Zinc oxide nanoparticle causes toxicity to the development of mouse oocyte and early embryo

Zinc oxide nanoparticle (ZnO NP) is one of the most widely used nanomaterial in industrial and commercial products. Here, we reported hazardous effects of ZnO NP on the development of mouse oocyte and pre implantation embryo. ZnO NP compromises meiosis partially by induction of oxidative stress as antioxidant rescues the development of ZnO NP-exposed oocytes, albeit with limited efficiency. It causes mitochondrialand endoplasmic reticulum stresss which thereby activates autophagy and apoptosis to trigger oocyte demise. Examining ZnO NP-exposed oocytes that complete M-phase entry witnesses a disruption in meiotic cytoskeleton architecture. Intriguingly, loss of Grp78, a chaperone in the ER, phenocopies ZnO NP-induced meiotic defects and cytoskeleton disorganization. Importantly however, ZnO NP commences cytotoxicity by more than releasing of Zn2+ in that ZnCl2 to a much less extent recapitulates ZnO NP-induced phenomena. The prevailing DNA damage is another causative to developmental arrest and degeneration of oocytes and early embryos, but compared with oocytes, embryos are more sensitive to ZnO NP and succumb to death. ZnO NP is demonstrated in this study to be toxic for oocytes and enbryos in mammals, which warrants careful evaluation of human exposure with regard to its influence on reproductive health. (C) 2022 Elsevier B.V. All rights reserved.

Automated summary

This study reported the hazardous effects of zinc oxide nanoparticles (ZnO NP) on the development of mouse oocytes and pre-implantation embryos. ZnO NP compromised the meiosis process, caused cellular stress, activated autophagy and apoptosis, disrupted cytoskeleton architecture, and induced DNA damage, leading to developmental arrest and degeneration of oocytes and early embryos. The study suggests that ZnO NP is toxic to oocytes and embryos in mammals, highlighting the need for careful evaluation of human exposure and its impact on reproductive health.