Abstract
The effect of maternal smoking as a source of exposure to toxic metals Cd and Pb on superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity, metallothionein (MT), Cd, Pb, Cu, Fe, Mn, Se and Zn concentrations were assessed in maternal and umbilical cord blood and placenta in 74 healthy mother-newborn pairs after term delivery. Sparse discriminant analysis (SDA) was used to identify elements with the strongest impact on the SOD, GPx and MT in the measured compartments, which was then quantified by multiple regression analysis. SOD activity was lower in maternal and cord plasma, and higher in the placenta of smokers compared to non-smokers, whereas GPx activity and MT concentration did not differ between the groups. Although active smoking during pregnancy contributed to higher maternal Cd and Pb concentrations, its contribution to the variability of SOD, GPx or MT after control for other elements identified by SDA was not significant. However, an impaired balance in the antioxidant defence observed in the conditions of relatively low-to-moderate exposure levels to Cd and Pb could contribute to an increased susceptibility of offspring to oxidative stress and risk of disease development later in life. Further study on a larger number of subjects will help to better understand complex interactions between exposure to toxic elements and oxidative stress related to maternal cigarette smoking.
Highlights
There is emerging evidence that maternal exposure to various environmental stressors may have an important role in programming the susceptibility of offspring to adverse health effects
No significant differences between smokers and non-smokers were found in parity, body mass index (BMI) before pregnancy, BMI before delivery, and weight gain during pregnancy
We found a significantly lower superoxide dismutase (SOD) in maternal and umbilical cord plasma, a higher SOD in the placenta of smoking compared to non-smoking participants, whereas glutathione peroxidase (GPx) and MT did not differ between the study groups
Summary
There is emerging evidence that maternal exposure to various environmental stressors may have an important role in programming the susceptibility of offspring to adverse health effects. Any changes during the perinatal period can increase the risk of developing a disease later in life. This concept is referred to as the developmental origins of health and disease (DOHaD) [1,2]. The mechanisms of the health consequences due to environmental exposures and conditions manifested postnatally may be oxidative stress, which is recognised as one of the key mediators included in the programming of future health and diseases of the offspring [3,4]. Cigarette smoking during pregnancy is one of the leading environmental factors that can adversely affect the health of women during the reproductive period and her progeny. A smoking pregnant woman exposes her embryo/foetus to a variety of chemicals from tobacco smoke as well as to increased risk of detrimental effects, directly via placental transfer of the toxicants and indirectly by affecting placental vasculature, umbilical artery blood flow, and impaired placental nutrient passage [6,7]
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