Article

Placental oxidative stress: From miscarriage to preeclampsia

Department of Anatomy, University of Cambridge, Cambridge, United Kingdom.
Journal of the Society for Gynecologic Investigation (Impact Factor: 2.33). 10/2004; 11(6):342-52. DOI: 10.1016/j.jsgi.2004.03.003
Source: PubMed

ABSTRACT

To review the role of oxidative stress in two common placental-related disorders of pregnancy, miscarriage and preeclampsia.
Review of published literature.
Miscarriage and preeclampsia manifest at contrasting stages of pregnancy, yet both have their roots in deficient trophoblast invasion during early gestation. Early after implantation, endovascular trophoblast cells migrate down the lumens of spiral arteries, and are associated with their physiological conversion into flaccid conduits. Initially these cells occlude the arteries, limiting maternal blood flow into the placenta. The embryo therefore develops in a low oxygen environment, protecting differentiating cells from damaging free radicals. Once embryogenesis is complete, the maternal intervillous circulation becomes fully established, and intraplacental oxygen concentration rises threefold. Onset of the circulation is normally a progressive periphery-center phenomenon, and high levels of oxidative stress in the periphery may induce formation of the chorion laeve. If trophoblast invasion is severely impaired, plugging of the spiral arteries is incomplete, and onset of the maternal intervillous circulation is premature and widespread throughout the placenta. Syncytiotrophoblastic oxidative damage is extensive, and likely a major contributory factor to miscarriage. Between these two extremes will be found differing degrees of trophoblast invasion compatible with ongoing pregnancy but resulting in deficient conversion of the spiral arteries and an ischemia-reperfusion-type phenomenon. Placental perfusion will be impaired to a greater or lesser extent, generating commensurate placental oxidative stress that is a major contributory factor to preeclampsia.
Miscarriage, missed miscarriage, and early- and late-onset preeclampsia represent a spectrum of disorders secondary to deficient trophoblast invasion.

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Available from: Graham J Burton, Dec 15, 2014
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    • "Placenta supports the normal growth and development of the fetus by coordinating exchanges of nutrients and wastes between maternal and fetal circulatory systems and by secreting numerous hormones. Therefore, placental dysfunctions are commonly associated to pregnancy disorders, such as miscarriage or preeclampsia (Ball et al. 2006; Burton and Jauniaux 2004; Goldman-Wohl and Yagel 2002; Sebire et al. 2002). Pregnancy disorders can be consecutive to pollutants exposure so it is of most importance to conceive placenta as a target organ for toxic agents and not just as a barrier between mother and fetus. "
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    • "Although ROS and antioxidants remain in balance during a healthy pregnancy , and cellular damage is repaired effectively, this balance can be easily disrupted (Furness et al., 2011). High OS during the first trimester of pregnancy increases the risk of spontaneous abortion (Agarwal et al., 2006; Burton and Jauniaux, 2004), as it causes the premature oxygenation of the early embryonic environment, which should occur later in the pregnancy (Jauniaux et al., 2000). OS is involved in defective embryo development and retardation of embryo growth, preeclampsia, maternal hypertension, and the risk of preterm delivery (reviewed in Ruder et al., 2009). "
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