[The role of reactive oxygen species in cisplatin-induced apoptosis of esophageal cancer cell line EC-109].

BACKGROUND & OBJECTIVE: Reactive oxygen species (ROS), in vivo oxygen metabolites and important signaling molecules, play a vital role in cell apoptosis. This study was to investigate the role of ROS in cisplatin (DDP)-induced apoptosis of esophageal cancer cell line EC-109, and explore the mechanism.

METHODS

EC-109 cells were treated with different concentrations (0, 1, 5, 10, and 15 microg/ml) of DDP. MTT assay was used to evaluate the influence of DDP on cell proliferation. Flow cytometry was used to test ROS levels, intracellular mitochondrial transmembrane potential (Delta psi m), and hypodiploid apoptosis peak in EC-109 cells. Cell apoptosis after pretreatment with hydrogen peroxide-scavenging enzyme catalase (CAT) was also detected.

RESULTS

DDP obviously suppressed proliferation of EC-109 cells. When treated with 0, 1, 5, 10, 15 microg/ml of DDP for 2 h, ROS levels were (3.3+/-1.0)%, (21.6+/-2.0)%, (32.6+/-3.2)%, (44.7+/-2.2)%, and (53.1+/-3.6)%, respectively; when treated for 12 h, Delta psi m were (97.2+/-1.9)%, (90.6+/-1.9)%, (85.5+/-1.4)%, (67.8+/-2.0)%, and (62.4+/-3.0)%, respectively; when treated for 24 h, cell apoptotic rates were (3.4+/-1.2)%, (16.2+/-2.3)%, (28.1+/-1.5)%, (33.2+/-3.9)%, and (45.5+/-3.8)%, respectively. Pretreatment with CAT significantly rescued cells from apoptosis (P<0.05).

CONCLUSION

DDP generates ROS in esophageal cancer EC-109 cells, which causes mitochondrial membrane permeabilization and Delta psi m decrease, therefore, leads to apoptosis of EC-109 cells.