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The effect of reproductive toxicity induced by ZnO NPs in mice during early pregnancy through mitochondrial apoptotic pathway
Environmental Toxicology ( IF 4.5 ) Pub Date : 2021-02-18 , DOI: 10.1002/tox.23113
Ling Chen 1, 2 , Haifang Wu 2, 3 , Wuding Hong 2 , Zoraida P. Aguilar 4 , Fen Fu 1 , Hengyi Xu 2
Affiliation  

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.

中文翻译:

ZnO NPs诱导的线粒体凋亡途径对孕早期小鼠生殖毒性的影响

氧化锌纳米颗粒(ZnO NPs)对人类的潜在毒性已成为广泛关注的问题。本研究探讨了ZnO NPs对早期妊娠小鼠的生殖毒性及其毒性机理。结果显示体重异常变化,诱发炎症,血清性激素水平降低,子宫受损,流产增加和胎儿发育异常。在子宫中,ZnT-1,HO-1,Bax,Bax / Bcl-2,JNK和Caspase-3的转录水平显着上调,而Bcl-2,ER-1和PR的转录水平显着下调。 。暴露于高水平的ZnO NPs的TUNEL阳性细胞增加。总而言之,这些结果表明,高水平暴露于子宫中积累的ZnO NPs中的Zn可能导致ROS形成,从而导致氧化应激,
更新日期:2021-04-20
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