mitoquinone and Fetal-Hypoxia

Pregnancy complications associated with prenatal hypoxia lead to increased placental oxidative stress. Previous studies suggest that prenatal hypoxia can reduce mitochondrial respiratory capacity and mitochondrial fusion, which could lead to placental dysfunction and impaired fetal development. We developed a placenta-targeted treatment strategy using a mitochondrial antioxidant, MitoQ, encapsulated into nanoparticles (nMitoQ) to reduce placental oxidative stress and (indirectly) improve fetal outcomes. We hypothesized that, in a rat model of prenatal hypoxia, nMitoQ improves placental mitochondrial function and promotes mitochondrial fusion in both male and female placentae. Pregnant rats were treated with saline or nMitoQ on gestational day (GD) 15 and exposed to normoxia (21% O

Topics: Animals; Antioxidants; Cell Respiration; Female; Fetal Hypoxia; Male; Mitochondria; Mitochondrial Dynamics; Nanoparticles; Organophosphorus Compounds; Placenta; Pregnancy; Rats; Rats, Sprague-Dawley; Sex Factors; Ubiquinone

Intrauterine growth restriction, a common consequence of prenatal hypoxia, is a leading cause of fetal morbidity and mortality with a significant impact on population health. Hypoxia may increase placental oxidative stress and lead to an abnormal release of placental-derived factors, which are emerging as potential contributors to developmental programming. Nanoparticle-linked drugs are emerging as a novel method to deliver therapeutics targeted to the placenta and avoid risking direct exposure to the fetus. We hypothesize that placental treatment with antioxidant MitoQ loaded onto nanoparticles (nMitoQ) will prevent the development of cardiovascular disease in offspring exposed to prenatal hypoxia. Pregnant rats were intravenously injected with saline or nMitoQ (125 μM) on gestational day (GD) 15 and exposed to either normoxia (21% O

Topics: Age Factors; Animals; Antioxidants; Cardiovascular Diseases; Disease Models, Animal; Female; Fetal Hypoxia; Gestational Age; Hemodynamics; Male; Maternal Exposure; Myocardial Contraction; Nanoparticles; Organophosphorus Compounds; Oxidative Stress; Placenta; Pregnancy; Prenatal Exposure Delayed Effects; Rats, Sprague-Dawley; Sex Factors; Ubiquinone; Ventricular Function, Left