title: New insight into mitochondrial changes in vascular endothelial cells irradiated by gamma ray.
abstract: To investigate alterations of mitochondria in irradiated endothelial cells to further elucidate the mechanism underlying radiation-induced heart disease.
  
  
  
  Experiments were performed using human umbilical vein endothelial cells (HUVECs). HUVECs were irradiated with single gamma ray dose of 0, 5, 10 and 20 Gy, respectively. Apoptosis was assessed by flow cytometry at 24, 48 and 72 h post-irradiation, respectively. The intracellular reactive oxygen species (ROS) was measured with 2',7'-dichlorofluorescein-diacetate (DCFH-DA) at 24 h post-irradiation. Mitochondrial membrane potential (ΔΨm) by JC-1 and the opening of mitochondrial permeability transition pore (mPTP) by a calcein-cobalt quenching method were detected at 24 h post-irradiation in order to measure changes of mitochondria induced by gamma ray irradiation.
  
  
  
  Gamma ray irradiation increased HUVECs apoptosis in a dose-dependent and time-dependent manner. Irradiation also promoted ROS production in HUVECs in a dose-dependent manner. At 24 h post-irradiation, the results showed that irradiation decreases ΔΨm, however, paradoxically, flow cytometry showed green fluorescence instensity higher in irradiated HUVECs than in control HUVECs in an irradiation dose-dependent manner which indicated gamma ray irradiation inhibited mPTP opening in HUVECs.
  
  
  
  Gamma ray irradiation induces apoptosis and ROS production of endothelial cells, and decreases ΔΨm meanwhile contradictorily inhibiting the opening of mPTP.
authors.affiliation: a Department of Cardiology , Chinese PLA General Hospital , Beijing , China.
authors.forename: Shunying
authors.initials: S
authors.lastname: Hu
authors.affiliation: b Beijing Institute of Radiation Medicine , Beijing , China.
authors.forename: Yajing
authors.initials: Y
authors.lastname: Gao
authors.affiliation: a Department of Cardiology , Chinese PLA General Hospital , Beijing , China.
authors.forename: Hao
authors.initials: H
authors.lastname: Zhou
authors.affiliation: b Beijing Institute of Radiation Medicine , Beijing , China.
authors.forename: Fanxuan
authors.initials: F
authors.lastname: Kong
authors.affiliation: b Beijing Institute of Radiation Medicine , Beijing , China.
authors.forename: Fengjun
authors.initials: F
authors.lastname: Xiao
authors.affiliation: b Beijing Institute of Radiation Medicine , Beijing , China.
authors.forename: Pingkun
authors.initials: P
authors.lastname: Zhou
authors.affiliation: a Department of Cardiology , Chinese PLA General Hospital , Beijing , China.
authors.forename: Yundai
authors.initials: Y
authors.lastname: Chen
mesh_terms: D017209:Apoptosis / Q000502:physiology* / Q000528:radiation effects; D002478:Cells, Cultured; D004307:Dose-Response Relationship, Radiation; D042783:Endothelial Cells / Q000502:physiology* / Q000528:radiation effects / Q000648:ultrastructure; D005720:Gamma Rays; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000502:physiology* / Q000528:radiation effects; D008928:Mitochondria / Q000502:physiology* / Q000528:radiation effects / Q000648:ultrastructure; D033681:Mitochondrial Membrane Transport Proteins / Q000502:physiology* / Q000528:radiation effects / Q000648:ultrastructure; D000083162:Mitochondrial Permeability Transition Pore; D011829:Radiation Dosage; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D017382:Reactive Oxygen Species
keywords: Mitochondrial membrane potential; apoptosis; gamma ray irradiation; human umbilical vein endothelial cells; mitochondrial permeability transition pore; reactive oxygen species