The effect of reproductive toxicity induced by ZnO NPs in mice during early pregnancy through mitochondrial apoptotic pathway
The effect of reproductive toxicity induced by ZnO NPs in mice during early pregnancy through mitochondrial apoptotic pathway
复制标题
ZnO NPs 通过线粒体凋亡途径对妊娠早期小鼠生殖毒性的影响。
DOI：
10.1002/tox.23113
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发表时间：
2021-02-18
影响因子：
4.5
通讯作者：
Xu, Hengyi
中科院分区：
文献类型：
--
作者：
Chen, Ling;Wu, Haifang;Xu, Hengyi
氧化锌纳米颗粒对人体的潜在毒性已成为人们普遍关注的问题。本研究旨在探讨氧化锌纳米颗粒对早孕小鼠的生殖毒性及其毒性机制。结果表明，异常体重变化，诱发炎症，血清性激素水平降低，子宫受损，流产增加，胎儿发育异常。子宫组织中ZnT-1、HO-1、Bax、Bax/Bcl-2、JNK和Caspase-3的转录水平显著上调，而Bcl-2、ER-1和PR的转录水平显著下调。TUNEL阳性细胞增加，暴露于高水平的ZnO纳米颗粒。总之，这些结果表明，来自高水平暴露于ZnO NPs的Zn在子宫中积累，这可能导致ROS的形成，从而导致氧化应激，这可能激活线粒体凋亡途径，这可能导致子宫损伤，从而诱导观察到的生殖毒性。
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.