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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.
Micro(nano)plastics (MNPs) are pervasive in aquatic environments, with aged MNPs being the predominant form due to environmental weathering. However, their developmental toxicity, particularly regarding skeletal formation, remains poorly understood. In this study, aged polystyrene nanoplastics (PSNPs) were prepared via 48-hour UV irradiation and compared with pristine PSNPs in zebrafish embryo exposures starting within 4 h post-fertilization (hpf) and lasting for 7 days. Both pristine and aged PSNPs induced skeletal malformations, but aged PSNPs caused more severe effects, including decreased hatching rates, increased mortality, and altered larval body length. Histopathological analysis revealed disrupted muscle fiber organization and lipid accumulation in the yolk sac. Elevated reactive oxygen species (ROS) and calcium ion levels were observed in both treatment groups. Aged PSNPs significantly upregulated GRP78 and RAB7 protein expression, increased transcription of the Endoplasmic Reticulum stress (ER stress) marker eif2α, and downregulated key genes involved in bone development (bmp2b, bmp4) and autophagy (atg13, atg5). These findings indicate that aged PSNPs exacerbate oxidative stress, activate ER stress pathways, inhibit autophagy, and impair skeletal development. This study highlights the heightened developmental toxicity of environmentally aged MNPs and underscores the necessity of including aged plastic particles in ecological risk assessments.
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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.
Aged polystyrene microplastics exposure affects apoptosis via inducing mitochondrial dysfunction and oxidative stress in early life of zebrafish
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Zebrafish embryos exposed to UV-aged polystyrene microplastics at environmental concentrations showed more severe developmental problems than those exposed to fresh microplastics. The aged particles caused greater oxidative stress and mitochondrial damage, triggering increased cell death during early development -- suggesting that weathered microplastics in the real environment may be more harmful than the pristine particles typically used in lab studies.
Impact of virgin and weathered microplastics on zebrafish: Bioaccumulation, developmental toxicity and molecular pathway disruptions
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Researchers compared the effects of brand-new versus environmentally weathered microplastics on zebrafish larvae and found that weathered particles were far more toxic, causing 80% mortality compared to 20% for new plastics. The weathered microplastics triggered more severe disruptions to oxidative stress pathways, cell death signaling, and DNA repair mechanisms. The study emphasizes that laboratory tests using only pristine microplastics may significantly underestimate the real-world dangers of plastic pollution.
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.
The neurodevelopmental toxicity induced by combined exposure of nanoplastics and penicillin in embryonic zebrafish: The role of aging processes
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Researchers studied how nanoplastics combined with the antibiotic penicillin affect brain development in zebrafish embryos, including how aging of the nanoplastics changes their toxicity. They found that pristine and UV-aged nanoplastics combined with penicillin caused more severe neurodevelopmental harm than either substance alone, suppressing heartbeat and movement. The findings suggest that environmental aging of nanoplastics can alter their interactions with common pollutants like antibiotics, potentially increasing risks to developing organisms.
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