Antimony (Sb) is a metalloid, widely presents in the environment and associates with human health. In this study, we aimed to decipher whether Sb exposure is harmful to female reproduction and explore the underlying mechanisms. The ICR mice were exposed to 0, 5, 10, and 20 mg/kg acetate potassium Sb tartrate trihydrate by intraperitoneal injection for 10 days, then mouse oocytes were collected for further analysis. We first found a significant decrease in the proportion of MII-stage oocytes obtained from supernumerary ovulation in the fallopian tubes and early embryo development under Sb treatment. Then a series of tests showed Sb affects oocyte maturation by damaging the cytoskeleton of microtubule and actin. Moreover, the abnormal distribution of cortical granules and their component Ovastacin in oocytes, combined with reduced expression levels of Juno, affected sperm-oocyte binding and led to fertilization failure. Based on the sequencing results and experimental validation, it was demonstrated that Sb exposure impairs mitochondrial distribution and membrane potential, elevated levels of mitochondrial superoxide, finally caused energy supply deficits. Mitochondrial damage in oocytes after Sb exposure results in the excessive oxidative stress and early apoptosis. Taken together, these data suggest that Sb exposure decreases oocyte quality and female fertilization ability by impairing mitochondrial function and redox perturbation.

Placental trophoblast dysfunction is one of the main causes of missed abortion (MA). The expression and regulation of specific molecules play crucial roles in this complex process. Among these, human deoxycytidine triphosphate pyrophosphatase 1 (DCTPP1), a key enzyme, not only participates in nucleotide metabolism but also plays an indispensable role in maintaining genomic stability. To delve deeper into the mechanism of DCTPP1 in placental trophoblast cell function, we used an immortalized human first-trimester extravillous trophoblast cell line (HTR8/SVneo) as an experimental model for functional studies. A decrease in DCTPP1 expression leads to an increase in oxidative stress and decreased cell viability ultimately leading to apoptosis. Further analysis revealed an interaction between DCTPP1 and the AU-rich element RNA-binding protein 1 (AUF1). A decrease of AUF1 induced oxidative stress imbalance, leading to apoptosis in HTR8/SVneo cells. These findings highlight DCTPP1 as a potential biomarker and an effective drug target for the treatment or prevention of MA.

染色体黏合是细胞分裂过程中由一环状蛋白复合物黏合素（cohesin）将染色体单体聚合在一起的细胞生物学过程，确保了染色体在后期的精确分离。除了黏合素，还有许多辅助因子共同参与组成了染色体黏合蛋白家族，在染色体黏合的建立、维持及解离过程中发挥重要功能。此外，该家族蛋白还参与调控DNA损伤修复、基因表达以及染色质高级结构形成等事件。虽然染色体黏合蛋白的功能和调控机理在有丝分裂中得到了比较深入的研究，但其在减数分裂，特别是第一次减数分裂中的作用及机制还不完全明确。本文对染色体黏合蛋白在各种生物学事件中的功能进行了概述，尤其阐释了它们在生殖细胞减数分裂中的非经典作用，并探讨了该领域未来的发展方向。