کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2789161 | 1154480 | 2014 | 7 صفحه PDF | دانلود رایگان |
The abnormally developed placenta is believed to be the pathophysiological cause of preeclampsia (PE). The resulting malperfusion of the placenta in PE can be associated with fluctuations in oxygen levels, leading to oxidative stress. How then do the placenta and the circulatory system of the mother adapt and respond to the increased oxidative challenge associated with PE? Many antioxidant systems have been shown to be upregulated or downregulated in the placenta and/or the maternal circulation during PE. Such altered antioxidant response can lead to increased lipid peroxidation. Oxidation of arachidonoyl residues in phospholipids generates bioactive lipids such as F2-isoprostanes, which are known vasoconstrictors. The consequences of changes in antioxidant status can also affect signal transduction and enzymatic pathways related to eicosanoid synthesis.
Journal: Placenta - Volume 35, Supplement, February 2014, Pages S32–S38