Oxidative stress in pre‐eclampsia

Bowen, Robin S.; Moodley, J.; Dutton, Michael F.; Theron, Annette J.

doi:10.1034/j.1600-0412.2001.080008719.x

Cited by 100 publications

(43 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Kato et al (8) reported a 26% higher mean concentration of malondialdehyde (MDA), another marker of oxidative stress, in preeclamptic pregnancies compared with controls, samples taken from umbilical vein at cordocentesis unaffected by labor. In contrast, Bowen et al (7) found no difference between preeclampsia and control concentrations of MDA in umbilical vein. Recently pentosidine, an advanced glycation end product, which can also be used as a marker of oxidative stress, was explored in fetal circulation in preeclampsia (10).…”

Section: Discussionmentioning

confidence: 86%

“…To what extent such placental agents affect the fetus, or are present in the fetal circulation at increased concentrations in preeclampsia, has not been fully explored. Few studies have addressed this issue, with conflicting results (7)(8)(9)(10). If endothelial activating agents are present in the fetal circulation, they could cause immediate effects, such as endothelial activation, or even long-term consequences, such as the programming of adult diseases.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Oxidative Stress and Antioxidant Status in Fetal Circulation in Preeclampsia

2006

View full text Add to dashboard Cite

Preeclampsia is associated with oxidative stress in maternal circulation. The purpose of this study was to explore oxidative stress and antioxidants in the fetal circulation in preeclampsia. Women with preeclampsia (n ϭ 19) or uncomplicated pregnancies (n ϭ 33) delivered by cesarean section were included. Blood was sampled separately from the umbilical vein and artery. 8-Isoprostaglandin F 2␣ (8-isoprostane), a stable product of lipid peroxidation, is a reliable marker of oxidative stress. Concentration of total 8-isoprostane in cord plasma was analyzed by gas chromatographymass spectrometry. Antioxidant status was evaluated measuring ferric reducing ability of plasma and vitamin E. There was no difference between preeclampsia and control groups regarding median plasma concentration of 8-isoprostane in umbilical vein (955 versus 780 pg/mL, p ϭ 0.41) or in umbilical artery (233 versus 276 pg/mL, p ϭ 0.65). Concentration of 8-isoprostane was much higher in plasma from the umbilical vein than artery, suggesting placenta as the source of 8-isoprostane. Median ferric reducing ability of plasma concentration was higher in preeclampsia than in controls, both in the umbilical vein and artery. Median vitamin E concentration in the umbilical vein was higher in preeclampsia, but no difference was found in the umbilical artery. In conclusion, no evidence of increased oxidative stress, evaluated by 8-isoprostane concentration, was found in fetal circulation in preeclampsia. (Pediatr Res 60: 560-564, 2006) P reeclampsia is a pregnancy specific disorder, characterized by hypertension and proteinuria developing in the second half of the pregnancy. For the fetus, the preeclampsia syndrome could have serious consequences, including increased risk of fetal growth restriction and induced premature delivery due to disease progression on the maternal or fetal side. Maternal endothelial dysfunction is believed to be the common final pathway leading to the syndrome of preeclampsia. A dominating hypothesis is that agents produced by the relatively hypoxic placenta is transferred to the maternal circulation, causing endothelial dysfunction (1). Several candidates have been proposed as possible agents that directly or indirectly could mediate the endothelial dysfunction, including lipid peroxidation products (2,3), activated leukocytes (4), placental debris (5), or sFlt1, a vascular endothelial growth factor (VEGF) antagonist (6). To what extent such placental agents affect the fetus, or are present in the fetal circulation at increased concentrations in preeclampsia, has not been fully explored. Few studies have addressed this issue, with conflicting results (7-10). If endothelial activating agents are present in the fetal circulation, they could cause immediate effects, such as endothelial activation, or even long-term consequences, such as the programming of adult diseases. The concept of intrauterine fetal programming, that an individual's adult health could be influenced by conditions and growth in utero, is convincingly do...

