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ZnO NPs 经早期妊娠小鼠生殖毒性作用及其线粒体凋亡途径的研究。

The effect of reproductive toxicity induced by ZnO NPs in mice during early pregnancy through mitochondrial apoptotic pathway.

机构信息

The Second Affiliated Hospital of Nanchang University, Nanchang University, Nanchang, China.

State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang, China.

出版信息

Environ Toxicol. 2021 Jun;36(6):1143-1151. doi: 10.1002/tox.23113. Epub 2021 Feb 18.

DOI:10.1002/tox.23113
PMID:33599401
Abstract

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.

摘要

氧化锌纳米粒子(ZnO NPs)对人类的潜在毒性已经引起了广泛关注。本研究探讨了 ZnO NPs 对孕早期小鼠的生殖毒性及其毒性机制。结果表明,ZnO NPs 可引起体重异常变化、诱导炎症、降低血清性激素水平、损伤子宫、增加流产和胎儿发育异常。在子宫中,ZnT-1、HO-1、Bax、Bax/Bcl-2、JNK 和 Caspase-3 的转录水平显著上调,而 Bcl-2、ER-1 和 PR 则显著下调。暴露于高水平 ZnO NPs 的 TUNEL 阳性细胞增加。综上所述,这些结果表明,暴露于高水平 ZnO NPs 中的 Zn 可能在子宫中蓄积,导致 ROS 形成,引发氧化应激,从而激活线粒体凋亡途径,导致子宫损伤,进而引起观察到的生殖毒性。

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