title: [Regulation role of superoxide dismutase coenzyme on Fas/FasL signal transduction and apoptosis in alveolar macrophages of pneumoconiosis patients].
abstract: OBJECTIVE
  To explore the role of superoxide dismutase (SOD) coenzyme in regulation of Fas/FasL signal transduction and apoptosis of alveolar macrophages in pneumoconiosis patients.
  
  
  METHODS
  50 male and Han nationality cases, including the dust exposed workers, Phase I, II pneumoconiosis patients confirmed by local pneumoconiosis diagnosis group according to GBZ 70 - 2002 diagnosis standard, who underwent whole lung lavage treatment were chosen as subjects. Their alveolar macrophages (AMs) were collected and purified. The cells were divided into three groups: the untreated group, the Fas/FasL group and the SOD group. 5 x 10(6) purified AMs were added into incubating bottles containing DMEM for 2 hours for purifying, added with SOD coenzyme and other block reagents separately, and then incubated for 24 hours in CO(2) incubation. The cells were harvested and lysed. Western-blot were used to analyze the expressions of Fas, FasL, Caspases-8 and Caspases-3. Software of Quantity One 7.0 was used to analyze the relative quantity of Fas, FasL, Caspase-8 and Caspase-3. TUNEL and DNA fragment analysis were used to analyze AMs apoptosis.
  
  
  RESULTS
  The apoptosis index in SOD coenzyme group (9.50 +/- 2.76)% and Fas/FasL group (14.01 +/- 2.56)% was significantly lower than that of in untreated group (19.18 +/- 2.83)% (P < 0.05). The catachrestic DNA ladder appeared in untreated group, was looming in Fas/FasL group, and was not found in the SOD group. The expressions of Fas, FasL, Caspase-8 and Caspase-3 of phase I and II in SOD group were higher than in the other two groups (P < 0.05). There was no significant difference in the expression of Fas, FasL, Caspase-8 and Caspase-3 among different phases of pneumoconiosis (P > 0.05).
  
  
  CONCLUSIONS
  SOD coenzyme can effectively regulate Fas/FasL signal transduction and block AMs apoptosis.
authors: Department of Preventive Medicine, North China Coal Medical University, Tangshan, Hebei province, 063000, China.
authors: San-Qiao
authors: SQ
authors: Yao
authors: Xi-Ying
authors: XY
authors: Zhang
authors: Zhi-Yuan
authors: ZY
authors: Chen
mesh_terms: D000328:Adult; D017209:Apoptosis; D002478:Cells, Cultured; D053222:Fas Ligand Protein / Q000378:metabolism*; D006801:Humans; D016676:Macrophages, Alveolar / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011009:Pneumoconiosis / Q000378:metabolism* / Q000473:pathology; D015398:Signal Transduction; D013482:Superoxide Dismutase / Q000378:metabolism*; D019014:fas Receptor / Q000378:metabolism*
chemical_list: C491901:FAS protein, human; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D019014:fas Receptor; D013482:Superoxide Dismutase