title: [Oxidative damage of NIH/3T3 cells induced by nickel smelting fumes].
abstract: OBJECTIVE
  To investigate the cytotoxicity and oxidative damage on NIH/3T3 cells induced by nickel smelting fume.
  
  
  METHODS
  NIH/3T3 cells were treated with nickel smelting fume collected from a nickel smelting factory in China with doses of 0, 6.25, 12.50, 25.00, 50.00, and 100.00 µg/ml for 6 h. Dose-dependent cytotoxicity in cells were assessed by Cell Counting Kit-8 (CCK-8), natural red uptake assay, and lactate dehydrogenase (LDH) leakage assay, and the level of oxidative damage was assessed based on the activity of catalase (CAT), percentage inhibition of superoxide dismutase (SOD), and content of malonaldehyde (MDA).
  
  
  RESULTS
  The relative survival of NIH/3T3 cells decreased with the increase in the dose of nickel smelting fume. In the CCK-8 assay, the group with 100 µg/ml nickel smelting fume showed a cell growth inhibition rate of 86%, with a significant difference compared with the control group (P < 0.05). LDH activity increased with increasing dose of nickel smelting fume: the groups of 12.50, 25, 50, and 100 µg/ml nickel smelting fume all showed increased LDH activities as compared with the control group (P < 0.05). The activities of CAT were significantly reduced in groups of 25, 50, and 100 µg/ml nickel smelting fume as compared with that of the control group (P < 0.05). As the dose of nickel smelting fume increased, the percentage inhibition of SOD and the content of MDA increased, with significant differences compared with the control group (P < 0.05).
  
  
  CONCLUSIONS
  Oxidative damage may be induced in NIH/3T3 cells after 6 h of exposure to nickel smelting fume, which leads to cell death.
authors.affiliation: Department of Occupational Medicine and Environment Health, School of Public Health, Harbin Medical University, Harbin 150086, China.
authors.forename: Jingchong
authors.initials: J
authors.lastname: Ba
authors.affiliation: Department of Occupational Medicine and Environment Health, School of Public Health, Harbin Medical University, Harbin 150086, China.
authors.forename: Yue
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Occupational Medicine and Environment Health, School of Public Health, Harbin Medical University, Harbin 150086, China.
authors.forename: Shengyuan
authors.initials: S
authors.lastname: Wang
authors.affiliation: Department of Occupational Medicine and Environment Health, School of Public Health, Harbin Medical University, Harbin 150086, China.
authors.forename: Dong
authors.initials: D
authors.lastname: Jiao
authors.affiliation: Department of Occupational Medicine and Environment Health, School of Public Health, Harbin Medical University, Harbin 150086, China. Email: wuyonghui777@163.com.
authors.forename: Yonghui
authors.initials: Y
authors.lastname: Wu
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D016923:Cell Death / Q000187:drug effects; D004391:Dust; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D008669:Metallurgy; D051379:Mice; D041681:NIH 3T3 Cells; D009532:Nickel / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D004391:Dust; D008315:Malondialdehyde; D009532:Nickel; D007770:L-Lactate Dehydrogenase; D002374:Catalase; D013482:Superoxide Dismutase