F<sub>2</sub>-Isoprostanes, tocopherols and normal pregnancy

Palm, Maria; Axelssön, Ove; Wernroth, Lisa; Basu, Samar

doi:10.1080/10715760902902737

Cited by 41 publications

(28 citation statements)

References 27 publications

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“…It anchors the conceptus, provides an interface for the exchange and modification of nutrients and gases, synthesizes and secretes a range of steroid and peptide hormones, and provided an immune barrier between the mother and the semi-allogeneic fetus. 27 Measurements of oxidative stress markers in maternal blood and urine 28 show that pregnancy per se is a state of oxidative stress due to the high metabolic activity of the placenta and maternal metabolism in pregnancy. 27 Our results showed that mild diabetes caused no change in the SOD activity and MDA concentration in the placental tissue samples, however, the catalase activity was increased.…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress in Maternal Blood and Placenta From Mild Diabetic Rats

et al. 2014

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The aim of the present study was at evaluating the effects of oxidative stress in blood and placenta of mild diabetic Wistar rats. At birth, Wistar rats received citrate buffer (nondiabetic group, n ¼ 15) and another group received streptozotocin (100 mg/kg, subcutaneous) to induce mild diabetes (diabetic, n ¼ 15). The glycemia of these pregnant adult female rats were evaluated at days 0, 7, 14, and 21 of pregnancy, and at term pregnancy, the blood and placental samples were collected for oxidative stress measurements. The mild diabetes caused glycemia superior to 120 mg/dL during pregnancy, increased superoxide dismutase, glutathione peroxidase, glutathione reductase activities, and malondialdehyde levels in the blood, and catalase activity in the placenta. Thus, mild diabetes increased activities of antioxidant substances aiming at defending against the exacerbated oxidative stress but were not enough. The placenta also answered to diabetic milieu and increased antioxidant defense, showing that even a mild hyperglycemia was enough to cause placental and maternal blood changes.

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Section: Discussionmentioning

confidence: 99%

Oxidative Stress in Maternal Blood and Placenta From Mild Diabetic Rats

et al. 2014

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“…We hypothesize that oxidative and nitrative stress can lead to altered placental function via covalent modification of protein structure and function. Measurements of markers of oxidative stress in maternal blood and urine [13–15] show that pregnancy per se is a state of oxidative stress due to the high metabolic activity of the placenta and maternal metabolism in pregnancy. However, this is heightened in pregnancies complicated by preeclampsia, IUGR and diabetes as measured by increased markers of production of reactive oxygen species and decreases in antioxidant defences [11, 16–18].…”

Section: Generation Of Oxidative and Nitrative Stress In The Placentamentioning

confidence: 99%

Review: Reactive oxygen and nitrogen species and functional adaptation of the placenta

2010

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The placenta regulates fetal growth and development via transport of nutrients and gases, and synthesis and secretion of steroid and peptide hormones. These functions are determined by vascular development and blood flow and by growth and differentiation of the trophoblast, which contains receptors, transporters and enzymes. The placenta generates reactive oxygen species which may contribute to the oxidative stress seen even in normal pregnancy but this is increased in pregnancies complicated by preeclampsia, IUGR and pregestational diabetes where oxidative and nitrative stress have been clearly documented. Nitrative stress is the covalent modification of proteins and DNA by peroxynitrite formed by the interaction of superoxide and nitric oxide. We have demonstrated nitrative stress by localizing nitrotyrosine residues in these placentas and found increased expression of NADPH oxidase (NOX) enzyme isoforms 1 and 5 as a potential source of superoxide generation. The presence of nitrative stress was associated with diminished vascular reactivity of the fetal placental circulation, a situation that could be reproduced by treatment with peroxynitrite in vitro. We find many nitrated proteins in the placenta, including p38 MAP kinase which has a role in development of the villous vasculature. Nitration of p38 MAPK was increased in the preeclamptic placenta and associated with loss of catalytic activity. We hypothesize that nitration of proteins in the placenta including receptors, transporters, enzymes and structural proteins can alter protein and placental function and this influences fetal growth and development. Increasing nitrative stress but a decrease in oxidative stress, measured as protein carbonylation, is found in the placenta with increasing BMI. Formation of peroxynitrite may then consume superoxide, decreasing nitrative stress. As protein carbonylation is a covalent modification at Lys, Arg, Pro and Thr residues the switch from carbonylation to nitration at tyrosine residues may alter protein function and hence placental function.

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“…Pregnancy, with a moderate state of systemic inflammation 4 and a state of increase oxidative stress, 5 is related to a higher production of reactive oxygen species (ROS) 6 . It has been proposed that an imbalance between the synthesis of nitric oxide and ROS produces endothelial dysfunction 7 .…”

Section: Introductionmentioning

confidence: 99%