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

Abstract

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.

Ceruloplasmin/Transferrin System Is Related to Clinical Status in Acute Stroke

“…Similarly to our patients, women with severe preeclampsia presented higher levels of lipid peroxidation and serum CP, and lower levels of Tf with respect to pregnant women healthy or with mild preeclampsia. [43][44] These findings suggest that CP/Tf system is involved in the oxidative stress generated in different body districts.…”

“…44,Pϭ0.012). No evidence of association between CP, Tf, Cu, "free" Cu, Fe, Ferritin, TAS, as well as NIHSS, with inflammation markers was found (all PϾ0.2, apart from CP and fibrinogen: rϭ0.37, Pϭ0.061).…”

miR-210 Targets Iron-Sulfur Cluster Scaffold Homologue in Human Trophoblast Cell Lines

“…Furthermore, serum levels of lipid peroxides, iron, and ceruloplasmin in severe preeclampsia are elevated, whereas the transferrin level was decreased; ischemic placental tissue was proposed to be a primary source of toxic iron in preeclampsia. 67 There are limitations of this study. First, although we report a robust increase in miR-210 expression in the villous placental tissues of preterm preeclampsia and SGA cases, increased iron deposition in trophoblasts after hypoxia and ISCU knockdown was found only in Swan 71 cells with an extravillous trophoblast phenotype and in placental bed interstitial trophoblasts.…”

The Role of Maternal Oxidative Stress, Iron/Zinc, Copper/Zinc Ratios and Trace Element Levels in the Pathogenesis of Preeclampsia

“…[7][8][9] Trace elements are necessary to biological processes in human Several trace elements and oxidant/antioxidant status have been implicated in the pathogenesis of preeclampsia. [13][14][15][16] In several of studies, trace element ratios have been used as an index related to increased inflammation and oxidative stress in the development or progression of the disease activities. However, there are various of studies in the literature, in which preeclamptic patients disclose the relationship of some characteristic features, trace element levels and oxidative stress parameters.…”

“…16,20 It has been suggested that transition metals, The disturbance of the prooxidant/antioxidant balance that results from increased free radical production, antioxidant enzyme inactivation, and excessive antioxidant consumption is the causative factor in oxidative damage. Oxidative stress is an important mediator of abnormal platelet function and dysfunctional endothelium-dependent vasodilation in the setting of cardiovascular disease.…”