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In preeclampsia, it is believed that widespread endothelial dysfunction leads to reduced placental perfusion and increased oxidative stress. Oxidative stress is the accumulation of reactive oxygen species (ROS) such as superoxide (O2-), nitric oxide (NO), and peroxynitrite (ONOO-). Our lab has previously established a colony of transgenic mice that do not express catechol-O-methyl transferase (COMT-/-). COMT produces 2-methoxyestradiol (2-ME), a potent vasodilator that is normally increased in pregnancy. Pregnant COMT-/- mice exhibit a phenotype similar to the one observed in preeclampsia. We hypothesize that COMT-/- mice have a decreased tolerance to prenatal hypoxic insults, characterized by an increase in placental oxidative stress when compared to control (C57) mice exposed to similar conditions.

Effects of maternal hypoxia on placental levels of oxidative stress markers in COMT-/- and C57 mice