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Oxidative stress in preeclampsia and the role of free fetal hemoglobin.

Hansson, Stefan LU orcid ; Nääv, Åsa LU and Erlandsson, Lena LU (2015) In Frontiers in Physiology 5.
Abstract
Preeclampsia is a leading cause of pregnancy complications and affects 3-7% of pregnant women. This review summarizes the current knowledge of a new potential etiology of the disease, with a special focus on hemoglobin-induced oxidative stress. Furthermore, we also suggest hemoglobin as a potential target for therapy. Gene and protein profiling studies have shown increased expression and accumulation of free fetal hemoglobin in the preeclamptic placenta. Predominantly due to oxidative damage to the placental barrier, fetal hemoglobin leaks over to the maternal circulation. Free hemoglobin and its metabolites are toxic in several ways; (a) ferrous hemoglobin (Fe(2+)) binds strongly to the vasodilator nitric oxide (NO) and reduces the... (More)
Preeclampsia is a leading cause of pregnancy complications and affects 3-7% of pregnant women. This review summarizes the current knowledge of a new potential etiology of the disease, with a special focus on hemoglobin-induced oxidative stress. Furthermore, we also suggest hemoglobin as a potential target for therapy. Gene and protein profiling studies have shown increased expression and accumulation of free fetal hemoglobin in the preeclamptic placenta. Predominantly due to oxidative damage to the placental barrier, fetal hemoglobin leaks over to the maternal circulation. Free hemoglobin and its metabolites are toxic in several ways; (a) ferrous hemoglobin (Fe(2+)) binds strongly to the vasodilator nitric oxide (NO) and reduces the availability of free NO, which results in vasoconstriction, (b) hemoglobin (Fe(2+)) with bound oxygen spontaneously generates free oxygen radicals, and (c) the heme groups create an inflammatory response by inducing activation of neutrophils and cytokine production. The endogenous protein α1-microglobulin, with radical and heme binding properties, has shown both ex vivo and in vivo to have the ability to counteract free hemoglobin-induced placental and kidney damage. Oxidative stress in general, and more specifically fetal hemoglobin-induced oxidative stress, could play a key role in the pathology of preeclampsia seen both in the placenta and ultimately in the maternal endothelium. (Less)
Please use this url to cite or link to this publication:
author
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type
Contribution to journal
publication status
published
subject
in
Frontiers in Physiology
volume
5
article number
516
publisher
Frontiers Media S. A.
external identifiers
  • pmid:25628568
  • wos:000348218500001
  • scopus:84926465859
  • pmid:25628568
ISSN
1664-042X
DOI
10.3389/fphys.2014.00516
language
English
LU publication?
yes
id
9b52c133-a154-41d7-8b92-010ec8e19af2 (old id 5039376)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25628568?dopt=Abstract
date added to LUP
2016-04-01 14:14:02
date last changed
2022-04-14 08:42:19
@article{9b52c133-a154-41d7-8b92-010ec8e19af2,
  abstract     = {{Preeclampsia is a leading cause of pregnancy complications and affects 3-7% of pregnant women. This review summarizes the current knowledge of a new potential etiology of the disease, with a special focus on hemoglobin-induced oxidative stress. Furthermore, we also suggest hemoglobin as a potential target for therapy. Gene and protein profiling studies have shown increased expression and accumulation of free fetal hemoglobin in the preeclamptic placenta. Predominantly due to oxidative damage to the placental barrier, fetal hemoglobin leaks over to the maternal circulation. Free hemoglobin and its metabolites are toxic in several ways; (a) ferrous hemoglobin (Fe(2+)) binds strongly to the vasodilator nitric oxide (NO) and reduces the availability of free NO, which results in vasoconstriction, (b) hemoglobin (Fe(2+)) with bound oxygen spontaneously generates free oxygen radicals, and (c) the heme groups create an inflammatory response by inducing activation of neutrophils and cytokine production. The endogenous protein α1-microglobulin, with radical and heme binding properties, has shown both ex vivo and in vivo to have the ability to counteract free hemoglobin-induced placental and kidney damage. Oxidative stress in general, and more specifically fetal hemoglobin-induced oxidative stress, could play a key role in the pathology of preeclampsia seen both in the placenta and ultimately in the maternal endothelium.}},
  author       = {{Hansson, Stefan and Nääv, Åsa and Erlandsson, Lena}},
  issn         = {{1664-042X}},
  language     = {{eng}},
  publisher    = {{Frontiers Media S. A.}},
  series       = {{Frontiers in Physiology}},
  title        = {{Oxidative stress in preeclampsia and the role of free fetal hemoglobin.}},
  url          = {{https://lup.lub.lu.se/search/files/3857686/7754330}},
  doi          = {{10.3389/fphys.2014.00516}},
  volume       = {{5}},
  year         = {{2015}},
}