The growing use of zinc oxide nanoparticles (ZnO NPs) in various applications has raised many concerns about the potential risks to human health. In this research, the protective effects of cellular oxidative stress inhibitor N-Acetyl-cysteine (NAC) and endoplasmic reticulum (ER) stress inhibitor Salubrinal (Sal) on reproductive toxicity induced by ZnO NPs were investigated. The results showed that application of these two kinds of cell stress inhibitors after oral ingestion of ZnO NPs could prevent the weight loss of pregnant mice; reduce zinc content in the uterus, placenta and fetus; reduce abnormal development of the offspring; and decrease fetal abortion. Furthermore, RT-qPCR and immunofluorescence assay results indicated that NAC restored the expression of Gclc, reduced the expression of ATF4, JNK and Caspase-12, and decreased the expression of eNOS and IGF-1, in the placenta. Sal decreased the expression of ATF4, JNK and Caspase-12, and increased the expression of eNOS and IGF-1caused by the oral ingestion of ZnO NPs. These results indicated that treatment with NAC and Sal after oral exposure could reduce reproductive and development toxicity caused by ZnO NPs which induced reproductive and development toxicity that was probably caused by the activation of oxide stress and ER stress.

氧化锌纳米颗粒（ZnO NPs）在各种应用中的日益增长的使用引起了人们对人类健康潜在风险的许多担忧。在这项研究中，研究了细胞氧化应激抑制剂N-乙酰半胱氨酸（NAC）和内质网（ER）应激抑制剂Salubrinal（Sal）对ZnO NPs诱导的生殖毒性的保护作用。结果表明，口服摄入ZnO NPs后使用这两种细胞应激抑制剂可以预防妊娠小鼠的体重减轻。减少子宫，胎盘和胎儿中的锌含量；减少后代的异常发育；并减少胎儿流产。进一步的RT-qPCR和免疫荧光检测结果表明，NAC可以恢复Gclc的表达，降低Gclc的表达。ATF4，JNK和Caspase-12并降低了胎盘中eNOS和IGF-1的表达。Sal会降低口服ZnO NPs引起的ATF4，JNK和Caspase-12的表达，并增加eNOS和IGF-1的表达。这些结果表明，口服暴露后用NAC和Sal治疗可以减少ZnO NPs引起的生殖和发育毒性，而ZnO NPs可能引起氧化应激和ER应激的激活而引起生殖和发育毒性。