Preeclampsia (PE) has a profound effect in increasing both maternal and fetal morbidity and
mortality especially in third World. Disturbances of extravillous trophoblast migration toward uterine
spiral arteries is characteristic feature of PE, which, in turn, leads to increased uteroplacental vascular
resistance and by vascular dysfunction resulting in reduced systemic vasodilatory properties. Underlying
pathogenesis appeared to be an altered bioavailability of nitric oxide (NO•) and tissue damage
caused by increased levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS). The
increase in ROS and RNS production or the decrease in antioxidant mechanisms generates a condition
called oxidative and nitrosative stress, respectively, defined as the imbalance between pro- and antioxidants
in favor of the oxidants. Additionally, ROS might trigger platelet adhesion and aggregation
leading to intravascular coagulopathy. ROS-induced coagulopathy causes placental infarction and impairs
the uteroplacental blood flow in PE. As a consequence of these disorders could result in deficiencies
in oxygen and nutrients required for normal fetal development resulting in fetal growth restriction.
On the one hand, enzymatic and nonenzymatic antioxidants scavenge ROS and protect tissues against
oxidative damage. More specifically, placental antioxidant enzymes including catalase, superoxide
dismutase (SOD), and glutathione peroxidase (GSH-Px) protect the vasculature from ROS, maintaining
the vascular function. On the other hand, ischemia in placenta in PE reduces the antioxidant activity.
Collectively, the extent of oxidative stress would increase and therefore leads to the development
of the pathological findings of PE including hypertension and proteinuria. Our goal in this article is to
review current literature about researches demonstrating the interplay between oxidative, nitrosative
stresses and PE, about their roles in the pathophysiology of PE and also about the outcomes of current
clinical trials aiming to prevent PE with antioxidant supplementation.