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The potential molecular mechanisms underlying these effects included disturbances in redox homeostasis (as evidence by the enhanced production of ROS and reactive nitrogen species), failure of enzymatic and nonenzymatic cytoprotective mechanisms involving the glutathione system as well as nuclear factor kappa B (NF-B) and fibroblast growth factor 2-mediated pathways, and impaired mitochondrial function

Further research revealed that during regular ovulation in women, ovarian epithelial cells undergo continuous repair damage, leading to the continuous proliferation and differentiation of OCSCs (62)

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