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Elucidating the underlying toxic mechanisms of nanoplastics on zebrafish hematological and circulatory systems
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This study demonstrated that nanoplastics disrupt early embryonic development and impair mitochondrial function in zebrafish by inhibiting PINK1/Parkin-mediated mitophagy, a cellular cleanup process. A mitophagy activator was able to mitigate these effects, pointing to mitochondrial dysfunction as a key mechanism of nanoplastic hematological and circulatory toxicity.
This study demonstrates that nanoplastics disrupt early embryonic development, impair mitochondrial function, and inhibit PINK1/Parkin-mediated mitophagy, which can be mitigated with a mitophagy activator.
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Lipophagy suppression: a novel mechanism for developmental disruption by nanoplastics/MC-LR in zebrafish
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Researchers co-exposed zebrafish embryos to polystyrene nanoplastics and microcystin-LR (a cyanobacterial toxin) and found that combined exposure suppressed lipophagy—a cellular process that breaks down lipid droplets—more severely than either substance alone. Disruption of lipophagy impaired early development, identifying this autophagy pathway as a novel target for nanoplastic developmental toxicity.
Lipid metabolic dysregulation: A novel developmental toxicity pathway of aged nanoplastics via inhibition of lipophagy in zebrafish
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Researchers showed that UV-aged polystyrene nanoplastics cause more severe developmental toxicity in zebrafish larvae than pristine particles by blocking lipophagy — the cellular process of breaking down stored fat via lysosomes — leading to abnormal lipid accumulation and disrupted early development.
Co-exposure to PFOA, PFBA and nanoplastics synergistically exacerbates neurotoxicity by impairing PINK1/Parkin-mediated mitophagy
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Researchers investigated the combined neurotoxic effects of two PFAS chemicals (PFOA and PFBA) with nanoplastics using zebrafish and human neuronal cells. They found that co-exposure synergistically worsened neurodevelopmental impairments and behavioral abnormalities by disrupting a key cellular cleanup pathway called PINK1/Parkin-mediated mitophagy. The study suggests that nanoplastics can amplify the neurotoxicity of PFAS compounds by impairing the cells' ability to clear damaged mitochondria.
Aged nanoplastics reprogram the ER stress-autophagy crosstalk: A mechanistic gateway to skeletal malformations in zebrafish
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Researchers exposed zebrafish embryos to both new and UV-aged nanoplastics and found that the aged particles caused significantly worse skeletal deformities, higher mortality, and lower hatching rates. The aged nanoplastics disrupted cellular stress responses and a self-cleaning process called autophagy in developing bone and cartilage cells. The study suggests that weathered nanoplastics in the environment may pose greater developmental risks than freshly produced particles.
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.
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