Background
Many reports investigated the effects of vitamin E succinate (VES) on cell growth inhibition and apoptosis in SGC-7901 cells, but the mechanisms are still unclear. This study assessed the effects of VES-induced oxidative stress on apoptosis in SGC-7901 cells and further explored its mechanism.
Material and Method
Cell growth and survival were detected by the MTT assay. Apoptosis was examined by DAPI fluorescence and an Annexin V-FITC apoptosis detection kit. The fluorescent probe CMXRos was used to analyze mitochondrial transmembrane potential by confocal microscopy. Accumulation of intracellular ROS was detected with DCFH-DA. DNA damage was evaluated by the comet assay in SGC-7901 cells. The total GSH concentration was detected by a total glutathione quantification kit. The expression level of Bcl-2 in response to VES treatment was determined by Western blot analysis.
Results
The results showed that VES induced growth inhibition and apoptosis in SGC-7901 cells as assessed by the MTT assay and apoptosis detection method. VES also induced a concentration-dependent generation of reactive oxygen species (ROS) and a concentration-dependent depletion of glutathione (GSH) in the cells. Mannitol, an inhibitor of mitochondrial oxidative damage, prevented ROS generation, GSH depletion, and apoptosis in response to VES in SGC-7901 cells.
Conclusions
VES abrogated the generation of intracellular ROS and the induction of apoptosis. The results indicate that VES induced apoptosis in SGC-7901 cells and this involved mitochondria, likely through mitochondrial- derived ROS.

Keywords: Reactive Oxygen Species - metabolism, Mitochondria - metabolism, Membrane Potentials, Microscopy, Confocal, Glutathione - metabolism, Cell Division - drug effects, Antioxidants - pharmacology, Vitamin E - pharmacology