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Regulation of Nitric Oxide by Cigarette Smoke in Airway Cells

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DOI: 10.4236/ojrd.2012.21002    3,963 Downloads   8,535 Views   Citations

ABSTRACT

Background and Objectives: Exhaled nitric oxide (NO) is decreased by smoking while oxides of nitrogen such as nitrites/nitrates (NOx) are increased. It was hypothesised that in vitro cigarette smoke extract (CSE) would either inhibit NO generation by increasing the NO synthase inhibitor, NG, NG-dimethyl-L-arginine (ADMA) or increase NOx levels via an oxidation pathway, which in turn could be inhibited by the antioxidant N-acetylcysteine NAC. Methods: Transformed airway cells (A549) were cultured with control medium, 1.0% CSE in culture medium, or 0.8 mM NAC with 1.0% CSE. Baseline L-arginine, NOx and ADMA levels were measured in the media. Conditioned media were then sampled at 1hour, 6 hours, 24 hours, 48 hours and 72 hours after incubation. Results: CSE induced significantly higher NOx levels (mean (SD) peak increase of 135.8 (126.6)% after incubation for 6 hours (p < 0.0005)). NAC pre-treatment partially reversed this effect to 35.6 (21.4)% at 6 hours (p = 0.009). ADMA levels were significantly higher in the CSE conditioned media compared with control media (p = 0.02) while NAC pre-treatment did not affect ADMA levels. Conclusions: CSE increased NOx which was partially reversed by NAC pre-treatment. ADMA levels were also increased after CSE exposure, suggesting that it activates the NO pathway via oxidative-stress while inhibition probably occurs via both ADMA and NOS.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

J. Liu, J. Wang, A. Sim, N. Mohan, S. Chow, D. Yates, X. Wang and P. Thomas, "Regulation of Nitric Oxide by Cigarette Smoke in Airway Cells," Open Journal of Respiratory Diseases, Vol. 2 No. 1, 2012, pp. 9-16. doi: 10.4236/ojrd.2012.21002.

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