298: Vitamin C does not prevent ROS-mediated syncytin expression or trophoblast differentiation


      Reactive Oxygen Species (ROS) have been implicated in the development of preeclampsia. Syncytin is expressed in placental trophoblasts and mediates syncytiotrophoblast formation via cell fusion. ROS-mediated Syncytin overexpression causes rapid cell fusion, which may lead to depletion of the trophoblast pool and contribute to the development of preeclampsia. This study was designed to investigate if antioxidant Vitamin C blocks the ROS effect in trophoblasts.

      Study Design

      Choriocarcinoma BeWo cells were treated with H202 or H202 and Vitamin C. A known antioxidant, NAC (N-acetylcysteine), served as the positive control. Following 48 hours of treatment, cells were harvested and syncytin mRNA measured by real-time PCR. Syncytin expression was compared to a GAPDH control. Syncytin protein levels were determined by Western blot analysis, and cell fusion effects were confirmed by two color imaging analysis.


      Syncytin expression was significantly increased in cells treated with H202. Vitamin C did not inhibit the induction of syncytin expression (Table I). Syncytin mRNA was present in greater concentration in cells treated with Vitamin C and H202 than in cells treated with Vitamin C or H2O2 alone.
      Tabled 1Syncytin mRNA expression 48 hours after treatment
      TreatmentRatio of Syncytin mRNA expression to GAPDH control (+/− SEM)
      Control3.21 (0.05)
      H20220.02 (1.09)
      NAC4.64 (0.14)
      H202 + NAC4.95 (0.19)
      Vitamin C (40 ng/ml)21.61 (1.20)
      Vitamin C (40 ng/ml) + H202130.81 (4.70)


      Vitamin C treatment did not block ROS-mediated upregulation of Syncitin or cell fusion.This data supports the clinical observation that Vitamin C does not decrease the risk of preeclampsia.