The effect of reproductive toxicity induced by ZnO NPs in mice during early pregnancy through mitochondrial apoptotic pathway.
Ling ChenHaifang WuWuding HongZoraida P AguilarFen FuHengyi XuPublished in: Environmental toxicology (2021)
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.
Keyphrases
- oxide nanoparticles
- oxidative stress
- induced apoptosis
- diabetic rats
- cell death
- room temperature
- quantum dots
- dna damage
- endoplasmic reticulum stress
- reduced graphene oxide
- signaling pathway
- transcription factor
- cell cycle arrest
- high glucose
- ischemia reperfusion injury
- visible light
- light emitting
- endothelial cells
- physical activity
- pi k akt
- pregnant women
- climate change
- risk assessment
- heavy metals
- skeletal muscle
- gold nanoparticles
- wild type
- pluripotent stem cells