From mothers to offspring: Polystyrene nanoplastics create a hidden toxic legacy via mitochondrial dysfunction

Plastic pollution has become a global concern, with nanoplastics (NPs) threatening aquatic ecosystems through their persistence, mobility, and biological effects. Although the ecological risks are increasingly recognized, the mechanisms of reproductive and transgenerational toxicity remain unclear. Here, we examined the effects of polystyrene nanoplastics (PSNPs) at 1, 10, 100 μg/L on zebrafish ( Danio rerio ) reproduction and offspring development. Sexually mature females were exposed to PSNPs for 30 days prior to mating with unexposed males, and the F1 progeny were subsequently reared in PSNP-free water. Maternal exposure to PSNPs at 100 μg/L significantly reduced hatching success and increased mortality, whereas lower concentrations caused malformations and premature hatching. These effects persisted in the absence of direct offspring exposure, indicating stable transgenerational toxicity. Transcriptomic and ultrastructural analyses revealed mitochondrial dysfunction in both ovaries and F1 offspring, including abnormal fission, impaired oxidative phosphorylation, and defective mitophagy. Protein expression analyses further indicated distinct molecular mechanisms in ovaries versus offspring. Collectively, our findings demonstrate that mitochondrial damage is the central driver of PSNP-induced transgenerational toxicity, providing novel mechanistic insights into reproductive and heritable risks posed by microplastics (MPs) and underscoring their long-term ecological threat to aquatic populations. • PSNPs exposure induces pronounced mitochondrial damage in zebrafish. • 2.Mitochondria act as the central hub mediating PSNP-induced transgenerational toxicity. • 3.The heritable toxic effects of PSNPs are irreversible across generations. • 4.Distinct mechanistic pathways underlie mitochondrial damage in ovaries and F1 offspring.