Oxidative stress in placental pathology

Abstract

The most important function of the placenta is the exchange of nutrients and oxygen between a mother and her fetus. To establish a healthy functioning placenta, placentation needs to occur with adequate remodelling of spiral arteries by extravillous trophoblasts. When this process is impaired, the resulting suboptimal and inadequate placenta function results in the manifestation of pregnancy complications. Impaired placenta function can cause preeclampsia and leads to fetal growth restriction due to hypoxia. Presence of hypoxia leads to oxidative stress due to an imbalance between reactive oxygen species and antioxidants, thereby causing damage to proteins, lipids and DNA. In the placenta, signs of morphological adaptation in response to hypoxia can be found. Different placental lesions like maternal or fetal vascular malperfusion or chronic villitis lead to a decreased exchange of oxygen between the mother and the fetus. Clinically, several biomarkers indicative for oxidative stress, e.g. malondialdehyde and reduced levels of free thiols are found. This review aims to give an overview of the causes and (potential) role of placental oxidative stress in the development of placental parenchymal pathology and its clinical consequences. Also, therapeutic options aiming at prevention or treatment of hypoxia of the placenta and fetus are described.

SIRT1 Alleviates LPS-Induced IL-1β Production by Suppressing NLRP3 Inflammasome Activation and ROS Production in Trophoblasts

“…NLRP3 inflammasome activation could be induced by ROS [55]. Hypoxia can cause placental tissue damage, including preeclampsia and IUGR, via the production of oxidative stress [56]. In the present study, intracellular ROS amounts were found to be elevated in Sw.71 cells after LPS treatment.…”

Hyperandrogenism and insulin resistance‐induced fetal loss: evidence for placental mitochondrial abnormalities and elevated reactive oxygen species production in pregnant rats that mimic the clinical features of polycystic ovary syndrome

“…; Schoots et al . ), there is also mounting evidence for oxidative stress, elevated ROS production, and decreased mitochondrial mass in the circulation (Zhang et al . ) and in the ovarian granulosa cells (Lai et al .…”

Role of aspirin‐triggered lipoxin A4, aspirin, and salicylic acid in the modulation of the oxidative and inflammatory responses induced by plasma from women with pre‐eclampsia

“…5,[48][49][50] In preeclampsia, increased reactive oxygen species generation, as well as decreased activity of the principal anti-oxidant enzyme, produces oxidative stress factors in placental tissue, which pass to maternal circulation leading to its characteristic alterations. Impaired remodeling of the spiral artery leads to hypoxia or re-oxygenation episodes, that could generate reactive oxygen species and also oxidized lipids, leading to placental oxidative stress and endothelial dysfunction.…”

“…Impaired remodeling of the spiral artery leads to hypoxia or re-oxygenation episodes, that could generate reactive oxygen species and also oxidized lipids, leading to placental oxidative stress and endothelial dysfunction. 5,[48][49][50] In preeclampsia, increased reactive oxygen species generation, as well as decreased activity of the principal anti-oxidant enzyme, produces oxidative stress factors in placental tissue, which pass to maternal circulation leading to its characteristic alterations. 6,10,11 Since reactive oxygen species have extremely short half-lives, they are difficult to measure directly, and several products of the damage produced by oxidative stress can be measured, such as TBARS.…”