Roles of selenoprotein K and selenium status in the etiopathogenesis of preeclampsia: Their relationships with maternal lipid peroxidation, oxidative DNA damage, and glutathione peroxidase

摘要

Objective: Preeclampsia (PE) is a complex disease and the underlying mechanisms are not known yet. It is well known that selenium and oxidative stress play a role in the pathogenesis of various diseases as well as PE. The aim of the study was to investigate the changes in selenium status, as an essential trace element, and selenoprotein K (SelK), a newly described selenoprotein which has been suggested to have an antioxidant function in some tissues in patients with preeclampsia. We also aimed at investigating their relationships with maternal lipid peroxidation, oxidative DNA damage, and glutathione peroxidase (GPx) activities. Materials and methods: 38 healthy pregnant and 48 pregnant women with PE were included in the study. Serum selenium levels were measured by graphite-furnace atomic absorption spectrophotometry. Plasma TBARS levels were analyzed by spectrophotometric method; GPx activities, 8OHdG, and SelK levels were determined by ELISA. Results: Plasma TBARS and 8OHdG levels were found to be increased in the PE group compared to the healthy pregnant group. Plasma SelK levels and GPx activities were found to be lower in the PE group than in the healthy control group. However, there was no significant difference in serum selenium levels between two groups. Furthermore, a significant correlation was determined between plasma SelK levels and GPx activities in PE patients group (r = 0.743; p 0.01). Likewise, a significant positive correlation was found between plasma 8OHdG and TBARS levels (r = 0.457; p 0.01), serum selenium levels and plasma GPx activities (r = 0.663; p 0.01), serum selenium and plasma SelK levels (r = 0.851; p 0.01) in PE. Conclusion: Our findings indicated that a selenoprotein SelK and a selenoenzyme GPx play a role in the etiopathogenesis of PE. Decreases in these antioxidant systems were associated with increase in lipid and DNA oxidation in PE patients. Underlying mechanisms of SelK and its interactions with selenium status and GPx in PE should be clarified in details with further studies.