Abstract: BACKGROUND ＆ AIM: To study the possible effect of Bax in vitamin E succinate-induced apoptosis of human gastric carcinoma. MATERIALS AND METHODS: Fluorescent staining was used to detect apoptosis and the mitochondrial transmembrane potential(ΔΨm) of human gastric carcinoma SGC-7901 cells. The expression of Bax was measured by Western Blot analysis after the cells were treated with VES at 5, 10, 20 μg/ml. The translocation of Bax and cytochrome c were determined by Western Blot analysis in mitochondrial and cytosolic-enriched cellular fractions. RESULTS: VES caused apoptosis of SGC-7901 cells. The expression of Bax was increased in whole cell lysate with a dose-dependent relationship. Bax was translocated from the cytosol to the mitochondria. The permeabilization of mitochondrial membranes was increased as determined by the loss of ΔΨm. And cytochrome c was released from the mitochondria to the cytosol. CONCLUSION: VES could induce apoptosis of human gastric carcinoma SGC-7901 cells through mitochondrial pathway by Bax.

Key words: vitamin E succinate, Bax, mitochondria, cytochrome c