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Articles in PresS, published online ahead of print April 5, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00059.2002
Submitted on February 12, 2002
Accepted on April 2, 2002
1 Pulmonary Division, Seoul Adventist Hospital, Seoul, Korea, Republic of; Pulmonary and Critical Care Medicine Section, University of Nebraska Medical Center, Omaha, NE, USA
2 Pulmonary and Critical Care Medicine Section, University of Nebraska Medical Center, Omaha, NE, USA
3 Pathology and Laboratory Medicine, Mt. Sinai Hospital, Toronto, Ontario, Canada
4 Department of Respiratory Medicine, University of Tokyo, Tokyo, Japan
5 Colt Research Labs, ELEGI, Edinburgh, Scotland, United Kingdom
6 Department of Respiratory Medicine, University of Edinburgh, Edinburgh, Scotland, United Kingdom
* To whom correspondence should be addressed. E-mail: srennard{at}unmc.edu.
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 (COPD). 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, the effect of 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 glutathione content. Pre-treatment 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 glutathione levels.
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