Journal
CELL BIOLOGY INTERNATIONAL
Volume 33, Issue 3, Pages 268-275Publisher
WILEY
DOI: 10.1016/j.cellbi.2008.11.012
Keywords
Acetylcholinesterase; Erythrocyte; Nitric oxide; Redox thiol status; S-nitrosothiols
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Funding
- GAPIC Department (Gabinete de Apoio a 'Investigacao Cientifica, Tecnologica e de Inovacao) of Lisbon University Faculty of Medicine
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We assessed the redox thiol status influence on nitric oxide (NO) metabolism and efflux in erythrocytes stimulated with acetylcholinesterase substrate (acetylcholine, ACh) and inhibitor (velnacrine maleate, VM). Erythrocyte suspensions from healthy donors were incubated with increasing concentrations of dithiothreitol (1-50 mu M), in the presence and absence of acetylcholine/velnacrine (10 mu M). Levels of NO, nitrite/nitrate, S-nitrosohemoglobin, peroxynitrite and S-nitrosoglutathione were determined by spectrofluorimetric and spectrophotometric methods. Dithiothreitol significantly mobilized NO toward nitrite/nitrate and S-nitrosoglutathione, and decreased the amount of NO efflux. Both ACh/VM induce changes on the levels of erythrocyte nitrite/nitrate dependent on the DTT concentration. Higher levels of peroxynitrite and S-nitrosoglutathione were seen with velnacrine in presence of DTT 1 and 50 mu M. We concluded that dithiothreitol-induced activation of erythrocyte thiol status decreases NO efflux and allows greater intracellular NO mobilization onto different derivative molecules, both in the absence and presence of acetylcholinesterase substrate and inhibitor. (C) 2008 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.
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