Abstract
Zinc oxide (ZnO) nanoparticles (NPs) are extensively utilized in the commercial and biomedical sectors, posing heightened risks of potential cytotoxicity through various mechanisms. Nonetheless, the regulatory framework governing the gestational toxicity of ZnO NPs and the corresponding intervention strategies remain largely obscure. In this study, using the Drosophila model, we observed that gestational exposure to ZnO NPs led to growth and developmental anomalies in a dose-dependent manner when compared with the control (no ZnO NP exposure). Subsequent dietary administration of Quercetin and Astragaloside IV resulted in effective mitigation of the developmental toxicity induced by exposure to ZnO NPs. Moreover, the latter also triggered activation of the ferroptosis pathway. The associated parameters were successfully ameliorated by the administration of Quercetin and Astragaloside IV. Notably, treatment with Ferrostatin-1 also alleviated developmental disorders arising from exposure to ZnO NPs. In conclusion, our investigation demonstrated that exposure to ZnO NPs during gestation interfered with growth and development via the ferroptosis pathway, underscoring the significance of dietary supplementation with Quercetin and Astragaloside IV for protection against developmental toxicity.