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The potential toxicity of Zinc oxide nanoparticles (ZnO NPs) to human beings has become a widespread concern. This study explored the reproductive toxicity and the mechanism of toxicity of ZnO NPs in early pregnant mice. The results showed that abnormal weight changes, induced inflammation, reduced level of serum sex hormones, damaged uterus, increased abortion, and abnormal development of fetus. In the uterus, the transcription levels of ZnT‐1, HO‐1, Bax, Bax/Bcl‐2, JNK, and Caspase‐3 were significantly up‐regulated while Bcl‐2, ER‐1 and PR were significantly down‐regulated. The TUNEL‐positive cells increased that were exposed to high levels of ZnO NPs. In summary, those results indicated that Zn from high levels of exposure to ZnO NPs accumulated in the uterus that could have caused the formation of ROS that led to oxidative stress, which might have activated the mitochondrial apoptotic pathway that could have caused the uterine injury which induced the observed reproductive toxicity. [ABSTRACT FROM AUTHOR]

ZnO nanoparticles (NPs) are among the most manufactured nanoparticles in the consumer products, industries, and researches. An increasing body of evidence indicated that ZnO NPs show toxicological effects in vivo. Sex differences in the toxicity of ZnO NPs are not clear, thus the aim of this study was to investigate the effects of ZnO NPs on the female and male reproductive organs (uterus, ovary and testes). ZnO NPs were orally administered to female and male mice at dosages level of 0 and 100 mg/kg body weight. The biological material was sampled 3 days after tube feeding. The results demonstrated that Zinc contents were accumulated in the reproductive organs of treated mice. Furthermore, ZnO NPs administration induced significant decrease in the testes weight, an imbalance of hematological and serum biochemical parameters in male mice. The histopathological examinations showed that structural disorder and the appearance of cell apoptosis and death in the ZnO NPs‐exposed mice. Additionally, the RT‐qPCR data indicated ZnO NPs can activate mitochondrial‐mediated signaling pathway and induce caspase depend damage that ultimately injured the uterus. In the ovary, ZnO NPs induce cell apoptosis in Shh pathway activated ovary cells, and affect the synthesis of steroidogenesis. In the testes, ZnO NPs effectively changed the expression level of genes related to oxidant stress, detox/metabolic process, and apoptosis. It was found that ZnO NPs caused more serious reproductive toxicity in the male mice than female mice. Overall, these findings indicated that ZnO NPs could induce exposure‐related risks to reproductive health, especially in those who are at the occupational level. [ABSTRACT FROM AUTHOR]