It has been suggested that curcumin and other sarcoplasmic/endoplasmic reticulum Ca2+-pump inhibitors could correct the defect in the most common mutation (ΔF508) in cystic fibrosis (CF), and restore normal chloride transport. In the present study, the effect of curcumin was tested on baby hamster kidney (BHK) cells transfected with ΔF508-CFTR, a CF airway epithelial cell line (CFBE), and cells isolated from the nasal epithelium of CF-patient homozygous for the ΔF508-mutation. Curcumin had a small effect on basal (non-CFTR-mediated) chloride efflux in CFBE and CF nasal epithelial cells, but did not increase the net cAMP-activated (CFTR-mediated) chloride efflux. Curcumin caused a small increase in net cAMP-activated chloride efflux from ΔF508-CFTR BHK cells. Immunocytochemical analysis failed to show significant movement of ΔF508-CFTR to the plasma membrane in ΔF508-CFTR BHK cells or CFBE cells. It is concluded that it is unlikely that curcumin has a significant positive effect on CFTR-mediated chloride transport in airway epithelial cells.