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Maternal Exposure to Polystyrene Nanoplastics Disrupts Spermatogenesis in Mouse Offspring by Inducing Prdm14 Overexpression in Undifferentiated Spermatogonia
Summary
When pregnant mice were exposed to nanoplastics (extremely small plastic particles), their male offspring had lower testosterone, fewer sperm, and damaged sperm-producing cells. The nanoplastics caused inflammation in the cells responsible for sperm production, disrupting a key gene (Prdm14) that controls sperm development. This suggests that a mother's plastic exposure during pregnancy could affect her sons' fertility later in life.
Undifferentiated spermatogonia (Undiff-SPG) plays a critical role in maintaining continual spermatogenesis. However, the toxic effects and molecular mechanisms of maternal exposure to nanoplastics on offspring Undiff-SPG remain elusive. Here, we utilized a multiomics combined cytomorphological approach to explore the reproductive toxicity and mechanisms of polystyrene nanoplastics (PS-NPs) on offspring Undiff-SPG in mice after maternal exposure. The results indicated that PS-NPs decreased testosterone levels and reduced sperm concentration and quality in offspring male mice through maternal exposure. Moreover, PS-NPs could enter offspring Undiff-SPG, increase ROS levels, and decrease the viability of Undiff-SPG. According to the transcriptomics and proteomics analyses, PS-NPs caused offspring male mice Undiff-SPG inflammation by increasing the expression of Tnfsf18/Nlrp6. Mechanistically, we found that inflammation induced overexpression of the transcription factor Prdm14 in Undiff-SPG, which suppressed the expression of Ccdc33 and Tcirg1. Additionally, PS-NPs disrupted offspring spermatogenesis by inhibiting the Osbp2/Zcwpw1/Dhps expression. Furthermore, PS-NPs reduced the Undiff-SPG autophagic flux by reducing the expression of Igbp1/Gabarapl2. In conclusion, maternal exposure to PS-NPs caused inflammation in offspring Undiff-SPG, which resulted in Prdm14 overexpression that could disrupt spermatogenesis and normal autophagy.
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