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Polystyrene microplastics impaired decidualization in mice via oxidative stress and inflammation and disrupted the reproductive function of their female offspring
Summary
Mouse experiments found that polystyrene microplastics impaired uterine decidualization and embryo implantation via oxidative stress and inflammation, and that maternal PS-MP exposure also disrupted the reproductive function of female offspring.
The extensive utilization of plastics has heightened concerns regarding microplastics exposure. However, the effects of polystyrene microplastics (PS-MPs) on early pregnancy remain inadequately investigated. This study aimed to examine the impact of PS-MPs on decidualization and embryo implantation in female mice, as well as the reproductive function of their offspring following maternal exposure to PS-MPs. We investigated the harmful effects of different PS-MPs sizes on mouse endometrial stromal cells (mESCs) during in vitro decidualization. Pregnant mice were orally given various concentrations of PS-MPs to examine their impact on decidualization. We evaluated oxidative stress and inflammation markers to understand their roles in abnormal decidualization. Additionally, we assessed potential reproductive health impacts on female offspring. Our findings indicated that 5 µm PS-MPs effectively penetrated mESCs and significantly disrupted decidualization compared to smaller or larger particles. Pregnant mice that were exposed to 5 µm PS-MPs at a dose of 1000 mg/(kg·day) exhibited substantial reductions in the decidual area and downregulation of decidualization markers such as BMP2. Inflammatory cytokines increased significantly in mESCs following 5 µm PS-MPs exposure, and the elevated malondialdehyde levels in uterine tissue were mitigated by antioxidant treatment. Moreover, offspring exhibited decreased uterine wet weight, uterine organ coefficients, decidual areas, and expression of BMP2 due to maternal exposure to PS-MPs. These results highlighted the detrimental effects of PS-MPs on maternal decidualization and embryo implantation, suggesting a link to oxidative stress and inflammation, and maternal exposure to PS-MPs during pregnancy impaired reproductive function in offspring females.
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