title: [Nickel exposure to A549 cell damage and L-ascorbic acid interference effect].
abstract: OBJECTIVE
  Studying different concentrations of nickel smelting smoke subjects of human lung adenocarcinoma cells (A549) carcinogenic effects, discusses the influence of L-ascorbic acid protection.
  
  
  METHODS
  The A549 cells were divided into experimental and L-ascorbic acid in the intervention group. Plus exposure group concentration of nickel refining dusts were formulated 0.00, 6.25, 12.50, 25.00, 50.00, 100.00 µg/ml suspension, the intervention group on the basis of the added exposure group containing L-ascorbic acid (100 mmol/L), contact 24 h. Detection of cell viability by MTT assay. When the test substance concentration select 0.00, 25.00, 50.00, 100.00 µg/ml experiment for internal Flou-3 fluorescent probe to detect cell Ca²⁺ concentration, within DCFH-DA detect intracellular reactive oxygen (ROS) content, real-time quantitative PCR (real time, in the RT-PCR) was used to detect cell HIF-1α gene expression.
  
  
  RESULTS
  With the increase of concentration, subjects increased cell growth inhibition rate, intracellular Ca²⁺ concentration increases, ROS content increased, HIF-1α gene expression increased, differences were statistically significant (P < 0.05). After L-ascorbic acid intervention treatment, the results of the intervention group were lower than that of the experimental group, and the difference was statistically significant (P < 0.05), so L-ascorbic acid can effectively protect the nickel exposure damage to cells.
  
  
  CONCLUSIONS
  With subjects following exposure to nickel concentration increased, its effect on A549 cell damage increases, L-ascorbic acid cell damage caused by nickel has certain protective effect.
authors.affiliation: School of Public Heath, Harbin Medical University, Harbin 150081, China.
authors.forename: Yao
authors.initials: Y
authors.lastname: Fu
authors.affiliation: School of Public Heath, Harbin Medical University, Harbin 150081, China.
authors.forename: Yue
authors.initials: Y
authors.lastname: Wang
authors.affiliation: School of Public Heath, Harbin Medical University, Harbin 150081, China.
authors.forename: Han
authors.initials: H
authors.lastname: Dan
authors.affiliation: School of Public Heath, Harbin Medical University, Harbin 150081, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Zhang
authors.affiliation: School of Public Heath, Harbin Medical University, Harbin 150081, China.
authors.forename: Wenhan
authors.initials: W
authors.lastname: Ma
authors.affiliation: School of Public Heath, Harbin Medical University, Harbin 150081, China.
authors.forename: Yulin
authors.initials: Y
authors.lastname: Pan
authors.affiliation: School of Public Heath, Harbin Medical University, Harbin 150081, China; E-mail: wuyonghui777@163.com.
authors.forename: Yonghui
authors.initials: Y
authors.lastname: Wu
mesh_terms: D000230:Adenocarcinoma; D000077192:Adenocarcinoma of Lung; D001205:Ascorbic Acid / Q000737:chemistry*; D002118:Calcium / Q000378:metabolism; D045744:Cell Line, Tumor; D002470:Cell Survival; D003470:Culture Media / Q000737:chemistry; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D008175:Lung Neoplasms; D008669:Metallurgy; D009532:Nickel / Q000633:toxicity*; D016273:Occupational Exposure; D020011:Protective Agents / Q000737:chemistry*; D017382:Reactive Oxygen Species / Q000378:metabolism; D012906:Smoke
chemical_list: D003470:Culture Media; C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D020011:Protective Agents; D017382:Reactive Oxygen Species; D012906:Smoke; D009532:Nickel; D001205:Ascorbic Acid; D002118:Calcium