An antioxidant role of nitric oxide in modulation of oxidative stress in human placental trophoblastic cells

Nitric oxide (NO) has recently attracted great interest as a mediator of cell and organ functions. During pregnancy, larger amounts of NO are known to be produced in systemic circulation on the maternal side than those in nonpregnant females. Placental trophoblastic cells (PTCs), which are major constituents of placenta and are in direct contact with maternal blood, can produce NO via the reaction of endothelial form of NO synthase during pregnancy. Endogenously produced NO in placenta can relax vascular tone, inhibit platelet aggregations, and attenuate adherent reactions of leukocytes and platelets. By contrast, the decrease of NO generation in the placenta is correlated with impairment of uteroplacental perfusion, which elicits severe perinatal complications such as preeclampsia (PE) and intrauterine growth retardation (IUGR). Although the mechanisms through which endogenous NO modulates a variety of cellular functions in the placenta have not been revealed yet, our results provide new insight into molecular mechanisms of endogenous NO in PTCs, suggesting that alterations in placental NO formation may not only play a role in the physiological changes of advancing gestation but may also contribute to the pathophysiology of PE and IUGR.