Increased levels of carboxyhemoglobin and serum iron as an indicator of increased red cell turnover in preeclampsia

Entman, Stephen S.; Kambam, J. R.; Bradley, Charles; Cousar, John B.

doi:10.1016/0002-9378(87)90134-7

Cited by 52 publications

(15 citation statements)

References 15 publications

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“…11,12,39 Iron is particularly abundant in the placenta and may arise in the ischaemic placenta by destruction of red blood cells from thrombotic, necrotic and haemorrhagic areas. 37,40 Additionally, low pH in the microenvironment of the ischaemic artery wall could lead to local release of iron from transferrin. 13,37 In the present study, we observed a significant increase in serum iron levels in mild and severe preeclampsia when compared to normotensive healthy Figure 1.…”

Section: Discussionmentioning

confidence: 99%

Serum iron and copper status and oxidative stress in severe and mild preeclampsia

Serdar

Gür

Develíoğlu

2006

Cell Biochem. Funct.

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Our aim was to investigate parameters of iron and copper status and oxidative stress and antioxidant function in women with healthy pregnancy, mild and severe preeclampsia with a view to exploring the possible contribution of these parameters to the aetiology. Thirty healthy, 30 mild preeclamptic and 30 severe preeclamptic pregnant women were included. Serum and placental lipid peroxides, and serum vitamin E and total carotene levels were measured by colorimetric assay. Cholesterol, copper, iron, total iron binding capacity (TIBC), ceruloplasmin and transferrin concentrations were measured by commercially available procedures. Data were analysed statistically using one-way analysis of variance and Pearson correlation test. Logistic regression procedures were used to calculate odds ratios. Lipid peroxides in serum and placental tissue, and iron, copper and ceruloplasmin levels in serum were significantly increased, and transferrin, TIBC, vitamin E/total cholesterol and total carotene/total cholesterol ratios in serum were significantly decreased especially in women with severe preeclampsia. Significant correlations were detected between serum iron and lipid peroxides in serum and placental tissue and between serum iron and vitamin E/total cholesterol in severe preeclamptic pregnancy. Furthermore, there were significant correlations between serum malondialdehyde and ceruloplasmin and vitamin E/total cholesterol in women with severe preeclampsia, and changes in serum and placental lipid peroxides and serum iron concentrations were significantly associated with preeclampsia. In conclusion, ischaemic placental tissue may be a primary source of potentially toxic iron in preeclampsia and the released iron species may contribute to the aetiology and would exacerbate lipid peroxidation and endothelial cell injury, which may be abated by antioxidant supplementation.

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Section: Discussionmentioning

confidence: 99%

Serum iron and copper status and oxidative stress in severe and mild preeclampsia

Serdar

Gür

Develíoğlu

2006

Cell Biochem. Funct.

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“…After exhaustion of the antioxidant systems, the RBCs are the sources of free Hb/heme, which can inhibit the vasodilator effect of NO [32]. Enhanced RBC destruction is a frequent complication of mild preeclampsia, even in the absence of overt intravascular hemolysis [33].…”

Section: Discussionmentioning

confidence: 99%

Blood glutathione redox status in gestational hypertension

Németh

Orvos

Boda

2001

Free Radical Biology and Medicine

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Abstract-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 ϭ 19) vs. normotensive pregnant subjects (n ϭ 18) and controls (n ϭ 20). An erythrocyte GSH depletion with an increase in the oxidized form (GSSG) resulted in an elevated ratio GSSG/GSH (0.305 Ϯ 0.057; mean Ϯ SD) in hypertensive pregnant women vs. normotensive pregnant or control subjects (0.154 Ϯ 0.025; 0.168 Ϯ 0.073; p Ͻ .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.

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“…Antioxidant therapy with vitamins C and E has been tried, but was ineffective in preventing preeclampsia in clinical trials 39, 40 . The high doses of vitamin C used in these trials may have been counter productive because vitamin C is a potent oxidant in the presence of free iron, which is elevated in blood of women with preeclampsia 41, 42 . On the other hand, meta-analysis of low-dose aspirin trials demonstrates aspirin is effective in preventing preeclampsia 43, 44 , the effectiveness of which is related to patient compliance 45 .…”

Section: Perspectivesmentioning

confidence: 99%

Mechanisms of Enhanced Vascular Reactivity in Preeclampsia

et al. 2011

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Preeclamptic women have enhanced blood pressure response to angiotensin II and extensive systemic vascular infiltration of neutrophils. Neutrophils release reactive oxygen species that might activate the RhoA kinase pathway to enhance vascular reactivity. We hypothesized that enhanced vascular reactivity in preeclampsia is due to neutrophil mediated reactive oxygen species activation of the RhoA kinase pathway. Omental arteries were obtained at cesarean section and studied using a myograph system. We found that arteries of preeclamptic women had extensive infiltration of neutrophils and enhanced reactivity to angiotensin II. Treatment of arteries of normal pregnant women with reactive oxygen species or activated neutrophils enhanced vessel reactivity to angiotensin II mimicking preeclamptic vessels. Pretreatment with superoxide dismutase/catalase to quench reactive oxygen species, or RhoA kinase inhibitor blocked enhanced responses in preeclamptic and normal vessels. Reactive oxygen species also enhanced vessel reactivity to norepinephrine, which was blocked by RhoA kinase inhibition. Treatment of arteries with reactive oxygen species increased RhoA kinase activity 3-fold, whereas culture of human vascular smooth muscle cells with angiotensin II and activated neutrophils or reactive oxygen species resulted in phosphorylation of key proteins in the RhoA kinase pathway. We conclude that enhanced vascular reactivity of omental arteries in preeclampsia is due to reactive oxygen species activation of the RhoA kinase pathway, and that enhanced vascular reactivity is likely due to the infiltration of neutrophils. We speculate that neutrophil infiltration into systemic vasculature of preeclamptic women is an important mechanism for hypertension.

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Increased levels of carboxyhemoglobin and serum iron as an indicator of increased red cell turnover in preeclampsia

Cited by 52 publications

References 15 publications

Serum iron and copper status and oxidative stress in severe and mild preeclampsia

Serum iron and copper status and oxidative stress in severe and mild preeclampsia

Blood glutathione redox status in gestational hypertension

Mechanisms of Enhanced Vascular Reactivity in Preeclampsia

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