Cytotoxic effects of cigarette smoke extract on an alveolar type II cell-derived cell line

• Published in: American journal of physiology. Lung cellular and molecular physiology 2001-08, Vol.281 (2), p.509-L516
• Main Authors: Hoshino, Yuma, Mio, Tadashi, Nagai, Sonoko, Miki, Hiroyuki, Ito, Isao, Izumi, Takateru
• Format: Article
• Language: English
• Subjects: Aldehydes - pharmacology; Cell Line; Cell Survival - drug effects; Humans; Intracellular Membranes - drug effects; Intracellular Membranes - metabolism; Nicotiana; Oxidants - pharmacology; Oxidation-Reduction; Plants, Toxic; Pulmonary Alveoli - drug effects; Pulmonary Alveoli - metabolism; Pulmonary Alveoli - pathology; Pulmonary Alveoli - physiology; Smoke
• ISSN: 1040-0605; 1522-1504
• DOI: 10.1152/ajplung.2001.281.2.l509

Department of Respiratory Medicine, Kyoto University Hospital, Shogo-in, Sakyo-ku, Kyoto 606-8507, Japan Injury of the alveolar epithelium by cigarette smoke is presumed to be an important process in the pathogenesis of smoking-related pulmonary diseases. We investigated the cytotoxic effects of cigarette smoke extract (CSE) on an alveolar type II cell-derived cell line (A549). CSE caused apoptosis at concentrations of 5% or less and necrosis at 10% or more. When CSE was exposed to air before application to A549 cells, the cytotoxic effects were attenuated. CSE caused cell death without direct contact with the cells. Acrolein and hydrogen peroxide, two major volatile factors in cigarette smoke, caused cell death in a similar manner. Aldehyde dehydrogenase, a scavenger of aldehydes, and N -acetylcysteine, a scavenger of oxidants and aldehydes, completely inhibited CSE-induced apoptosis. CSE and acrolein increased intracellular oxidant activity. In conclusion, apoptosis of alveolar epithelial cells may be one of the mechanisms of lung injury induced by cigarette smoking. This cytotoxic effect might be due to an interaction between aldehydes and oxidants present in CSE or formed in CSE-exposed cells. apoptosis; oxidant; aldehyde