The accumulation of nanoparticles (NPs) in the female body has raised global concerns regarding potential effects on the reproductive system. This study aimed to investigate the toxic effects of nano-titanium dioxide (nano-TiO₂) exposure on the ovaries and the underlying mechanisms. By establishing a nano-TiO₂ accumulation model in mice, our research systematically evaluated the effects of different concentrations of nano-TiO₂ exposure on the development and reproductive endocrine functions of mice. The results showed that nano-TiO₂ exposure significantly reduced the littering rate, sex hormone levels, and ovarian index of mice, and the effects were dose-dependent. Studies on the mechanisms involved revealed that nano-TiO₂ induces an excessive production of reactive oxygen species (ROS), leading to the potential collapse of the mitochondrial membrane and an increase in the apoptosis rate of granulosa cells, thereby triggering oxidative stress and inhibiting the expression of ovarian-specific genes and granulosa-cell function genes. This study reveals the “dual blow” mechanism of nano-TiO₂-mediated ovarian morphology and function through oxidative stress in granulosa cells, namely directly disrupting cellular homeostasis and interfering with the reproductive-related gene network, ultimately leading to decreased ovarian function. This provides experimental evidence for assessing the reproductive risks of nanomaterials in women.

Porcine reproductive and respiratory syndrome (PRRS), which is caused by the porcine reproductive and respiratory syndrome virus (PRRSV), results in substantial economic losses for the global pig farming industry. A critical step in the infection process is the binding of PRRSV to the CD163 receptor on the surface of porcine alveolar macrophages. This study successfully generated CD163−/− Landrace pigs using CRISPR/Cas9 gene editing technology. Following an experimental challenge with two distinct Type II PRRSV strains, the edited pigs exhibited complete resistance to infection. Virological and pathological examinations confirmed the absence of viral replication and the presence of characteristic pulmonary lesions and other organ damage in CD163−/− pigs. In contrast, wild-type control pigs exhibited high viral loads and severe pulmonary lesions, as well as damage to other organs. Our findings provide direct evidence that CD163 is an essential receptor for PRRSV infection in vivo. The CD163−/− pig model offers an effective genetic strategy for breeding pigs with an inherent resistance to PRRSV.