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Gut microbiota contributes to polystyrene nanoplastics-induced fetal growth restriction by disturbing placental nicotinamide metabolism

Journal of Nanobiotechnology 2025 4 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Yijing He, Qiao Li, Qinfeng Sun, Heran Li, Tianhang Yu, Miaoyu Chen, Genkui Zhang, Biao Zhang, Weihan Wang, Shiqiang Ju

Summary

Researchers found that pregnant mice exposed to polystyrene nanoplastics experienced placental damage and metabolic disruptions that restricted fetal growth. The nanoplastics altered the mothers' gut bacteria, which in turn disturbed nicotinamide metabolism in the placenta, a key pathway for fetal development. The study suggests that nanoplastic exposure during pregnancy may harm offspring development through indirect effects on the gut-placenta connection.

Polymers
Body Systems
Models

Polystyrene nanoplastics (PS-NPs) are ubiquitous in the environment, eliciting significant concerns about their possible risks to human health, especially reproductive health. Various reproductive toxicities of PS-NPs have been reported, however, information regarding the effects of PS-NPs exposure during pregnancy on offspring development and the underlying mechanisms remains limited. In this study, pregnant mice were orally administered PS-NPs (approximately 100 nm in diameter) at different concentrations (1, 10, and 100 mg/kg/day) for 17.5 consecutive days, from gestational day (GD) 0.5 to GD 17.5. The relevant samples were collected on GD 18.5 to investigate the intergenerational effects. The results indicated that PS-NPs induced placental injury and metabolic abnormalities, leading to adverse pregnancy outcomes. Specifically, PS-NPs exposure observably reduced the levels of nicotinamide (NAM) and nicotinamide adenine dinucleotide (NAD) in the placenta, resulting in decreased ATP production, increased oxidative stress and ferroptosis. Meanwhile, PS-NPs disrupted the maternal gut microbiome, specifically manifested as a reduction in Lactobacillus levels and abundances of norank_f_Muribaculaceae, Turicibacter, Alloprevotella, Parabacteroides and Ruminococcus. Fecal microbial transplant (FMT) experiments demonstrated that the microbiota from PS-NPs-administered pregnant mice could similarly induce intestinal barrier damages and placental injury. Treatment with NAM effectively mitigated disruptions in placental metabolism and reversed the adverse pregnancy outcomes caused by PS-NPs. These findings highlight the novel role of the gut microbiota in PS-NPs-induced placental injury and adverse pregnancy outcomes, and suggest that NAM could serve as a promising preventative strategy against this intergenerational damage caused by PS-NPs.

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