%0 Journal Article
%T Regulation of Nitric Oxide by Cigarette Smoke in Airway Cells
%A Jia Liu
%A Jun Wang
%A Ah Siew Sim
%A Nitin Mohan
%A Sharron Chow
%A Deborah H. Yates
%A Xingli Wang
%A Paul S. Thomas
%J Open Journal of Respiratory Diseases
%P 9-16
%@ 2163-9418
%D 2012
%I Scientific Research Publishing
%R 10.4236/ojrd.2012.21002
%X Background and Objectives: Exhaled nitric oxide (NO) is decreased by smoking while oxides of nitrogen such as nitrites/nitrates (NO<sub>x</sub>) are increased. It was hypothesised that <i>in vitro</i> cigarette smoke extract (CSE) would either inhibit NO generation by increasing the NO synthase inhibitor, NG, NG-dimethyl-L-arginine (ADMA) or increase NO<sub>x</sub> 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, NO<sub>x</sub> 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 NO<sub>x</sub> levels (mean (SD) peak increase of 135.8 (126.6)% after incubation for 6 hours (p &lt; 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 NO<sub>x</sub> 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.
%K Airway
%K Cigarette
%K Nitric Oxide
%K Nitric Oxide Synthase
%K N-Acetylcysteine
%K NG
%K NG-Dimethyl-L-Arginine
%U http://www.scirp.org/journal/PaperInformation.aspx?PaperID=17714