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Maternal polystyrene nanoplastics suppress zebrafish offspring development and locomotion through mitochondrial dysfunction
Summary
Researchers found that zebrafish mothers exposed to nanoplastics at environmentally relevant concentrations passed developmental harm to offspring, with transcriptomic analysis pointing to suppressed oxidative phosphorylation genes as the mechanism — showing nanoplastics can impair embryo energy metabolism across generations even when offspring are not directly exposed.
Plastic pollution is ubiquitous in aquatic ecosystem, posing growing threats to ecosystem health. Maternal transfer of polystyrene nanoplastics (PS-NPs) is known to impair offspring development, yet the underlying molecular mechanisms driving these transgenerational effects remain poorly understood. This study aimed to elucidate the mechanisms by which maternal PS-NPs exposure disrupts embryonic development and locomotion in zebrafish offspring, with a specific focus on mitochondrial dysfunction. We investigated the transgenerational consequences of maternal exposure to environmentally relevant concentrations (1-100 μg/L) of europium-chelated PS-NPs (50 nm PS-Eu) over 120 days. Developmental, behavioral, mitochondrial respiration, and transcriptomic endpoints were assessed in offspring. Keys findings revealed that maternal exposure to 10 (p < 0.01) and 100 μg/L (p < 0.001) PS-Eu significantly reduced offspring head area and body length while increasing malformation rates compared to controls. Locomotor behavior was markedly inhibited in offspring from mother exposed to 10 (p < 0.01) and 100 μg/L PS-Eu (p < 0.05). Furthermore, maternal exposure to 100 μg/L PS-Eu suppressed offspring mitochondrial respiration including reduced basal respiration (p < 0.01), ATP-linked respiration (p < 0.01), and maximal respiration (p < 0.05). Transcriptomic analysis identified oxidative phosphorylation as the most significantly suppressed pathway, with 15 related genes (e.g., atp5po, uqcrq, atp5pd, atp5l, atp6v0a2b, uqcrc2a, and others) downregulated. Protein-protein interaction networks pinpointed atp5po, uqcrq, atp5pd, and atp5l as hub genes, and their suppression was validated via RT-qPCR. These integrated results demonstrate that maternal PS-NPs inhibit embryonic development and locomotion in offspring, by disrupting mitochondrial energy metabolism and oxidative phosphorylation-related genes. Our study provides crucial mechanistic understanding of maternal PS-NPs toxicity and contributes significantly to environmental risk assessments for nanoplastics in aquatic species.
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