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Am J Physiol Lung Cell Mol Physiol 283: L409-L417, 2002. First published April 5, 2002; doi:10.1152/ajplung.00059.2002
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Vol. 283, Issue 2, L409-L417, August 2002

Glutathione prevents inhibition of fibroblast-mediated collagen gel contraction by cigarette smoke

Hui Jung Kim1,2, Xiangde Liu2, Hangjun Wang3, Tadashi Kohyama4, Tetsu Kobayashi2, Fu-Qiang Wen2, Debra J. Romberger2, Shinji Abe2, William MacNee5, Irfan Rahman6, and Stephen I. Rennard2

1 Pulmonary Division, Department of Internal Medicine, Seoul Adventist Hospital, Seoul 130-650, Korea; 2 Pulmonary and Critical Care Medicine Section, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska 68198-5125; 3 Mount Sinai Hospital, Pathology and Laboratory Medicine, Toronto, Ontario, Canada M5G 1X5; 4 Department of Respiratory Medicine, University of Tokyo, Tokyo 113-8655, Japan; 5 Edinburgh Lung and the Environment Group Initiative, Colt Research Labs, Edinburgh; and 6 Department of Respiratory Medicine, Medical School, University of Edinburgh, Edinburgh EH8 9AG, United Kingdom

Cigarette smoke, the major risk factor for the development of emphysema, contains over 4,700 chemical compounds, including free radicals and other oxidants (1014/puff). An imbalance between oxidants and antioxidants has been proposed in the pathogenesis of chronic obstructive pulmonary disease. Inhibition of repair processes has been suggested to be one pathway contributing to the development of emphysema. We hypothesized that cigarette smoke inhibition of repair might result from a shift of the oxidant/antioxidant balance in favor of oxidants. To evaluate this hypothesis, N-acetyl-L-cysteine (NAC), which serves as a substrate for glutathione (GSH) production, and buthionine sulfoximine (BSO), which inhibits GSH production, were incubated in the presence and absence of cigarette smoke extract (CSE) with fibroblasts in three-dimensional collagen gels. Neither agent alone altered gel contraction. CSE inhibition of gel contraction, however, was mitigated by NAC and potentiated by BSO. Parallel effects were observed on cigarette smoke inhibition of fibronectin production and mRNA expression as well as by changes in intracellular GSH content. Pretreatment of fibroblasts with NAC or BSO resulted in similar effects, suggesting that neither agent was acting directly on smoke but, rather, was altering cellular response to smoke. In conclusion, smoke inhibition of fibroblast repair, as reflected by collagen gel contraction and fibronectin production, may be modulated by intracellular GSH levels.

chronic obstructive pulmonary disease; oxidants


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