Effects of exposure to cigarette smoke prior to pregnancy in diabetic rats

<p>Abstract</p> <p>Background</p> <p>The purpose of this study was to evaluate the effects of cigarette smoke exposure before pregnancy on diabetic rats and their offspring development.</p> <p>Methods</p> <p>Diabetes was induced by streptozotocin and cigarette smoke exposure was conducted by mainstream smoke generated by a mechanical smoking device and delivered into a chamber. Diabetic female Wistar rats were randomly distributed in four experimental groups (n minimum = 13/group): nondiabetic (ND) and diabetic rats exposed to filtered air (D), diabetic rats exposed to cigarette smoke prior to and into the pregnancy period (DS) and diabetic rats exposed to cigarette smoke prior to pregnancy period (DSPP). At day 21 of pregnancy, rats were killed for maternal biochemical determination and reproductive outcomes.</p> <p>Results</p> <p>The association of diabetes and cigarette smoke in DSPP group caused altered glycemia at term, reduced number of implantation and live fetuses, decreased litter and maternal weight, increased pre and postimplantation loss rates, reduced triglyceride and VLDL-c concentrations, increased levels of thiol groups and MDA. Besides, these dams presented increased SOD and GSH-Px activities. However, the increased antioxidant status was not sufficient to prevent the lipid peroxidation observed in these animals.</p> <p>Conclusion</p> <p>Despite the benefits stemming from smoking interruption during the pregnancy of diabetic rats, such improvement was insufficient to avoid metabolic alterations and provide an adequate intrauterine environment for embryofetal development. Therefore, these results suggest that it is necessary to cease smoking extensive time before planning pregnancy, since stopping smoking only when pregnancy is detected may not contribute effectively to fully adequate embryofetal development.</p

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