RT Journal Article
SR Electronic
T1 Oxidative stress in lung epithelial cells from patients with idiopathic interstitial pneumonias
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 232
OP 240
DO 10.1183/09031936.03.00063203
VO 21
IS 2
A1 K. Kuwano
A1 N. Nakashima
A1 I. Inoshima
A1 N. Hagimoto
A1 M. Fujita
A1 M. Yoshimi
A1 T. Maeyama
A1 N. Hamada
A1 K. Watanabe
A1 N. Hara
YR 2003
UL http://erj.ersjournals.com/content/21/2/232.abstract
AB 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 IIPs 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. This work was supported by a Grant-in-Aid for Scientific Research (13670604) from the Ministry of Education, Science and Culture of Japan.