title: The sensitivity of digestive tract tumor cells to As2O3 is associated with the inherent cellular level of reactive oxygen species.
abstract: OBJECTIVE
  To explore the correlation of the inherent cellular ROS level with the susceptibility of the digestive tract tumor cells to apoptosis inducted by As2O3.
  
  
  METHODS
  Two gastric carcinoma cell lines, SGC7901 and MKN45, and two esophageal carcinoma cell lines, EC/CUHK1(alternatively named EC1.71) and EC1867 with low concentration(2 micromol x L(-1))of As2O3 were cultured espectly, which confirmed the difference in apoptosis susceptibility between SGC7901 and MKN45, and between EC/CUHK1 and EC1867. The cells were incubated with dihydrogenrhodamine123 (DHR123), used as a ROS capture in absence of As2O3. The fluorescent intensity of rhodamine123, which was the product of cellular oxidation of DHR123, was detected by flow cytometry, and ROS was measured.
  
  
  RESULTS
  Apoptosis induced by a low concentration of As2O3 was more readily to occur in SGC7901(22.4%+/-2.4%) and EC/CUHK1(27.0%+/-2.9%) than in MKN45(2.1%+/-0.5%) and EC1867(0.8%+/-0.5%). In other words, SGC7901 was more sensitive than MKN45 to As2O3, meanwhile EC/CUHK1 was more sensitive than EC1867 to As2O3. The level of inherent cellular ROS in SGC7901(650+/-37) was higher than that in MKN45(507+/-22)(P<0.01), and the level of inherent cellular ROS in EC/CUHK1(462+/-17) was higher than that in EC1867(187+/-12)(P<0.01).
  
  
  CONCLUSIONS
  The cellular sensitivity to apoptosis induced by As2O3 is associated with the difference in cellular ROS level. The inherent ROS level might determinate the apoptotic sensitivity of tumor cells to As2O3.
authors.affiliation: Department of Cell Biology, Shanghai Second Medical University, Shanghai 200025 China.
authors.forename: Fei
authors.initials: F
authors.lastname: Gao
authors.forename: Jing
authors.initials: J
authors.lastname: Yi
authors.forename: Gui-Ying
authors.initials: GY
authors.lastname: Shi
authors.forename: Hui
authors.initials: H
authors.lastname: Li
authors.forename: Xue-Geng
authors.initials: XG
authors.lastname: Shi
authors.forename: Xue-Ming
authors.initials: XM
authors.lastname: Tang
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D000077237:Arsenic Trioxide; D001152:Arsenicals / Q000494:pharmacology*; D004938:Esophageal Neoplasms; D005434:Flow Cytometry; D006801:Humans; D010087:Oxides / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013274:Stomach Neoplasms; D014407:Tumor Cells, Cultured / Q000166:cytology / Q000187:drug effects / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D001152:Arsenicals; D010087:Oxides; D017382:Reactive Oxygen Species; D000077237:Arsenic Trioxide