Sulfate transport in human neutrophils.

The Journal of General Physiology
L Simchowitz, A O Davis

Abstract

The mechanism by which SO4(2-) is transported across the plasma membrane of isolated human neutrophils was investigated. Unlike the situation in erythrocytes, SO4(2-) and other divalent anions are not substrates for the principal Cl-/HCO3- exchange system in these cells. At an extracellular concentration of 2 mM, total one-way 35SO4(2-) influx and efflux in steady-state cells amounted to approximately 17 mumol/liter of cell water per min. The intracellular SO4(2-) content was approximately 1 mM, approximately 25-fold higher than the passive distribution level. Internal Cl- trans stimulated 35SO4(2-) influx. Conversely, 35SO4(2-) efflux was trans stimulated by external Cl- (Km approximately 25 mM) and by external SO4(2-) (Km approximately 14 mM), implying the presence of a SO4(2-)/Cl- countertransport mechanism. The exchange is noncompetitively inhibited by 4-acetamido-4'-isothiocyanostilbene-2,2' -disulfonate (SITS) (Ki approximately 50 microM) and competitively blocked by alpha-cyano-4-hydroxycinnamate (Ki approximately 230 microM) and by ethacrynate (Ki approximately 7 microM); furosemide and probenecid also suppressed activity. The carrier exhibits broad specificity for a variety of monovalent (NO3- approximately Cl- greater...Continue Reading

Citations

Nov 1, 1992·Pediatric Nephrology : Journal of the International Pediatric Nephrology Association·D R Pena, R E Neiberger
Aug 1, 1997·The Journal of General Physiology·C W ChowS Grinstein
Jan 7, 2003·The Tohoku Journal of Experimental Medicine·Hideki MitsuhashiYoshihisa Nojima
Jan 14, 2004·Canadian Journal of Physiology and Pharmacology·David CauviOdile M Chabaud
Apr 18, 1997·The Journal of Biological Chemistry·S M KrischerM J Mueller
Apr 1, 1992·The American Journal of Physiology·Z I Cabantchik, R Greger

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