title: Oxidative stress in lung epithelial cells from patients with idiopathic interstitial pneumonias.
abstract: Lung epithelial cells are a primary target for reactive oxygen species (ROS). ROS can cause oxidative deoxyribonucleic acid modification, such as 8-hydroxy-deoxyguanosine (8-OHdG). A human homologue of the MutT protein (hMTH1) prevents this modification. Mitochondria are the most important cellular source of ROS and may be susceptible to oxidative damage. The purpose of this study is to investigate oxidative stress and mitochondrial damage in lung epithelial cells from idiopathic interstitial pneumonias (IIPs). The authors analysed 8-OHdG, hMTH1, and mitochondrial proteins on lung specimens from 13 patients with IlPs consisted of eight patients with usual interstitial pneumonia and five patients with nonspecific interstitial pneumonia using Western blot analysis and immunohistochemistry. Immunoreactivity for 8-OHdG and hMTH1 was significantly increased in the lung epithelial cells from patients with IIPs compared with controls. The expression of hMTH1 was localised in the nuclear and cytoplasmic, but not the mitochondrial, fraction of lung homogenates. Immunoreactivity for mitochondrial protein and cytochrome c oxidase complex subunit IV was increased in the lung epithelial cells from patients with IIPs compared with controls. The current study concludes that oxidative stress may participate in epithelial cell damage in idiopathic interstitial pneumonia, and that increased mitochondrial mass may associate with increased reactive oxygen species production in idiopathic interstitial pneumonia.
authors.affiliation: Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. kkuwano@kokyu.med.kyushu-u.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Kuwano
authors.forename: N
authors.initials: N
authors.lastname: Nakashima
authors.forename: I
authors.initials: I
authors.lastname: Inoshima
authors.forename: N
authors.initials: N
authors.lastname: Hagimoto
authors.forename: M
authors.initials: M
authors.lastname: Fujita
authors.forename: M
authors.initials: M
authors.lastname: Yoshimi
authors.forename: T
authors.initials: T
authors.lastname: Maeyama
authors.forename: N
authors.initials: N
authors.lastname: Hamada
authors.forename: K
authors.initials: K
authors.lastname: Watanabe
authors.forename: N
authors.initials: N
authors.lastname: Hara
mesh_terms: D015153:Blotting, Western; D045643:DNA Repair Enzymes; D003839:Deoxyadenosines / Q000032:analysis; D003576:Electron Transport Complex IV / Q000032:analysis; D004847:Epithelial Cells / Q000502:physiology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008168:Lung / Q000737:chemistry / Q000378:metabolism* / Q000473:pathology; D017563:Lung Diseases, Interstitial / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D008928:Mitochondria / Q000473:pathology; D024101:Mitochondrial Proteins / Q000032:analysis; D018384:Oxidative Stress; D010744:Phosphoric Monoester Hydrolases / Q000032:analysis
chemical_list: D003839:Deoxyadenosines; D024101:Mitochondrial Proteins; C078251:2'-deoxy-7,8-dihydro-8-oxoadenosine; D003576:Electron Transport Complex IV; D010744:Phosphoric Monoester Hydrolases; C078207:8-oxodGTPase; D045643:DNA Repair Enzymes