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Polystyrene/polylactic acid microplastics impair transzonal projections and oocyte maturation via gut microbiota-mediated lipoprotein lipase inhibition
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Researchers found that both conventional polystyrene and biodegradable polylactic acid microplastics impaired egg development and fertility in female mice by disrupting the connections between egg cells and their surrounding support cells. The microplastics altered gut bacteria, which led to metabolic changes that reduced a key enzyme needed for healthy ovarian function. The study suggests that microplastic exposure could affect reproductive health through the gut-ovary connection, and that biodegradable plastics are not necessarily safer.
This study focuses on the impacts of polystyrene/polylactic acid microplastics (PS/PLA-MPs) on ovarian reserve and oocyte maturation in female mice, along with the underlying mechanisms. 1 μm PS-MPs and PLA-MPs were prepared, with PLA-MPs having a rougher surface and broader size distribution. In vitro, PLA-MPs showed higher cytotoxicity to granulosa cells compared to PS-MPs. In vivo, MPs exposure disrupted the estrous cycle, and damaged ovarian reserve. Granulosa cell apoptosis and cytokine activation led to transzonal projection retraction, oocyte oxidative stress, meiotic abnormalities, and reduced oocyte retrieval and polar body extrusion rate, thus reducing litter size. PS-MPs induced more severe intestinal and ovarian impairment. Analysis of feces 16S rRNA, serum metabolomics, and ovarian RNA sequencing revealed that lipoprotein lipase (LPL) was suppressed by both MPs, linking gut microbiota, lipid metabolism, and ovarian injury. Fecal microbiota transplantation as a rescue strategy in MPs exposed mice upregulated LPL, alleviating ovarian reserve decline. In PLA-MPs exposed mice, ovarian reserve related indicators partially recovered after a two-week exposure cessation. These results clarify the similarities and differences in how PS-MPs and PLA-MPs impair ovarian function via gut-ovary axis and lipid metabolism dysregulation.
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Impact of polystyrene microplastics (PS-MPs) on the entire female mouse reproductive cycle: Assessing reproductive toxicity of microplastics through in vitro follicle culture
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Female mice exposed to polystyrene microplastics suffered significant damage to their reproductive systems, including ovarian cell death, abnormal egg development, and fewer offspring. The microplastics accumulated in the ovaries and triggered cell death pathways while disrupting survival signaling in the cells that support egg development, suggesting microplastic exposure could contribute to declining fertility.
Gut microbiota participates in polystyrene microplastics-induced defective implantation through impairing uterine receptivity
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Researchers found that oral exposure to polystyrene microplastics in mice impaired the ability of embryos to implant in the uterus by disrupting uterine receptivity. The study revealed that microplastics altered gut bacteria composition, which in turn affected hormone signaling and gene expression in the uterus. These findings suggest a gut-reproductive axis through which microplastic exposure could potentially affect fertility.
Characterization of microplastics in human follicular fluid and assessment of their potential impact on mouse oocyte maturation in vitro
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Scientists found microplastics in human follicular fluid, the liquid surrounding eggs in the ovaries, after analyzing samples from 19 women. When they tested how these particles affect egg development in mice, they found that certain types of microplastics reduced the ability of eggs to mature properly, raising concerns about potential effects on fertility.
Polystyrene microplastics induced female reproductive toxicity in mice
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Researchers exposed female mice to polystyrene microplastics for 35 days and found the particles accumulated in multiple organs including the ovaries, where they caused inflammation and oxidative stress. The microplastics reduced egg quality by lowering protective antioxidants, disrupting mitochondrial function, and altering calcium levels in the cells. This study provides evidence that microplastic exposure could harm female fertility by directly damaging the ovaries and the eggs they produce.
Polystyrene nanoplastics induce apoptosis, autophagy, and steroidogenesis disruption in granulosa cells to reduce oocyte quality and fertility by inhibiting the PI3K/AKT pathway in female mice
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Researchers found that polystyrene nanoplastics (tiny plastic particles under 1 micrometer) impair egg cell quality in female mice by damaging the ovarian support cells that help eggs mature, triggering cell death and disrupting hormone production. These findings raise important questions about the potential reproductive risks of nanoplastic exposure in women.
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