Abstract:

OBJECTIVE:  To study four key enzyme complexes in the mitochondria that contribute to vitamin E succinate (VES)-inhibited cell growth in human gastric cancer cells SGC-7901. METHODS：Gastric cancer cells SGC-7901 were grown in vitro. Cells were treated with rotenone(ROT)，thenoyltri?uoroacetone(TTFA)，antimycin A(AA) or sodium azide(SA) alone before treatment with VES for 2 h. Then cells were treated with VES at 20 μg/ml. MTT assay was used to evaluate cell growth. ROS was detected by confocal microscope. FITC/Annexin V was used to assess apoptosis. RESULTS：Cell growth inhibition induced by VES were obviously down-regulated after complex Ⅱ was inhibited by TTFA (5 μg/ml) (P<0.05). ROS induced by VES was all down-regulated after four complexes were inhibited respectively. Percentage of apoptosis induced by VES was all up-regulated after four complexes were inhibited respectively (P<0.05). However，levels of ROS and apoptosis were obviously lower than other three groups after complex Ⅱ was inhibited by TTFA (5 μg/ml) (all P<0.05). Cytochrome C and caspase-3 induced by VES were all down-regulated after cells treated with ROT，TTFA，AA or SA，respectively (P<0.05). Cytochrome C and caspase-3 were obviously down-regulated compared with other three groups (P<0.05). CONCLUSION：Key enzyme of complex Ⅱ (succinate dehydrogenase，SDH) was affected by VES. SDH induced ROS retention in cells. This may be the mechanism that VES contributes to vitamin E succinate-induced apoptosis in human gastric cancer cells.

Key words: vitamin E succinate, complex, ROS, apoptosis