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Antioxidative defense enzymes in placenta protect placenta and fetus in inherited thrombophilia from hydrogen peroxide.

Authors
Type
Published Article
Journal
Oxidative Medicine and Cellular Longevity
1942-0994
Publisher
Hindawi Limited
Publication Date
Volume
2
Issue
1
Pages
14–18
Identifiers
PMID: 20046640
Source
Medline
Keywords
License
Unknown

Abstract

Our aim was to investigate the activities of antioxidative defense enzymes in the placenta, fetal blood and amnion fluid in inherited thrombophilia. Thrombophilia was associated with nearly threefold increase of activity (p < 0.001) of the placental catalase (81.1 +/- 20.6 U/mg of proteins in controls and 270.0 +/- 69.9 U/mg in thrombophilic subjects), glutathione (GSH) peroxidase (C: 20.2 +/- 10.1 U/mg; T: 60.0 +/- 15.5 U/mg), and GSH reductase (C: 28.9 +/- 5.6 U/mg; T: 72.7 +/- 23.0 U/mg). The placental activities of superoxide dismutating enzymes--MnSOD and CuZnSOD, did not differ in controls and thrombophilia. Likewise, the activities of catalase and SOD in the fetal blood, and the level of ascorbyl radical which represents a marker of oxidative status of amniotic fluid, were similar in controls and thrombophilic subjects. From this we concluded that in thrombophilia, placental tissue is exposed to H(2)O(2)-mediated oxidative stress, which could be initiated by pro-thrombic conditions in maternal blood. Increased activity of placental H(2)O(2)-removing enzymes protects fetus and mother during pregnancy, but may increase the risk of postpartum thrombosis.

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