Tamoxifen does not inhibit the swell activated chloride channel in human neutrophils during the respiratory burst
- Leukocyte and Ion Channel Research Laboratory, School of Health and Biosciences, University of East London, Stratford Campus, London E15 4LZ (United Kingdom)
Effective functioning of neutrophils relies upon electron translocation through the NADPH oxidase (NOX). The electron current generated (I{sub e}) by the neutrophil NADPH oxidase is electrogenic and rapidly depolarises the membrane potential in activated human neutrophils. Swelling activated chloride channels have been demonstrated in part to counteract the depolarisation generated by the NADPH oxidase I{sub e}. In the present study, the effects of inhibitors of swell activated chloride channels on ROS production and on the swelling activated chloride conductance was investigated in activated human neutrophils. Tamoxifen (10 {mu}M), a specific inhibitor for swell activated chloride channels in neutrophils, completely inhibited both the PMA and FMLP stimulated respiratory burst. This inhibition of the neutrophil respiratory burst was not due to the blocking effect of tamoxifen on the swelling activated chloride conductance in these cells. These results demonstrate that a tamoxifen insensitive swell activated chloride channel has important significance during the neutrophil respiratory burst.
- OSTI ID:
- 21143920
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 375, Issue 4; Other Information: DOI: 10.1016/j.bbrc.2008.08.067; PII: S0006-291X(08)01591-X; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
Similar Records
Intracellular shunting of O{sub 2}{sup −} contributes to charge compensation and preservation of neutrophil respiratory burst in the absence of voltage-gated proton channel activity
Chloride channels activated by swell can regulate the NADPH oxidase generated membrane depolarisation in activated human neutrophils