title: [Effect of phosgene on apoptosis of alveolar type II cells and vascular endothelial growth factor in exposed mice].
abstract: OBJECTIVE
  To study the apoptosis of alveolar type II cells, alterations of vascular endothelial growth factor (VEGF), VEGF receptor (Flt1) in serum and lung and expression of VEGF mRNA in lung in pulmonary edema mice induced by phosgene.
  
  
  METHODS
  Twenty-six BALB/C mice were randomly divided into 2 groups: control group, exposed group (13 mice in each group). Mice of exposed group were intoxicated by inhalation of phosgene 11.9 mg/L for 5 minutes. Mice of control group were treated as the same way by inhalation of air. Isolation of mice alveolus type II cells 4 h after intoxication was carried out to observe their apoptosis under electron microscope. Contents of VEGF and Flt1 in lung and serum by ELISA, and expression of VEGF mRNA were determined.
  
  
  RESULTS
  Alveolar type II cells were identified by tannic acid staining and electron microscopy. After exposed to 11.9 mg/L of phosgene for 5 minutes, the apoptotic body in alveolus type II cells was found in exposed group. The contents of VEGF in serum and lung and Flt1 in lung of exposed mice [(134.07 +/- 120.26), (477.76 +/- 98.06), (1,2818.48 +/- 2,304.15) pg/ml] were significantly lower than those of control group [(445.57 +/- 173.30), (1,026.87 +/- 474.56), (21,976.51 +/- 7,421.01) pg/ml, P < 0.05] but the content of Flt1 in serum [(2,369.56 +/- 381.70) pg/ml] was higher than that in control group [(1,898.00 +/- 453.69) pg/ml, P < 0.05]. The expression of VEGF mRNA in pulmonary edema mice was decreased.
  
  
  CONCLUSIONS
  Phosgene can induce apoptosis of alveolar type II cells, and decrease in the content of VEGF and Flt1, and expression of VEGF mRNA in lung.
authors.affiliation: Department of Toxicology, The Fourth Military Medical University, Xi'an 710033, China.
authors.forename: Wen-li
authors.initials: WL
authors.lastname: Li
authors.forename: Chun-xu
authors.initials: CX
authors.lastname: Hai
authors.forename: Xu-jun
authors.initials: XJ
authors.lastname: Qin
authors.forename: Xin
authors.initials: X
authors.lastname: Liang
authors.forename: Hong-li
authors.initials: HL
authors.lastname: Chen
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002478:Cells, Cultured; D002619:Chemical Warfare Agents / Q000633:toxicity; D016228:Endothelial Growth Factors / Q000096:biosynthesis / Q000235:genetics; D004797:Enzyme-Linked Immunosorbent Assay; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010705:Phosgene / Q000633:toxicity*; D011650:Pulmonary Alveoli / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D011654:Pulmonary Edema / Q000139:chemically induced*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011897:Random Allocation; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis / Q000235:genetics / Q000502:physiology*; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000032:analysis / Q000235:genetics
chemical_list: D002619:Chemical Warfare Agents; D016228:Endothelial Growth Factors; D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; D010705:Phosgene; D040281:Vascular Endothelial Growth Factor Receptor-1