Blood glutathione redox status in gestational hypertension

Citation
I. Nemeth et al., Blood glutathione redox status in gestational hypertension, FREE RAD B, 30(7), 2001, pp. 715-721
Citations number
40
Categorie Soggetti
Biochemistry & Biophysics
Journal title
FREE RADICAL BIOLOGY AND MEDICINE
ISSN journal
08915849 → ACNP
Volume
30
Issue
7
Year of publication
2001
Pages
715 - 721
Database
ISI
SICI code
0891-5849(20010401)30:7<715:BGRSIG>2.0.ZU;2-V
Abstract
Gestational hypertension during the third trimester reflects an exaggerated maternal inflammatory response to pregnancy. We hypothesized that oxidativ e stress present even in normal pregnancy becomes uncompensated in hyperten sive patients. A glucose-6-phosphate dehydrogenase (G6PD) activity sufficie nt to meet the increased reductive equivalent need of the cells is indispen sable for defense against oxidative stress. The erythrocyte glutathione red ox 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 oxidati ve challenge in pregnant women with gestational hypertension (n = 19) vs. n ormotensive pregnant subjects (n = 18) and controls (n = 20). An erythrocyt e 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 pr egnant women vs, normotensive pregnant or control subjects (0.154 +/-: 0.02 5; 0.168 +/- 0.073; p <.001). In hypertensive pregnant patients, a "GSH sta bility" decrease after an in vitro oxidative challenge suggested a reduced GSH recycling capacity resulting from an insufficient NADPH supply. The ery throcyte GSSG/GSH ratio may serve as an early and sensitive parameter of th e oxidative imbalance and a relevant target for future clinical trials to c ontrol the effects of antioxidant treatment in women at increased risk of t he pre-eclampsia syndrome. <(c)> 2001 Elsevier Science Inc.