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Updated: Jun 25, 2026

Studying Neurobehavioral Effects of Environmental Pollutants on Zebrafish Larvae
Published on: February 5, 2020
Maternal polystyrene nanoplastics suppress zebrafish offspring development and locomotion through mitochondrial
Fangjie Cao1, Bingyue Liu2, Xinran Hou3
1National-Regional Joint Engineering Research Center for Soil Pollution Control and Remediation in South China, Guangdong Key Laboratory of Integrated Agro-environmental Pollution Control and Management, Institute of Eco-environmental and Soil Sciences, Guangdong Academy of Sciences, Guangzhou, 510650, China.
Abstract:
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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