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Introduction Zinc oxide nanoparticles (ZnO NPs) participate in all aspects of our lives, but with their wide application, more and more disadvantages are exposed. The goal of this study was to investigate the toxicity of ZnO NPs in female mice ovaries and explore its potential mechanism. Methods In this study, adult female mice were orally exposed to 0, 100, 200, and 400 mg/kg ZnO NPs for 7 days. We explored the underlying mechanisms via the intraperitoneal injection of N-acetyl-cysteine (NAC), an inhibitor of oxidative stress, and salubrinal (Sal), an inhibitor of endoplasmic reticulum (ER) stress. Results The results indicated that serum estradiol and progesterone levels declined greatly with increasing ZnO NPs dosage. Hematoxylin and eosin (HE) staining revealed increased atretic follicles and exfoliated follicular granulosa cells. Moreover, at the transcriptional level, antioxidant-related genes such as Keap1 and Nrf2 , and ER stress-related genes PERK, eIF2α , and ATF4 were markedly upregulated. In addition, the expression of Caspase12, Caspase9 , and Caspase3 , which are genes related to apoptosis, was also upregulated in all ZnO NPs treatment groups. Serum malondialdehyde (MDA) content was remarkably up-regulated, whereas superoxide dismutase (SOD) activity was down-regulated. The 400 mg/kg ZnO NPs treatment group suffered the most substantial harm. However, ovarian damage was repaired when NAC and Sal were added to this group. Conclusion ZnO NPs had toxic effects on the ovary of female mice, which were due to oxidative stress, ER stress, and the eventual activation of apoptosis.

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The stem cell origin theory of endometriosis (EMS) is a significant area of new research but the sources of this have yet to be adequately summarized. Existing treatments for EMS are commonly associated with a high recurrence rate; consequently, there is an urgent need to develop new therapeutic measures for the future treatment of this disease from the view of stem cells and gene therapy. Recently, we describe the evidence for the potential sources of EMS stem cells and other key molecules participating in the establishment of lesions, and predict the miRNAs that target these key genes via bioinformatics analysis for further research. The review highlights the origin of EMS stem cells and potential therapy targets.