title: [Role of calcium activated-potassium channels in the injury to rat alveolar macrophages induced by quartz].
abstract: OBJECTIVE
  To investigate the role of calcium activated-potassium channels (KCa) in the injury to rat alveolar macrophages induced by quartz.
  
  
  METHODS
  The experiments were conducted on a rat alveolar macrophage cell line (NR8383) in vitro, where crystal silica (100 üg/ml) and amorphous silica (100 üg/ml) were used as the test substances and the cells without any treatment as negative controls. At first the effects of two kinds of quartz were compared. Then KCa special inhibitors (Paxilline for BK, Tram-34 for IK, Apamin for SK) were added in different doses to the in vitro test system with 100 üg/ml crystal quartz as matrix, to observe the function of such channels. Cell viability, lactate dehydrogenase (LDH), interleukin-1β (IL-1β) and tumor necrosis factor-a (TNF-α) were tested.
  
  
  RESULTS
  Comparing to the negative control group, cell viability reduced, LDH leakage, IL-1β and TNF-α release increased significantly in the amorphous quartz group, furthermore, the effects by crystal quartz were much more serious than those by amorphous quartz, with a statistical significance (P < 0.01). Comparing to the crystal quartz group, IK blockers (Tram-34) led to increase in cell viability significantly, with a statistical significance (P < 0.01); all the KCa specific blockers (Paxilline, Tram-34, Apamin) could reduce LDH leakage and IL-1β release, with a statistical significance (P < 0.05); meanwhile, BK and IK blockers (Paxilline,Tram-34) were able to reduce TNF-α release,with a statistical significance (P < 0.05).Reduction of IL-1β and TNF-α by Tram-34 was dose-dependent, but not so in the other two blockers.
  
  
  CONCLUSIONS
  Blocking calcium-activated potassium channels (KCa) could reduce cell membrane damage as well as IL-1β and TNF-α release induced by crystal quartz in the rat alveolar macrophages cell line in vitro, which might serve as a signal in the early regulation of inflammatory responses by quartz.
authors.affiliation: MOE Key Lab of Environmental and Occupational Health, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science & Technology, Wuhan 430030, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Li
authors.affiliation: E-mail: sunjzh@yahoo.com.cn.
authors.forename: Jingzhi
authors.initials: J
authors.lastname: Sun
authors.forename: Li
authors.initials: L
authors.lastname: Yang
authors.forename: Jing
authors.initials: J
authors.lastname: Zhao
authors.forename: Zhenglun
authors.initials: Z
authors.lastname: Wang
authors.affiliation: E-mail: Leiyang@mails.tjmu.edu.cn.
authors.forename: Lei
authors.initials: L
authors.lastname: Yang
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D002460:Cell Line; D053583:Interleukin-1beta / Q000378:metabolism; D016676:Macrophages, Alveolar / Q000166:cytology / Q000378:metabolism*; D024681:Potassium Channels, Calcium-Activated / Q000378:metabolism*; D011791:Quartz / Q000633:toxicity*; D051381:Rats; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D024681:Potassium Channels, Calcium-Activated; D014409:Tumor Necrosis Factor-alpha; D011791:Quartz; D002118:Calcium