0
Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Gut & Microbiome Nanoplastics Reproductive & Development Sign in to save

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. Score: 58 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
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.

Sign in to start a discussion.

More Papers Like This

Article Tier 2

Maternal exposure to polystyrene microplastics alters placental metabolism in mice

Researchers exposed pregnant mice to polystyrene microplastics and examined how placental metabolism was affected. The study found significant changes in placental metabolic pathways that could help explain the fetal growth restriction previously observed in microplastic-exposed pregnancies. These findings suggest that microplastic exposure during pregnancy may interfere with the placenta's ability to support normal fetal development.

Article Tier 2

Maternal Exposure to Polystyrene Micro- and Nanoplastics Causes Fetal Growth Restriction in Mice

Researchers exposed pregnant mice to polystyrene micro and nanoplastics and found that exposure caused fetal growth restriction and placental abnormalities. The study observed that plastic particles accumulated in placental tissue and disrupted normal placental function. These findings raise concern that maternal exposure to plastic particles during pregnancy may interfere with fetal development.

Article Tier 2

Polystyrene nanoparticles induced adverse pregnancy outcomes via the activation of placental ferroptosis and gut microbiota dysfunction

Researchers exposed pregnant mice to 50-nanometer polystyrene nanoparticles and found that the particles caused adverse pregnancy outcomes through two interconnected mechanisms: disruption of gut microbiota and activation of ferroptosis in placental tissue. The nanoparticle exposure altered the composition of beneficial gut bacteria and triggered iron-dependent cell death in the placenta. The study suggests that maternal exposure to nanoplastics during pregnancy may threaten reproductive health through gut-placenta axis disruption.

Article Tier 2

Maternal exposure to polystyrene nanoparticles retarded fetal growth and triggered metabolic disorders of placenta and fetus in mice

Researchers exposed pregnant mice to polystyrene nanoplastics through drinking water and found that higher concentrations led to significantly reduced fetal weight. The nanoplastics caused abnormal cell structures in the placenta and disrupted metabolic processes in both placental tissue and fetal livers. The study suggests that maternal nanoplastic exposure during pregnancy can cross the placental barrier and interfere with normal fetal growth and metabolism.

Article Tier 2

Intergenerational neurotoxicity of polystyrene nanoplastics in offspring mice is mediated by dysfunctional microbe-gut-brain axis

Researchers found that mother mice exposed to polystyrene nanoplastics during pregnancy and nursing passed neurological harm to their offspring, with the babies showing brain inflammation, disrupted dopamine and serotonin signaling, and gut microbiome imbalances — suggesting that nanoplastic exposure before birth can damage the developing brain through the gut-brain connection.

Share this paper