| Popis: |
Background: Two-dimensional ultrathin Ti3C2 nanosheets are increasingly being used in biomedical applications owing to their special physicochemical properties. Meanwhile, the biological effects of its exposure, especially on the reproductive system, deserve attention. However, this effect on the reproductive system has not been studied yet. Results: In the present study, we established an in vivo Ti3C2 nanosheet exposure model in mice and an in vitro Ti3C2 nanosheet exposure model in GC-1 cells. In vivo, Ti3C2 nanosheets accumulated in the testes of mice, leading to male reproductive dysfunction, including diminished sperm quantity and quality. Furthermore, they also induced elevated reactive oxygen species (ROS) and DNA damage in testis tissues and activated the DNA damage response signaling pathway (ATM/p53). In vitro, they entered the GC-1 cytoplasm and reduced cell viability. Ti3C2 nanosheets also induced elevated ROS levels and DNA double-strand breaks, activated the ATM/p53 signaling pathway, caused cell cycle arrest in the G1/G0 phase, inhibited proliferation, and increased apoptosis in GC-1 cells. Conclusions: Ti3C2 nanosheet-induced suppression of spermatogonia proliferation disrupted normal spermatogenic function, which was mediated by the ATM/p53 signaling pathway. Thus, our findings shed more lights on the mechanisms of male reproductive toxicity induced by Ti3C2 nanosheets. |
