title: Single-fraction γ-60Co radiation induces apoptosis in cultured rat C6 cells.
abstract: OBJECTIVE
  Radiotherapy is frequently applied in the treatment of malignant gliomas, but it is unclear if radiotherapy exerts its effects via induction of apoptosis. The present study was designed to determine whether a single-fraction γ-60Co radiation can induce apoptosis.
  
  
  METHODS
  In vitro cytological controlled study performed at a military medical university from October 2006 to June 2008.
  
  
  METHODS
  C6 cells were treated with a single fraction of ?-60Co radiation at various doses (0, 4, 16, and 64 Gy). The 3-(4,5)-dimethylthiazol-2)-2,5-diphenyl tetrazolium bromide (MTT) assay, apoptosis assays using Annexin V-fluorescein isothiocyanate /propidium iodide or Hoechst 33258 staining, and the cell cycle assay were performed, and the expression of p53 and p21 proteins was evaluated.
  
  
  RESULTS
  The C6 cell numbers in the 16 Gy and 64 Gy groups were much lower than in the control group at 48, 96, and 144 hours after irradiation. The irradiated cells underwent apoptosis in a dose-dependent manner. Irradiation also impacted cell cycle progression, arresting cells in the G1 phase. The p53 protein expression was shown in both the nucleus and the cytoplasm of irradiated cells, whereas p53 was only expressed in the nucleus of control (untreated) cells. The p21 protein was expressed in irradiated cells but not in control cells.
  
  
  CONCLUSIONS
  Single-fraction ?-60Co radiation inhibited C6 cell growth by inducing apoptosis and G1 arrest, which correlated with the up-regulation of the p53-p21 pathway. The extent of apoptosis and G1 arrest was positively correlated with the dose of radiation. Better understanding of apoptosis induced by radiation therapy will help design optimal dosing schedules for radiation therapy, especially in combination with chemotherapy.
authors.affiliation: Department of Vascular Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China. jfbian@yahoo.com
authors.forename: Jiefang
authors.initials: J
authors.lastname: Bian
authors.forename: Xiling
authors.initials: X
authors.lastname: Wang
authors.forename: Jun
authors.initials: J
authors.lastname: Yun
authors.forename: Ruifeng
authors.initials: R
authors.lastname: Cao
authors.forename: Yunxin
authors.initials: Y
authors.lastname: Cao
authors.forename: Jingwen
authors.initials: J
authors.lastname: Liang
authors.forename: B Fucheng
authors.initials: BF
authors.lastname: Ma
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000528:radiation effects*; D059447:Cell Cycle Checkpoints / Q000528:radiation effects*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000528:radiation effects*; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism; D004307:Dose-Response Relationship, Radiation; D059585:G1 Phase Cell Cycle Checkpoints / Q000528:radiation effects; D005720:Gamma Rays; D015972:Gene Expression Regulation, Neoplastic / Q000528:radiation effects*; D005910:Glioma / Q000235:genetics / Q000532:radiotherapy; D051381:Rats; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D050759:Cyclin-Dependent Kinase Inhibitor p21; D016159:Tumor Suppressor Protein p53