Blood glutathione redox status in gestational hypertension

Gestational hypertension during the third trimester reflects an exaggerated maternal inflammatory response to pregnancy. We hypothesized that oxidative stress present even in normal pregnancy becomes uncompensated in hypertensive patients. A glucose-6-phosphate dehydrogenase (G6PD) activity sufficie...

Full description

Saved in:
Bibliographic Details
Published inFree radical biology & medicine Vol. 30; no. 7; pp. 715 - 721
Main Authors Németh, Ilona, Orvos, Hajnalka, Boda, Domokos
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.04.2001
Subjects
Online AccessGet full text
ISSN0891-5849
1873-4596
DOI10.1016/S0891-5849(00)00516-5

Cover

Loading…
More Information
Summary:Gestational hypertension during the third trimester reflects an exaggerated maternal inflammatory response to pregnancy. We hypothesized that oxidative stress present even in normal pregnancy becomes uncompensated in hypertensive patients. A glucose-6-phosphate dehydrogenase (G6PD) activity sufficient to meet the increased reductive equivalent need of the cells is indispensable for defense against oxidative stress. The erythrocyte glutathione redox system was studied, where G6PD is the only NADPH source. The glutathione (GSH) redox status was measured both in vivo and after an in vitro oxidative challenge in pregnant women with gestational hypertension ( n = 19) vs. normotensive pregnant subjects ( n = 18) and controls ( n = 20). An erythrocyte GSH depletion with an increase in the oxidized form (GSSG) resulted in an elevated ratio GSSG/GSH (0.305 ± 0.057; mean ± SD) in hypertensive pregnant women vs. normotensive pregnant or control subjects (0.154 ± 0.025; 0.168 ± 0.073; p < .001). In hypertensive pregnant patients, a “GSH stability” decrease after an in vitro oxidative challenge suggested a reduced GSH recycling capacity resulting from an insufficient NADPH supply. The erythrocyte GSSG/GSH ratio may serve as an early and sensitive parameter of the oxidative imbalance and a relevant target for future clinical trials to control the effects of antioxidant treatment in women at increased risk of the pre-eclampsia syndrome.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0891-5849
1873-4596
DOI:10.1016/S0891-5849(00)00516-5