| Literature DB >> 27212609 |
E Jauniaux1, G J Burton2.
Abstract
In normal pregnancies, the earliest stages of development take place in a low oxygen (O2) environment. This physiological hypoxia of the early gestational sac protects the developing fetus against the deleterious and teratogenic effects of O2free radicals. Oxidative stress is manifested at the maternal-fetal interface from early pregnancy onwards. In early pregnancy, a well-controlled oxidative stress plays a role in modulating placental development, functions and remodelling. Focal trophoblastic oxidative damage and progressive villous degeneration trigger the formation of the fetal membranes, which is an essential developmental step enabling vaginal delivery. Our data have demonstrated that the first trimester placenta in humans is histiotrophic and not haemochorial. The development and maintenance of a physiological O2 gradient between the uterine and fetal circulations is also essential for placental functions, such as transport and hormonal synthesis. Pathological oxidative stress arises when the production of reactive O2 species overwhelms the intrinsic anti-oxidant defences causing indiscriminate damage to biological molecules, leading to loss of function and cell death. We here review the role of oxidative stress in the pathophysiology of miscarriage, pre-eclampsia and fetal growth restriction.Entities:
Keywords: Fausse couche; Intra-uterine growth retardation (IUGR); Miscarriage; Oxidative stress; Oxygen; Oxygène; Placenta; Pre-eclampsia; Pré-éclampsie; Retard de croissance intra-utérin (RCIU); Stress oxydatif
Mesh:
Year: 2016 PMID: 27212609 DOI: 10.1016/j.jgyn.2016.02.012
Source DB: PubMed Journal: J Gynecol Obstet Biol Reprod (Paris) ISSN: 0150-9918