Premium
The effect of reproductive toxicity induced by ZnO NPs in mice during early pregnancy through mitochondrial apoptotic pathway
Author(s) -
Chen Ling,
Wu Haifang,
Hong Wuding,
Aguilar Zoraida P.,
Fu Fen,
Xu Hengyi
Publication year - 2021
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.23113
Subject(s) - reproductive toxicity , toxicity , apoptosis , oxidative stress , uterus , hormone , andrology , reactive oxygen species , bcl 2 associated x protein , chemistry , inflammation , biology , programmed cell death , endocrinology , microbiology and biotechnology , medicine , caspase 3 , immunology , biochemistry
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.