show abstract

Section: Discussionmentioning

confidence: 86%

mentioning

confidence: 99%

Oxidative Stress and Antioxidant Status in Fetal Circulation in Preeclampsia

2006

View full text Add to dashboard Cite

show abstract

“…The pancreatic beta cells require large amounts of ATP to allow glucose stimulated insulin secretion to take place. Studies in humans have shown that intrauterine growth retardation can lead to increased production of reactive oxygen species (ROS) in the fetus (71)(72)(73) along with low levels of oxygen which lead to impaired function of the electron transport chain, which can then increase ROS production further (74,75). The oxidative damage M a n u s c r i p t 12 caused by ROS is not limited to the mitochondria -proteins, lipids and nucleic acids within the cell can also be damaged.…”

Section: Mechanisms Of Intrauterine Programmingmentioning

confidence: 99%

Fetal programming of glucose–insulin metabolism

Jones

Ozanne

2009

Molecular and Cellular Endocrinology

View full text Add to dashboard Cite

Epidemiological studies have shown a link between poor fetal growth and increased risk of developing type 2 diabetes. These observations are highly reproducible in many populations worldwide although the mechanisms behind them remain elusive.The 'Thrifty Phenotype Hypothesis' was proposed to explain the underlying causes of these relationships. Animal models of poor intrauterine nutrition have been utilised to help to define the causal factors and identify the molecular mechanisms. Programmed changes in beta cell function and insulin action have been a common feature of animal models of poor intrauterine nutrition. Fundamental underlying mechanisms are starting to emerge, including changes in the epigenotype and mitochondrial function.

show abstract

“…Other studies demonstrated that bilateral uterine vessel ligation resulted in IUGR rat offspring with increased arterial vascular stiffness and selective endothelial uterine artery dysfunction (73) and caused nephron deficits and modest renal insufficiency (74) . Placental insufficiency in both animal models of uterine placental ligation (75) and in human studies (76)(77)(78)(79) is strongly associated with the development of oxidative stress, and it is thought that the mitochondria plays an important role in mediating this effect. Mitochondria are a major source of ROS generation in cells and are generated from the mitochondrial electron transport chain (ETC).…”

Section: Uterine Placental Ligationmentioning

confidence: 99%

The impact of early nutrition on the ageing trajectory

Tarry-Adkins

Ozanne

2014

Proc. Nutr. Soc.

View full text Add to dashboard Cite

Epidemiological studies, including those in identical twins, and in individuals in utero during periods of famine have provided robust evidence of strong correlations between low birthweight and subsequent risk of disease in later life, including type 2 diabetes (T2D), CVD, and metabolic syndrome. These and studies in animal models have suggested that the early environment, especially early nutrition, plays an important role in mediating these associations. The concept of early life programming is therefore widely accepted; however the molecular mechanisms by which early environmental insults can have long-term effects on a cell and consequently the metabolism of an organism in later life, are relatively unclear. So far, these mechanisms include permanent structural changes to the organ caused by suboptimal levels of an important factor during a critical developmental period, changes in gene expression caused by epigenetic modifications (including DNA methylation, histone modification and microRNA) and permanent changes in cellular ageing. Many of the conditions associated with early-life nutrition are also those which have an age-associated aetiology. Recently, a common molecular mechanism in animal models of developmental programming and epidemiological studies has been development of oxidative stress and macromolecule damage, specifically DNA damage and telomere shortening. These are phenotypes common to accelerated cellular ageing. Thus, this review will encompass epidemiological and animal models of developmental programming with specific emphasis on cellular ageing and how these could lead to potential therapeutic interventions and strategies which could combat the burden of common age-associated disease, such as T2D and CVD.

show abstract

Oxidative stress in pre‐eclampsia

Cited by 100 publications

References 47 publications

Oxidative Stress and Antioxidant Status in Fetal Circulation in Preeclampsia

Oxidative Stress and Antioxidant Status in Fetal Circulation in Preeclampsia

Fetal programming of glucose–insulin metabolism

The impact of early nutrition on the ageing trajectory

Contact Info

Product

Resources

About