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...
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| Dokumentumtípus: | Cikk |
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Elsevier
2001
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| Sorozat: | FREE RADICAL BIOLOGY AND MEDICINE
30 No. 7 |
| doi: | 10.1016/S0891-5849(00)00516-5 |
| mtmt: | 1388253 |
| Online Access: | http://publicatio.bibl.u-szeged.hu/12883 |
| Tartalmi kivonat: | 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. <(c)> 2001 Elsevier Science Inc. |
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| Terjedelem/Fizikai jellemzők: | 715-721 |
| ISSN: | 0891-5849 |