Selenium Supplementation Protects Trophoblast Cells from Mitochondrial Oxidative Stress (#272)
Oxidative stress plays an important role in the pathogenesis of preeclampsia, a placental disorder affecting 7% of mothers and babies. Trophoblast cells are susceptible to oxidative stress which causes increased cell death and placental turnover. In this study we used inhibitors of the mitochondrial respiratory chain to induce oxidative stress and studied the effect that selenium supplementation had on trophoblast viability.
Materials and Methods:
Trophoblast cells (BeWo, JEG-3 and Swan-71) were treated with Na Selenite (100nM) or Selenomethionine (500nM) to increase the biological activity of antioxidants Glutathione Peroxidase and Thioredoxin Reductase. The cells were then oxidatively stressed with the addition of increasing doses of Antimycin C and Rotenone. The Resazurin end point assay was used to measure the cellular viability.
There was a dose dependent decrease in the cellular activity in BeWo, JEG3 and Swan71 when treated with increasing concentrations of Antimycin or Rotenone. For Antimycin concentrations of 320µM and 160µM, applied for 4 hours, resulted in a significant decrease in cellular activity whereas Rotenone concentrations of 400 nM and 200 nM also showed a significant decrease. Prior incubation with NaSelenite or Selenomethionine was able to protect trophoblast cells from oxidative stress.
These data suggest that selenoproteins such as GPx and ThxRed have an important role in protecting trophoblast mitochondria from oxidative stress. This emphasises the importance of maintaining an adequate selenium supply during pregnancy and especially in pregnancies complicated by conditions such as preeclampsia.