Fig. 3

Uterine arterial hypoxia, or placental ischemia, triggers oxidative stress (OS), generating superoxide radical (O₂ ^*) as a byproduct by specific enzymes such as xanthine or nicotinamide adenine dinucleotide phosphate (NADPH) oxidases. O₂ ^* may stimulate the production of cytokines (particularly IL-6), thus increasing the intensity of OS and inflammation and further increasing the generation of O₂ *_, leading to such adverse pregnancy outcomes as altered placental growth, reduced fetoplacental blood flow, and preeclampsia. Sufficient availability of Se may alleviate OS by increasing antioxidant capacities, such as superoxide dismutase (SOD) which converts O₂ * to hydrogen peroxide (H2O2), and inhibiting cytokine formation and activity