Cigarette smoke extract induces oxidative stress and apoptosis in human lung fibroblasts.

نویسندگان

  • Stefano Carnevali
  • Stefano Petruzzelli
  • Biancamaria Longoni
  • Renato Vanacore
  • Roberto Barale
  • Monica Cipollini
  • Fabrizio Scatena
  • Pierluigi Paggiaro
  • Alessandro Celi
  • Carlo Giuntini
چکیده

Cigarette smoke is a mixture of chemicals having direct and/or indirect toxic effects on different lung cells. We investigated the effect of cigarette smoke on human lung fibroblasts (HFL-1) oxidation and apoptosis. Cells were exposed to various concentrations (1, 5, and 10%) of cigarette smoke extract (CSE) for 3 h, and oxidative stress and apoptosis were assessed by fluorescence-activated cell sorting and confocal laser fluorescence microscopy. Both oxidative stress and apoptosis exhibited a dose-response relationship with CSE concentrations. Lung fibroblasts also showed marked DNA fragmentation at the Comet assay after exposure to 10% CSE. Coincubation of HLF-1 cells with N-acetylcysteine (1 mM) during CSE exposure significantly reduced oxidative stress, apoptosis, and DNA fragmentation, whereas preincubation (3 h) with the glutathione-depleting agent buthionine sulfoximine (125 microM) produced a significant increase of oxidative stress. Cigarette smoke is a potent source of oxidative stress, DNA damage, and apoptosis for HFL-1 cells, and we speculate that this could contribute to the development of pulmonary emphysema in the lungs of smokers.

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عنوان ژورنال:
  • American journal of physiology. Lung cellular and molecular physiology

دوره 284 6  شماره 

صفحات  -

تاریخ انتشار 2003