Figure 2
Investigation of cytotoxicity mechanism of [PtCl 2 (L)] and [PdCl 2 (L)]. (A) [PdCl2 (L)] induced apoptosis on CDDP-resistant gastric cancer cell lines. Apoptosis was assessed by analyzing activation of caspase-3 and caspase-7. Mean of three independent experiments in triplicate; bars, SE. Values for apoptosis of cells in FBS alone were used as controls. Significance was determined by Welch’s t-test. *, P < 0.05, **, P < 0.01 relative to parental cell line. (B) [PdCl2 (L)] induced DNA double-strand breaks in CDDP-resistant gastric cancer cells. Cells were labeled with antibody against phosphorylated histone H2AX (γ-H2AX), which detects double-strand breaks caused by drugs such as CDDP. An evaluation of γ-H2AX protein expression was investigated by Western blotting at 24 or 48 h after treatment.