2.5, cmlc-2, and myh-7 in response to PSNPs. Additionally, PSNPs significantly up-regulated the mRNA level associated with the Notch signaling pathway (notch-1a, jag-1a, and her-7) while remarkably suppressing the expression of the Wnt signaling pathway gene (wnt-3a). Further research showed that PSNPs significantly increased the expression of endoplasmic reticulum stress genes atf-6 and chop, while noticeably inhibiting mitochondrial copy numbers. Moreover, PSNPs were found to decrease calcium ion level and superoxide dismutase (SOD) activity in zebrafish larvae. Additionally, prolonged exposure to PSNPs for 7 days exacerbated abnormalities in various indicators compared to a 4-day exposure. In conclusion, our study demonstrates that PSNPs induce oxidative stress in zebrafish larvae, thereby activating endoplasmic reticulum stress and inhibiting mitochondrial activity, ultimately disrupting the Notch and Wnt signaling pathways. These disruptions result in abnormalities in cardiac developmental genes, ultimately leading to cardiac developmental abnormalities in zebrafish. The present research contributes to a novel understanding of the cardiotoxicity of PSNPs.
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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.
Polystyrene nanoplastics induce developmental impairments and vasotoxicity in zebrafish (Danio rerio)
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Zebrafish exposed to polystyrene nanoplastics at environmentally realistic concentrations showed developmental problems including heart defects, brain abnormalities, blood vessel damage, and reduced swimming ability. The nanoplastics accumulated on the fish's body and triggered cell damage and oxidative stress even at very low doses. Since zebrafish are commonly used to model human developmental processes, these findings raise concerns about what nanoplastic exposure could mean for early human development.
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.
Aged polystyrene nanoplastics induce cardiac developmental toxicity associated with mitochondrial dysfunction in zebrafish larvae
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Zebrafish embryos exposed to plastic nanoparticles (polystyrene) that had been artificially aged by UV light showed more heart defects, faster heart rates, and disrupted heart development than those exposed to unaged particles. Aged particles also caused greater damage to mitochondria, the cell structures that produce energy, which may help explain the stronger effects.
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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