Short communicationOxidant Status in Maternal and Cord Plasma and Placental Tissue in Gestational Diabetes
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
References (39)
- et al.
Lipid peroxidation products and antioxidant enzymes in red blood cells during normal and diabetic pregnancy
Eur J Obstet Gynecol Reprod Biol
(1993) - et al.
Oxidative and antioxidative status in pregnant women with either gestational or type 1 diabetes
Clin Biochem
(2004) - et al.
The thiobarbituric acid reaction and the autooxidations of polyunsaturated fatty acid methyl esters
Arch Biochem Biophys
(1962) - et al.
Protein measurement with folin phenol reagent
J Biol Chem
(1951) - et al.
Oxidant-mediated lung disease in newborn infants
J Free Radic Biol Med
(1986) Free radicals, antioxidants, and human disease: curiosity, cause or consequence?
Lancet
(1994)- et al.
Proceedings of the fourth international workshop—conference on gestational diabetes mellitus
Diabetes Care
(1998) Epidemiology of glucose intolerance and gestational diabetes in women of childbearing age
Diabetes Care
(1998)- et al.
Alterations in transfer and lipid distribution of arachidonic acid in placentas of diabetic pregnancies
Diabetes
(1990) - et al.
Altered levels of scavenging enzymes in embryos subjected to a diabetic environment
Free Radic Res
(1996)