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Investigating polystyrene nanoplastics-induced reproductive toxicity in vitro: Focus on Nrf2-PKM2-autophagy signaling pathway
Summary
This lab study investigated how polystyrene nanoplastics damage male reproductive cells, finding they triggered autophagy (cellular self-digestion) and disrupted key proteins in a signaling pathway important for sperm cell survival. The findings suggest nanoplastics could impair male fertility by causing programmed cell death in testicular cells. This adds to growing evidence that plastic nanoparticles can harm reproductive health.
Abstract As an issue of widespread concern, microplastics pollution has emerged as a harmful environmental pollutant. Nanoplastics (NaPs) has reported to accumulate in the testes and cause degeneration in the seminiferous tubules. However, the current research involving NaPs-induced reproductive toxicity remains poorly understood. The current work aimed to investigate the mechanisms of NaPs-induced reproductive injury in vitro . At first, we found that 80 nm fluorescent NaPs could enter into GC-2spd(ts) cells by fluorescent inverted microscope. Our results also demonstrated that suppression of reactive oxygen species (ROS) inhibited NaPs-triggered mitochondrial apoptosis and autophagy in GC-2spd(ts) cells. We also found that NaPs treatment did not change the interaction between nuclear factor erythroid-derived 2-related factor (Nrf2) and Kelch-like ECH associated protein 1 (Keap1), while inhibiting nuclear accumulation of Nrf2 protein. Further in vitro experiments showed that NaPs-induced reproductive toxicity associated with reducing dimerize pyruvate kinase M2 (PKM2), which are ascribed to the loss of Nrf2. Meanwhile, improving nuclear accumulation of Nrf2 might interact with PKM2 to rescue mitochondrial apoptosis caused by NaPs. Together, this study highlight that disturbing Nrf2-PKM2 signaling is essential process of NaPs-induced reproductive toxicity and provide valuable insights into the mechanism of microplastics-induced reproductive toxicity.