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These environments include ischemia-hypoxia-reperfusion during placental development, pathological changes in physiological uterine contractions or superficial placental perfusion, trophoblastic iron enrichment, evidence of lipotoxicity during the pathophysiology of major placenta-related diseases such as PE, fetal growth restriction, and preterm birth, and decreased GSH redox capacity and lipid peroxidation repair capacity during placental injury [29]