Oxidative stress in pregnancies complicated by diabetes

The placenta is essential for normal foetal metabolism and growth. However, maternal diabetes is an unfavourable environment for embryonic and fetoplacental development, which may disrupt normal foetal programming, leading later to metabolic disease. Additionally, an adverse in utero environment may lead to foetal congenital anomalies. Existing diabetes before pregnancy (pregestational type 1 and or type 2 diabetes mellitus) may have negative effects on the embryonic development, while gestational diabetes mellitus (GDM) that occurs during late stages of pregnancy may affect the growth and maturation of the foetus. Many of the damaging effects of diabetes in pregnancy have been attributed to oxidative stress. Reactive oxygen and nitrogen species are by-products of a number of important biological pathways of pregnancy, including embryo development, implantation, angiogenesis, placental development and function. In healthy pregnancies, these reactive oxygen and nitrogen species can be controlled to ensure no damage ensues. However, in pregnancies complicated by diabetes, their excessive production and/or a reduction in antioxidant defence mechanisms results in a number of damaging outcomes. Animal models of diabetes in pregnancy have provided supportive evidence of reactive oxygen and nitrogen species generation and their damaging effects, which are dependent on the developmental stage. In this chapter, we will review the available data on oxidative stress in human diabetic pregnancies as well as in animal models of diabetes in pregnancy during early gestation, fetoplacental development and the perinatal period, as well as on its postnatal consequences. Human and animal data supportive of antioxidant treatments will be also discussed