Role of intracellular Ca~(2+) in diallyl trisulfide induction of apoposis in gastric cancer cells

Aim To investigate whether DATS induce MGC803 cell apoptosis and the relationship betweenapoptosis and Ca~(2+) disruption. Methods MGC-803 cell growth inhibition was measured by MTT assay. Tunnel and flow cytometry methods were used to determine the induction of apoptosis and Ca2+ homeostasis disruption. Result MTT assay showed that the inhibitory rates on MGC-803 cell growth of different concentrations of DATS 4,8,12,16 and 24 mg·L-1 were 0.231±0.037,0.305±0.036,0.455±0.029,0.607±0.058,0.751±0.019 respectively. Flow cytometry analysis showed that treating MGC803 cell with DATS significantly increased the percentage of apoptosis cells and intracellular Ca2+. Treatment of cells with 1,2-bis(2-aminophenoxye-thane)-N,N,N-tetraacetic acid tetrakis acetoxymethyl ester (BAPTA-AM), cellular Ca2+ chelator, resulted in abolishment of the elevation of intracellular Ca~(2+) and blockage of DATS induced apoptotic of MGC-803. Conclusoin DATS could induce apoptosis of MGC-803 cells through the mechanism of Ca~(2+) homeostasis disruption.