title: Evaluation of acute oxidative stress induced by NiO nanoparticles in vivo and in vitro.
abstract: OBJECTIVE
  Nickel oxide (NiO) is an important industrial material, and it is also a harmful agent. The toxicity of NiO is size-related: nanoparticles are more toxic than fine-particles. The toxic mechanism induced by NiO nanoparticles remains unexplained, and the relationship between in vitro and in vivo NiO toxicity results is unclear. In the present study, we focused on the oxidative stress caused by NiO nanoparticles by examining and comparing in vitro and in vivo acute responses induced by NiO nanoparticles.
  
  
  METHODS
  Cellular responses induced by black NiO nanoparticles with a primary particle size of 20 nm, were examined in human lung carcinoma A549 cells. In vivo responses were examined by instillation of NiO nanoparticles into rat trachea. Bronchoalveolar lavage fluid (BALF) was collected after intratracheal instillation at different time points, and concentrations of lipid peroxide heme oxygenase-1 (HO-1), surfactant protein-D (SP-D) and lactate dehydrogenase (LDH) in BALF were measured.
  
  
  RESULTS
  The levels of intracellular reactive oxygen species and lipid peroxidation in A549 cells increased with increasing exposure to NiO nanoparticles, and increases in gene expressions of HO-1 and SP-D were observed in A549 cells. The lipid peroxide level in BALF significantly increased after 24 h instillation but decreased three days later. LDH leakage was also observed three days later.
  
  
  CONCLUSIONS
  NiO nanoparticles induce oxidative stress-related lung injury. In vivo and in vitro oxidative stress was induced resulting in activation of antioxidant systems. Based on these responses, we conclude that the results of the in vivo and in vitro studies tend to correspond.
authors.affiliation: Health Research Institute, Ikeda, Osaka, Japan. masa-horie@aist.go.jp
authors.forename: Masanori
authors.initials: M
authors.lastname: Horie
authors.forename: Hiroko
authors.initials: H
authors.lastname: Fukui
authors.forename: Keiko
authors.initials: K
authors.lastname: Nishio
authors.forename: Shigehisa
authors.initials: S
authors.lastname: Endoh
authors.forename: Haruhisa
authors.initials: H
authors.lastname: Kato
authors.forename: Katsuhide
authors.initials: K
authors.lastname: Fujita
authors.forename: Arisa
authors.initials: A
authors.lastname: Miyauchi
authors.forename: Ayako
authors.initials: A
authors.lastname: Nakamura
authors.forename: Mototada
authors.initials: M
authors.lastname: Shichiri
authors.forename: Noriko
authors.initials: N
authors.lastname: Ishida
authors.forename: Shinichi
authors.initials: S
authors.lastname: Kinugasa
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Morimoto
authors.forename: Etsuo
authors.initials: E
authors.lastname: Niki
authors.forename: Yasukazu
authors.initials: Y
authors.lastname: Yoshida
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Iwahashi
mesh_terms: D000208:Acute Disease; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D005786:Gene Expression Regulation / Q000187:drug effects; D051547:Heme Oxygenase-1 / Q000235:genetics / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects*; D008168:Lung / Q000187:drug effects; D053758:Nanoparticles; D009532:Nickel / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects*; D037663:Pulmonary Surfactant-Associated Protein D / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D014407:Tumor Cells, Cultured
chemical_list: D037663:Pulmonary Surfactant-Associated Protein D; D017382:Reactive Oxygen Species; D009532:Nickel; C028007:nickel monoxide; D007770:L-Lactate Dehydrogenase; D051547:Heme Oxygenase-1