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.