Abstract
Preeclampsia is a persistent hypertensive gestational disease characterized by high blood pressure and proteinuria, which presents from the second trimester of pregnancy. At the cellular level, preeclampsia has largely been associated with the release of free radicals by the placenta. Placenta-borne oxidative and nitrosative stresses are even sometimes considered as the major molecular determinants of the maternal disease. In this review, we present the recent literature evaluating free radical production in both normal and pathological placentas (including preeclampsia and other major pregnancy diseases), in humans and animal models. We then assess the putative effects of these free radicals on the placenta and maternal endothelium. This analysis was conducted with regard to recent papers and possible therapeutic avenues.
Highlights
Preeclampsia (PE) is a major disease of human pregnancy, marked by hypertension and proteinuria, appearing during the second or third trimester of gestation
In these trophoblast cell lines, antioxidant molecules have proven to be able to reverse oxidative stress cascades. This is the case for Resveratrol [32], which normalized the activity of superoxide dismutase (SOD) in the HTR8-SVneo H/R stressed cells, as well as the concentration of Malondialdehyde, and decreased apoptosis
Oxygen is a vital gas that enables our cells to function via the production of mitochondrial ATP
Summary
Vascular endothelium consists of a single layer of epithelial cells covering the interior surface of blood vessels. A recent in vitro study has shown that treatment of ECs with PE serum, ox-LDL, progesterone, or sFlt-1 all leads to depressed KCas levels This inhibition seems to be the consequence of increased O2− production via high NOX2 and NOX4 expression and reduced SOD levels [121,122]. When HUVECs were treated for 24 h with 2% plasma from preeclamptic women, an increase of LOX-1 expression and oxidized LDL uptake was observed. This resulted in OS overproduction, as evidenced by increased NOX activity, O2−, and ONOO−. Production of O2− and its derivative, H2O2, by neutrophils results in increased neutrophilic CD11b expression and adhesion to ECs [132]
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