Placental oxidative stress and monoamine oxidase expression are increased in severe preeclampsia: a pilot study

Abstract

Preeclampsia (PE) is the most severe complication of pregnancy with substantial burden of morbidity and mortality for mother and neonate. The increased placental oxidative stress (OS) has been involved as central pathomechanism, yet the sources of reactive oxygen species (ROS) are partially elucidated. Monoamine oxidase (MAO) with 2 isoforms, A and B, at the outer mitochondrial membrane has emerged as a constant source of ROS in cardiometabolic pathologies. The present pilot study was purported to assess as follows: (i) the magnitude of placental OS in relation to the site of sampling and (ii) the expression of placental MAO in the setting of PE. To this aim, central and placental samples were harvested during cesarean section from mild and severe PE versus healthy pregnancies. ROS generation (dihydroethidium staining) and MAO expression were assessed (confocal microscopy). MAO gene transcript was evaluated by RT-PCR. The main findings are as follows: (i) a significant increase in placental OS was found in severe (but not in mild) PE with no regional differences between central and peripheral areas and (ii) placental MAO-A and B (gene and protein) were significantly increased in severe preeclampsia. The signal transduction of the latter finding, particularly in relation with mitochondrial dysfunction, is worth further studying.

Keywords: Human placental oxidative stress; Monoamine oxidase; Peripheral and central samples; Preeclampsia.