Elsevier

Placenta

Volume 27, Issues 2–3, February–March 2006, Pages 327-332
Placenta

Short communication
Oxidant Status in Maternal and Cord Plasma and Placental Tissue in Gestational Diabetes

https://doi.org/10.1016/j.placenta.2005.01.002Get rights and content

The aim of this study was to measure oxidant/antioxidant status in maternal and cord plasma and in placental tissue in gestational diabetes and to correlate the results with the quality of glycemic control of the mother. To achieve this, blood and placental tissue samples have been obtained from pregnant women with gestational diabetes mellitus (GDM) and from the umbilical cord of their fetuses. The same samples have been collected from pregnant women without GDM. In all the samples, oxidant and antioxidant parameters have been studied. It has been observed that the antioxidant defense system was impaired; xanthine oxidase, which is the main free radical-producing enzyme (XO) in the living cells, was activated; and oxidation reactions were accelerated in the samples obtained from patients with GDM. Results suggest presence of oxidant stress in the gestational diabetes, the reason probably being impaired antioxidant defense mechanism and increased free radical production through XO activation.

Introduction

Gestational diabetes mellitus is described as glucose intolerance of varying severity with the onset or first recognition during pregnancy [1]. Gestational diabetes complicates approximately 2–4% of pregnancies and it is the major cause of fetal macrosomia, prenatal mortality and may increase maternal long-term risk of developing type 2 diabetes mellitus [2]. However, possible molecular mechanisms leading to fetal abnormalities and maternal vascular complications such as preeclampsia has not been identified yet [3]. The clinical manifestations of gestational diabetes have been attributed to fetal hyperglycemia, hyperlipidemia, hyperinsuliemia or placental endothelial dysfunction [3]. As to the subject, oxidative mechanisms have recently drawn special attention [4], [5]. It has been reported that oxidative system is impaired owing to both overproduction of free radicals and/or a defect in the antioxidant defense [6]. The increased production of reactive oxygen species (ROS) has been attributed to protein glycation [7], [8] and glucose auto-oxidation in a hyperglycemic environment [9]. Impaired radical scavenger function has been attributed to the decreased activity of enzymatic and non-enzymatic scavengers. Present data demonstrate increased biomarkers of oxidant stress and impaired antioxidant defense in diabetic patients [10].

Previous studies revealed that superoxide dismutase (SOD), which converts superoxide radical to H2O2, and glutathione peroxidase (GSH-Px) and catalase (CAT), both of which detoxify H2O2 decrease in diabetic animals [11], [12]. Additionally, among the non-enzymatic scavengers, vitamin E, the main intra-cellular antioxidant, has been found to decrease in diabetic patients [12]. Experimental studies have revealed free oxygen radicals in diabetic pregnancy [13], [14]. Furthermore, it has been observed in an animal study that antioxidant support can decrease occurrence of malformations in offspring [15]. However, relatively limited data are available on the oxidative stress in gestational diabetes, and further studies need to be performed in order to elucidate possible molecular mechanism(s) involved.

The placenta provides the interface of the maternal and fetal circulations, and it may play a crucial role in protecting the fetus from adverse effects of maternal diabetic milieu, while disturbances in placental function may exacerbate this state.

To avoid reactive oxygen species (ROS)-induced damage of cellular components, several biochemical safety mechanisms are present in the placenta and serum including defense enzymes like SOD, glutathione peroxidase, and antioxidants like vitamin C, E, glutathione etc. ROS measurement is difficult given their high reactivity, very short half-life and low concentration [16]. Therefore, indirect markers are commonly used to evaluate secondary products of ROS damage.

In the present study, it is aimed to investigate whether there is oxidative stress in the placenta, maternal plasma and cord plasma in pregnant women with GDM compared to pregnant women with normal glucose tolerance test.

Section snippets

Materials and methods

Overall 26 women with singleton pregnancy between 38 and 40 weeks of gestation were registered as new patients in the Department of Obstetrics and Gynecology in Gazi University Hospital. In 13 women, pregnancy was complicated by gestational diabetes mellitus. The other 13 patients had a negative oral glucose tolerance test and were controls matched on gestational, maternal ages, and BMI. Gestational age was confirmed in all pregnant women by a routine ultrasonographic examination performed

Results

The main characteristics of all participants involved in the investigation are presented in Table 1. Fasting and 1-h glucose values at oral glucose tolerance test were significantly higher in women with GDM compared to healthy pregnant women (P < 0.05). Glysemic metabolic control is reflected by HbA1c percentage. While the mean HbA1c of controls was in the normal range of 4.71 ± 0.5%, women with diabetes at diagnosis and enrolment before dietary advice had a higher HbA1c mean (5.38 ± 0.7%) than their

Discussion

This is the first study evaluating simultaneously the antioxidant parameters in maternal and fetal compartments in GDM. In the present study, we found that oxidant reactions are enhanced in blood and tissue samples from patients with GDM. This is reflected by an increased activity of the xanthine oxidizes, elevated levels of lipid peroxidation, and a decrease of enzyme activity and of the antioxidant potential. In addition, an impairment of the antioxidant defense system is observed in the cord

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