Induction of apoptosis by arsenic trioxide and hydroxy camptothecin in gastriccancer cells in vitro

Math 1 Math(A1).

Figure 1 Cytotoxicity of As₂O₃ (A), and HCPT (B), on gastric cancer cells.

Figure 2 Electron microscopic observation of ultrastructural changes in gastric cancer cells treated with 10 μmol/L As₂O₃ for 48 h. The early change of apoptosis, nuclear chromatin condensation, looks like a new moon subjacent to the nuclear membranes (A). The intermediate stage of apoptosis presents cytoplasmic blebs, nuclear condensation, overflow of nuclear chromatin, and like-sprout (B). The late stage of apoptosis is characterized by splitting of nuclear membrane, nuclear chr omatin condensation, overflow of some parts of nuclear chromatin, and fragmentation of nucleus (C), and formation of apoptotic bodies (C) (D).

Figure 3 The index of apoptosis of gastric cancer cells induced by As₂O₃ (A) and by HCPT (B).

Figure 4 Nuclear DNA contents measured by flow cytometry in As₂O₃ and HCPT-induced apoptosis in gastric cancer cells at 48 h. Ap represents apoptotic cells. A: Untreated MKN-45 cells; B: Untreated SGC-7901 cells; C: Untreate d MKN-28 cells; D: MKN-45 cells treated with 10 μmol/L As₂O₃; E: SGC-79 01 cells treated with 10 μmol/L As₂O₃; F: MKN-28 cells treated with 10 μmol/L As₂O₃; G: MKN-45 cells treated with 10 mg/L HCPT; H: SGC-7901 cells treated with 10 mg/L HCPT; I: MKN-28 cells treated with 10 mg/L HCPT.