What question did this study set out to answer?

This study aims to investigate the effects of polystyrene microplastics on female reproductive health, specifically oocyte maturation.

March 21, 2026Environmental Sciences Europe0 citationsOpen Access

Polystyrene microplastics impair mouse oocyte maturation by interfering with fatty acid oxidation

ZLZhiqiang LiuChina Agricultural University XHXiaohan HuangChina Agricultural University YYYu YuChina Agricultural University

Key Points

This study aims to investigate the effects of polystyrene microplastics on female reproductive health, specifically oocyte maturation.
Female mice were exposed to varying doses of polystyrene microplastics via intragastric administration for 35 days.
Assessment of oocyte maturation was conducted by examining polar body extrusion and oxidative stress markers.
RNA sequencing analyzed changes in gene expression related to fatty acid oxidation and reproductive health.
Exposure to the highest PS-MPs dose (30 mg/kg) significantly reduced polar body extrusion and glutathione levels.
Oocytes exhibited increased spindle abnormalities and lipid droplet accumulation after PS-MP treatment.
Treatment with BEC2 partially reversed the negative effects of PS-MPs on fatty acid oxidation and improved oocyte maturation.

Abstract

Microplastics (MPs) represent a significant environmental pollutant and have raised considerable concern due to their tendency to accumulate in animals, plants, and humans, thereby posing potential health risks. In this study, female mice were exposed to different doses of polystyrene microplastics (PS-MPs) (0, 0.3, 3, and 30 mg/kg) via intragastric administration for 35 days to investigate their effects on female reproductive health. The results showed a significant reduction in first polar body extrusion (PBE) and glutathione (GSH) levels, accompanied by increased reactive oxygen species (ROS) levels in germinal vesicle (GV) stage oocytes in the 30 mg/kg group. Based on these findings, the 30 mg/kg dose was selected for subsequent reproductive toxicity assessments. Compared with the control group, oocytes from the PS-MPs treated group exhibited a significant increase in spindle abnormalities and lipid droplet accumulation. RNA sequencing and experimental validation in mouse oocytes demonstrated that PS-MPs exposure led to upregulation of SIRT4 protein expression and downregulation of genes associated with fatty acid oxidation. Treatment with BEC2, a CPT1A activator, partially reversed the inhibitory effects of PS-MPs on fatty acid oxidation and improved oocyte maturation. Further analyses revealed that PS-MPs exposure reduced HSPA1A protein expression, potentially contributing to the activation of endoplasmic reticulum (ER) stress in ovarian cells. In addition, PS-MP exposure significantly altered the expression of genes related to ovarian fibrosis, angiogenesis, and aging. Knockdown of Hspa1a in the mouse granulosa cell line KK1 reduced cell proliferation and viability, induced G2/M cell cycle arrest, and triggered ER stress. Collectively, these findings suggest that PS-MPs exposure may accelerate ovarian aging by disrupting protein homeostasis and impair oocyte maturation in mice by disrupting fatty acid oxidation.

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