Cell Biol Int. 2009 Oct 20
The effect of N-acetylcysteine on chloride efflux from airway epithelial cells.
Varelogianni G, Oliynyk I, Roomans GM, Johannesson M.
Defective chloride transport in epithelial cells increases mucus viscosity and leads to recurrent infections with high oxidative stress in patients with cystic fibrosis (CF). N-acetylcysteine (NAC) is a well known mucolytic and antioxidant drug, and an indirect precursor of glutathione.
Since S-nitrosoglutathione (GSNO) previously has been shown to be able to promote Cl- efflux from CF airway epithelial cells, it was investigated whether NAC also could stimulate Cl- efflux from CF and non-CF epithelial cells and through which mechanisms.
CF bronchial epithelial cells (CFBE) and normal bronchial epithelial cells (16HBE) were treated with 1mM, 5mM, 10mM or 15mM NAC for 4h at 37 degrees C. The effect of NAC on Cl- transport was measured by Chloride efflux measurements and by X-ray microanalysis. Cl- efflux from CFBE cells was stimulated by NAC in a dose dependent manner, with 10mM NAC causing a significant increase in Cl- efflux with nearly 80% in CFBE cells.
The intracellular Cl- concentration in CFBE cells was significantly decreased up to 60 % after 4h treatment with 10mM NAC. Moreover immunocytochemistry and Western Blot experiments revealed expression of CFTR channel on CFBE cells after treatment with 10mM NAC.
The stimulation of Cl- efflux by NAC in CF airway epithelial cells may improve hydration of the mucus and thereby be beneficial for CF patients.