Silica nanoparticles cause spermatogenesis dysfunction in mice via inducing cell cycle arrest and apoptosis

The widespread use of silica nanoparticles (SiNPs) has increased the risk of human exposure, which raised concerns about their adverse effects on human health, especially the reproductive system. Previous studies have shown that SiNPs could cause damage to reproductive organs, but the specific mechanism is still unclear. In this study, to investigate the underlying mechanism of male reproductive toxicity induced by SiNPs, 40 male mice at the age of 8 weeks were divided into two groups and then intraperitoneally injected with vehicle control or 10 mg/kg SiNPs per day for one week. The results showed that SiNPs could damage testicular structure, perturb spermatogenesis and reduce serum testosterone levels, leading to a decrease in sperm quality and quantity. In addition, the ROS level in the testis of exposed mice was significantly increased, followed by imbalance of the oxidative redox status. Further study revealed that exposure to SiNPs led to cell cycle arrest and apoptosis, as shown by downregulation of the expression of positive cell cycle regulators and the activation of TNF-alpha/TNFR I mediated apoptotic pathway. The results demonstrated that SiNPs could cause testicles injure via inducing oxidative stress and DNA damage which led to cell cycle arrest and apoptosis, and thereby resulting in spermatogenic dysfunction

Automated summary

The widespread use of silica nanoparticles has raised concerns about their adverse effects on human health, particularly on the reproductive system. This study demonstrated that silica nanoparticles can damage testicular structure, perturb spermatogenesis, and reduce testosterone levels, resulting in decreased sperm quality and quantity. Furthermore, exposure to silica nanoparticles induces oxidative stress and DNA damage, leading to cell cycle arrest and apoptosis in the testis, ultimately causing spermatogenic dysfunction.